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ATP + 1-phosphatidyl-1D-myo-inositol 4-phosphate
ADP + 1-phosphatidyl-1D-myo-inositol 3,4-bisphosphate
ATP + phosphatidylinositol
ADP + phosphatidylinositol 3-phosphate
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-
-
?
ATP + 1-phosphatidyl-1D-myo-inositol 4-phosphate
ADP + 1-phosphatidyl-1D-myo-inositol 3,4-bisphosphate
ATP + 1-phosphatidyl-1D-myo-inositol-4-phosphate
ADP + 1-phosphatidyl-1D-myo-inositol 3,4-bisphosphate
ATP + phosphatidylinositol
ADP + phosphatidylinositol 3-phosphate
ATP + phosphoinositides
ADP + ?
additional information
?
-
ATP + 1-phosphatidyl-1D-myo-inositol 4-phosphate
ADP + 1-phosphatidyl-1D-myo-inositol 3,4-bisphosphate
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-
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?
ATP + 1-phosphatidyl-1D-myo-inositol 4-phosphate
ADP + 1-phosphatidyl-1D-myo-inositol 3,4-bisphosphate
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-
-
?
ATP + 1-phosphatidyl-1D-myo-inositol 4-phosphate
ADP + 1-phosphatidyl-1D-myo-inositol 3,4-bisphosphate
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-
-
?
ATP + 1-phosphatidyl-1D-myo-inositol 4-phosphate
ADP + 1-phosphatidyl-1D-myo-inositol 3,4-bisphosphate
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-
-
?
ATP + 1-phosphatidyl-1D-myo-inositol 4-phosphate
ADP + 1-phosphatidyl-1D-myo-inositol 3,4-bisphosphate
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-
-
?
ATP + 1-phosphatidyl-1D-myo-inositol 4-phosphate
ADP + 1-phosphatidyl-1D-myo-inositol 3,4-bisphosphate
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-
-
?
ATP + 1-phosphatidyl-1D-myo-inositol 4-phosphate
ADP + 1-phosphatidyl-1D-myo-inositol 3,4-bisphosphate
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-
-
?
ATP + 1-phosphatidyl-1D-myo-inositol-4-phosphate
ADP + 1-phosphatidyl-1D-myo-inositol 3,4-bisphosphate
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-
-
?
ATP + 1-phosphatidyl-1D-myo-inositol-4-phosphate
ADP + 1-phosphatidyl-1D-myo-inositol 3,4-bisphosphate
at 10% of the activity with phosphatidylinositol, phosphorylation only in presence of Mg2+, not in presence of Ca2+
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?
ATP + phosphatidylinositol
ADP + phosphatidylinositol 3-phosphate
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-
-
?
ATP + phosphatidylinositol
ADP + phosphatidylinositol 3-phosphate
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-
?
ATP + phosphatidylinositol
ADP + phosphatidylinositol 3-phosphate
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-
-
?
ATP + phosphoinositides
ADP + ?
enzyme plays a role in cellular signalling pathways, e.g. the insulin signalling pathways acting via class Ia and PI3K-C2alpha isozymes synthesizing 1-phosphatidyl-1D-myo-inositol 3,4,5-trisphosphate and affecting the glucose metabolism, the enzyme antagonizes with phosphatases both regulating the signalling pathways together, the enzyme is also involved in insulin resistance in peripheral tissues, overview
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-
?
ATP + phosphoinositides
ADP + ?
phosphorylation of the D-3 position on the inositol ring
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-
?
additional information
?
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ATP and substrate binding of PI3K isozymes, overview
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-
-
additional information
?
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ATP and substrate binding of PI3K isozymes, overview
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additional information
?
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ATP and substrate binding of PI3K isozymes, overview
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-
-
additional information
?
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the class II phosphoinositide 3-kinase C2.alpha. is activated by clathrin and regulates clathrin-mediated membrane trafficking
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-
?
additional information
?
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PI3K-C2alpha and PI3K-C2beta represent two downstream targets of the activated epidermal growth factor
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-
?
additional information
?
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enzyme regulation, overview
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?
additional information
?
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isozyme PI3K-C2alpha is a crucial survival factor for the cell
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?
additional information
?
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the isozymes activate different signalling cascades via stem cell factor SCF in overexpressing cancer cell lines, e.g. association with c-Met, IGF-IR, regulation, class II PI3K C2beta blocks both protein kinase and small lung cell carcinoma in reponse to stem cell factor, polypeptide growth factors induce the recruitment of class IA and II isozymes to phosphotyrosine-containing signalling complexes, detailed overview
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-
?
additional information
?
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PI3KC2alpha functions in vascular smooth muscle contraction, priming of neurosecretory granule exocytosis, insulin signalling and clathrin-mediated membrane trafficking.
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?
additional information
?
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PI3KC2alpha functions in vascular smooth muscle contraction, priming of neurosecretory granule exocytosis, insulin signalling and clathrin-mediated membrane trafficking.
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?
additional information
?
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PI3KC2alpha functions in vascular smooth muscle contraction, priming of neurosecretory granule exocytosis, insulin signalling and clathrin-mediated membrane trafficking.
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?
additional information
?
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PI3KC2beta functions in cell migration, and PTK receptor signalling
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?
additional information
?
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PI3KC2beta functions in cell migration, and PTK receptor signalling
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?
additional information
?
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PI3KC2beta functions in cell migration, and PTK receptor signalling
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?
additional information
?
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PI3KC2beta regulates the migration and survival of human tumor cells by distinct molecular mechanisms. Phosphoinositide 3-kinase C2beta regulates cytoskeletal organization and cell migration via Rac-dependent mechanisms
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?
additional information
?
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ATP and substrate binding of PI3K isozymes, overview
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-
additional information
?
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ATP and substrate binding of PI3K isozymes, overview
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-
additional information
?
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ATP and substrate binding of PI3K isozymes, overview
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(5Z)-5-[[5-(4-fluoro-2-hydroxyphenyl)furan-2-yl]methylidene]-1,3-thiazolidine-2,4-dione
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2-amino-N-[(1S)-1-[8-[(1-methyl-1H-pyrazol-4-yl)ethynyl]-1-oxo-2-phenyl-1,2-dihydroisoquinolin-3-yl]ethyl]pyrazolo[1,5-a]pyrimidine-3-carboxamide
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3-amino-N-[3-(3,5-dimethoxyanilino)pyrazin-2-yl]benzene-1-sulfonamide
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5-[2,6-bis(morpholin-4-yl)pyrimidin-4-yl]-4-(trifluoromethyl)pyridin-2-amine
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6-[5-(2,2-dimethylpropane-1-sulfonyl)pyridin-3-yl]-8-fluoro[1,2,4]triazolo[1,5-a]pyridin-2-amine
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(2S)-N1-[4-methyl-5-[3-(trifluoromethyl)phenyl]-1,3-thiazol-2-yl]pyrrolidine-1,2-dicarboxamide
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2-([(1R)-1-[7-methyl-2-(morpholin-4-yl)-4-oxo-4H-pyrido[1,2-a]pyrimidin-9-yl]ethyl]amino)benzoic acid
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2-methyl-1-[[2-methyl-3-(trifluoromethyl)phenyl]methyl]-6-(morpholin-4-yl)-1H-benzimidazole-4-carboxylic acid
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3-amino-N-[3-(3,5-dimethoxyanilino)pyrazin-2-yl]benzene-1-sulfonamide
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3-[4-(morpholin-4-yl)pyrido[3',2':4,5]furo[3,2-d]pyrimidin-2-yl]phenol
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4-[(3-chloro-4-fluorophenyl)methyl]-6-[(Z)-(4-oxo-2-sulfanylidene-1,3-thiazolidin-5-ylidene)methyl]-2H-1,4-benzoxazin-3(4H)-one
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5-[2,6-bis(morpholin-4-yl)pyrimidin-4-yl]-4-(trifluoromethyl)pyridin-2-amine
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8-[(1R)-1-(3,5-difluoroanilino)ethyl]-N,N-dimethyl-2-(morpholin-4-yl)-4-oxo-4H-1-benzopyran-6-carboxamide
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adipokines
block insulin signalling via PI3K isozymes
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Caffeine
might inhibit the enzyme
ceramide
selective inhibition of PI3KC2beta
cytokines
block insulin signalling via PI3K isozymes
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N-(5-[4-chloro-3-[(2-hydroxyethyl)sulfamoyl]phenyl]-4-methyl-1,3-thiazol-2-yl)acetamide
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N-(7,8-dimethoxy-2,3-dihydroimidazo[1,2-c]quinazolin-5-yl)pyridine-3-carboxamide
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N-[2-[3-[(benzenesulfonyl)amino]phenyl]-4-(morpholin-4-yl)quinazolin-6-yl]acetamide
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N-[3-(2-chloro-5-hydroxyanilino)pyrazin-2-yl]benzenesulfonamide
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N-[4-(morpholin-4-yl)-2-[3-[(naphthalene-2-sulfonyl)amino]phenyl]quinazolin-6-yl]acetamide
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naringenin
might inhibit the enzyme
[6-(2-amino-1,3-benzoxazol-5-yl)imidazo[1,2-a]pyridin-3-yl](morpholin-4-yl)methanone
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LY294002
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LY294002
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IC50: 0.019 mM, maximal inhibition at 1 mM
Wortmannin
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Wortmannin
low inhibition
Wortmannin
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IC50: 420 nM, maximal inhibition at 10 mM
Wortmannin
class I isozyme inhibitor, isozyme PI3K-C2alpha is resistant to inhibition
additional information
no or poor inhibition by GDC-0941, (2S)-N1-[4-methyl-5-[3-(trifluoromethyl)phenyl]-1,3-thiazol-2-yl]pyrrolidine-1,2-dicarboxamide, 2-([(1R)-1-[7-methyl-2-(morpholin-4-yl)-4-oxo-4H-pyrido[1,2-a]pyrimidin-9-yl]ethyl]amino)benzoic acid, idelalisib, N-(7,8-dimethoxy-2,3-dihydroimidazo[1,2-c]quinazolin-5-yl)pyridine-3-carboxamide, N-(5-[4-chloro-3-[(2-hydroxyethyl)sulfamoyl]phenyl]-4-methyl-1,3-thiazol-2-yl)acetamide, 4-[(3-chloro-4-fluorophenyl)methyl]-6-[(Z)-(4-oxo-2-sulfanylidene-1,3-thiazolidin-5-ylidene)methyl]-2H-1,4-benzoxazin-3(4H)-one, dactolisib, ZSTK474, AZD 3147, 5-[4-[(methanesulfonyl)methyl]-6-(morpholin-4-yl)pyrimidin-2-yl]-1H-indole, gedatolisib, 4'-(cyclopropylmethyl)-N2-(pyridin-4-yl)[4,5'-bipyrimidine]-2,2'-diamine, 1-([2-[(2-chloropyridin-4-yl)amino]-4'-(cyclopropylmethyl)[4,5'-bipyrimidin]-2'-yl]amino)-2-methylpropan-2-ol, SAR405, (2S)-2-amino-1-(4-[4-[2-(difluoromethyl)-1H-benzimidazol-1-yl]-6-(morpholin-4-yl)-1,3,5-triazin-2-yl]piperazin-1-yl)-3-phenylpropan-1-one, N-[4-(morpholin-4-yl)-2-[3-[(naphthalene-2-sulfonyl)amino]phenyl]quinazolin-6-yl]acetamide, N-[2-[3-[(benzenesulfonyl)amino]phenyl]-4-(morpholin-4-yl)quinazolin-6-yl]acetamide, N-(3-[[3-(2-chloro-5-methoxyanilino)quinoxalin-2-yl]sulfamoyl]phenyl)-2-methylalaninamide, N-[3-(3,5-dimethoxyanilino)quinoxalin-2-yl]-4-fluorobenzene-1-sulfonamide, and N-[3-(2-chloro-5-hydroxyanilino)pyrazin-2-yl]benzenesulfonamide
-
additional information
no or poor inhibition by GDC-0941, (2S)-N1-[4-methyl-5-[3-(trifluoromethyl)phenyl]-1,3-thiazol-2-yl]pyrrolidine-1,2-dicarboxamide, 2-([(1R)-1-[7-methyl-2-(morpholin-4-yl)-4-oxo-4H-pyrido[1,2-a]pyrimidin-9-yl]ethyl]amino)benzoic acid, idelalisib, N-(7,8-dimethoxy-2,3-dihydroimidazo[1,2-c]quinazolin-5-yl)pyridine-3-carboxamide, N-(5-[4-chloro-3-[(2-hydroxyethyl)sulfamoyl]phenyl]-4-methyl-1,3-thiazol-2-yl)acetamide, 4-[(3-chloro-4-fluorophenyl)methyl]-6-[(Z)-(4-oxo-2-sulfanylidene-1,3-thiazolidin-5-ylidene)methyl]-2H-1,4-benzoxazin-3(4H)-one, dactolisib, ZSTK474, AZD 3147, 5-[4-[(methanesulfonyl)methyl]-6-(morpholin-4-yl)pyrimidin-2-yl]-1H-indole, gedatolisib, 4'-(cyclopropylmethyl)-N2-(pyridin-4-yl)[4,5'-bipyrimidine]-2,2'-diamine, 1-([2-[(2-chloropyridin-4-yl)amino]-4'-(cyclopropylmethyl)[4,5'-bipyrimidin]-2'-yl]amino)-2-methylpropan-2-ol, SAR405, (2S)-2-amino-1-(4-[4-[2-(difluoromethyl)-1H-benzimidazol-1-yl]-6-(morpholin-4-yl)-1,3,5-triazin-2-yl]piperazin-1-yl)-3-phenylpropan-1-one, N-[4-(morpholin-4-yl)-2-[3-[(naphthalene-2-sulfonyl)amino]phenyl]quinazolin-6-yl]acetamide, N-[2-[3-[(benzenesulfonyl)amino]phenyl]-4-(morpholin-4-yl)quinazolin-6-yl]acetamide, N-(3-[[3-(2-chloro-5-methoxyanilino)quinoxalin-2-yl]sulfamoyl]phenyl)-2-methylalaninamide, N-[3-(3,5-dimethoxyanilino)quinoxalin-2-yl]-4-fluorobenzene-1-sulfonamide, and N-[3-(2-chloro-5-hydroxyanilino)pyrazin-2-yl]benzenesulfonamide
-
additional information
no or poor inhibition by GDC-0941, (2S)-N1-[4-methyl-5-[3-(trifluoromethyl)phenyl]-1,3-thiazol-2-yl]pyrrolidine-1,2-dicarboxamide, 2-([(1R)-1-[7-methyl-2-(morpholin-4-yl)-4-oxo-4H-pyrido[1,2-a]pyrimidin-9-yl]ethyl]amino)benzoic acid, idelalisib, N-(7,8-dimethoxy-2,3-dihydroimidazo[1,2-c]quinazolin-5-yl)pyridine-3-carboxamide, N-(5-[4-chloro-3-[(2-hydroxyethyl)sulfamoyl]phenyl]-4-methyl-1,3-thiazol-2-yl)acetamide, 4-[(3-chloro-4-fluorophenyl)methyl]-6-[(Z)-(4-oxo-2-sulfanylidene-1,3-thiazolidin-5-ylidene)methyl]-2H-1,4-benzoxazin-3(4H)-one, dactolisib, ZSTK474, AZD 3147, 5-[4-[(methanesulfonyl)methyl]-6-(morpholin-4-yl)pyrimidin-2-yl]-1H-indole, gedatolisib, 4'-(cyclopropylmethyl)-N2-(pyridin-4-yl)[4,5'-bipyrimidine]-2,2'-diamine, 1-([2-[(2-chloropyridin-4-yl)amino]-4'-(cyclopropylmethyl)[4,5'-bipyrimidin]-2'-yl]amino)-2-methylpropan-2-ol, SAR405, (2S)-2-amino-1-(4-[4-[2-(difluoromethyl)-1H-benzimidazol-1-yl]-6-(morpholin-4-yl)-1,3,5-triazin-2-yl]piperazin-1-yl)-3-phenylpropan-1-one, N-[4-(morpholin-4-yl)-2-[3-[(naphthalene-2-sulfonyl)amino]phenyl]quinazolin-6-yl]acetamide, N-[2-[3-[(benzenesulfonyl)amino]phenyl]-4-(morpholin-4-yl)quinazolin-6-yl]acetamide, N-(3-[[3-(2-chloro-5-methoxyanilino)quinoxalin-2-yl]sulfamoyl]phenyl)-2-methylalaninamide, N-[3-(3,5-dimethoxyanilino)quinoxalin-2-yl]-4-fluorobenzene-1-sulfonamide, and N-[3-(2-chloro-5-hydroxyanilino)pyrazin-2-yl]benzenesulfonamide
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additional information
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introduction of phosphatidylserine, produces an 8fold decrease in Vmax for ATP using phosphatidylinositol. Without phosphatidylserine, phosphatidylinositol 4-phosphate produces non-linear enzyme kinetics
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additional information
enzyme is regulated by several feedback inhibition possibilities in the insulin signalling pathway, overview
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additional information
no or poor inhibition by buparlisib, (8S)-2-[(3R)-3-methylmorpholin-4-yl]-9-(3-methyl-2-oxobutyl)-8-(trifluoromethyl)-6,7,8,9-tetrahydro-4H-pyrimido[1,2-a]pyrimidin-4-one, AZD3147, 5-[4-[(methanesulfonyl)methyl]-6-(morpholin-4-yl)pyrimidin-2-yl]-1H-indole, gedatolisib, 4'-(cyclopropylmethyl)-N2-(pyridin-4-yl)[4,5'-bipyrimidine]-2,2'-diamine, 1-([2-[(2-chloropyridin-4-yl)amino]-4'-(cyclopropylmethyl)[4,5'-bipyrimidin]-2'-yl]amino)-2-methylpropan-2-ol, SAR405, (2S)-2-amino-1-(4-[4-[2-(difluoromethyl)-1H-benzimidazol-1-yl]-6-(morpholin-4-yl)-1,3,5-triazin-2-yl]piperazin-1-yl)-3-phenylpropan-1-one, N-(3-[[3-(2-chloro-5-methoxyanilino)quinoxalin-2-yl]sulfamoyl]phenyl)-2-methylalaninamide, and N-[3-(3,5-dimethoxyanilino)quinoxalin-2-yl]-4-fluorobenzene-1-sulfonamide
-
additional information
no or poor inhibition by buparlisib, (8S)-2-[(3R)-3-methylmorpholin-4-yl]-9-(3-methyl-2-oxobutyl)-8-(trifluoromethyl)-6,7,8,9-tetrahydro-4H-pyrimido[1,2-a]pyrimidin-4-one, AZD3147, 5-[4-[(methanesulfonyl)methyl]-6-(morpholin-4-yl)pyrimidin-2-yl]-1H-indole, gedatolisib, 4'-(cyclopropylmethyl)-N2-(pyridin-4-yl)[4,5'-bipyrimidine]-2,2'-diamine, 1-([2-[(2-chloropyridin-4-yl)amino]-4'-(cyclopropylmethyl)[4,5'-bipyrimidin]-2'-yl]amino)-2-methylpropan-2-ol, SAR405, (2S)-2-amino-1-(4-[4-[2-(difluoromethyl)-1H-benzimidazol-1-yl]-6-(morpholin-4-yl)-1,3,5-triazin-2-yl]piperazin-1-yl)-3-phenylpropan-1-one, N-(3-[[3-(2-chloro-5-methoxyanilino)quinoxalin-2-yl]sulfamoyl]phenyl)-2-methylalaninamide, and N-[3-(3,5-dimethoxyanilino)quinoxalin-2-yl]-4-fluorobenzene-1-sulfonamide
-
additional information
no or poor inhibition by buparlisib, (8S)-2-[(3R)-3-methylmorpholin-4-yl]-9-(3-methyl-2-oxobutyl)-8-(trifluoromethyl)-6,7,8,9-tetrahydro-4H-pyrimido[1,2-a]pyrimidin-4-one, AZD3147, 5-[4-[(methanesulfonyl)methyl]-6-(morpholin-4-yl)pyrimidin-2-yl]-1H-indole, gedatolisib, 4'-(cyclopropylmethyl)-N2-(pyridin-4-yl)[4,5'-bipyrimidine]-2,2'-diamine, 1-([2-[(2-chloropyridin-4-yl)amino]-4'-(cyclopropylmethyl)[4,5'-bipyrimidin]-2'-yl]amino)-2-methylpropan-2-ol, SAR405, (2S)-2-amino-1-(4-[4-[2-(difluoromethyl)-1H-benzimidazol-1-yl]-6-(morpholin-4-yl)-1,3,5-triazin-2-yl]piperazin-1-yl)-3-phenylpropan-1-one, N-(3-[[3-(2-chloro-5-methoxyanilino)quinoxalin-2-yl]sulfamoyl]phenyl)-2-methylalaninamide, and N-[3-(3,5-dimethoxyanilino)quinoxalin-2-yl]-4-fluorobenzene-1-sulfonamide
-
additional information
no or poor inhibition by NVP-BYL719/buparlisib, 5-fluoro-3-phenyl-2-[(1S)-1-[(9H-purin-6-yl)amino]propyl]quinazolin-4(3H)-one, 3-[4-(morpholin-4-yl)pyrido[3',2':4,5]furo[3,2-d]pyrimidin-2-yl]phenol, (8S)-2-[(3R)-3-methylmorpholin-4-yl]-9-(3-methyl-2-oxobutyl)-8-(trifluoromethyl)-6,7,8,9-tetrahydro-4H-pyrimido[1,2-a]pyrimidin-4-one, AZD3147, 5-[4-[(methanesulfonyl)methyl]-6-(morpholin-4-yl)pyrimidin-2-yl]-1H-indole, gedatolisib, 4'-(cyclopropylmethyl)-N2-(pyridin-4-yl)[4,5'-bipyrimidine]-2,2'-diamine, 1-([2-[(2-chloropyridin-4-yl)amino]-4'-(cyclopropylmethyl)[4,5'-bipyrimidin]-2'-yl]amino)-2-methylpropan-2-ol, SAR405, (2S)-2-amino-1-(4-[4-[2-(difluoromethyl)-1H-benzimidazol-1-yl]-6-(morpholin-4-yl)-1,3,5-triazin-2-yl]piperazin-1-yl)-3-phenylpropan-1-one, N-[4-(morpholin-4-yl)-2-[3-[(naphthalene-2-sulfonyl)amino]phenyl]quinazolin-6-yl]acetamide, N-[2-[3-[(benzenesulfonyl)amino]phenyl]-4-(morpholin-4-yl)quinazolin-6-yl]acetamide, N-(3-[[3-(2-chloro-5-methoxyanilino)quinoxalin-2-yl]sulfamoyl]phenyl)-2-methylalaninamide, N-[3-(3,5-dimethoxyanilino)quinoxalin-2-yl]-4-fluorobenzene-1-sulfonamide, 3-amino-N-[3-(3,5-dimethoxyanilino)pyrazin-2-yl]benzene-1-sulfonamide, and N-[3-(2-chloro-5-hydroxyanilino)pyrazin-2-yl]benzenesulfonamide
-
additional information
no or poor inhibition by NVP-BYL719/buparlisib, 5-fluoro-3-phenyl-2-[(1S)-1-[(9H-purin-6-yl)amino]propyl]quinazolin-4(3H)-one, 3-[4-(morpholin-4-yl)pyrido[3',2':4,5]furo[3,2-d]pyrimidin-2-yl]phenol, (8S)-2-[(3R)-3-methylmorpholin-4-yl]-9-(3-methyl-2-oxobutyl)-8-(trifluoromethyl)-6,7,8,9-tetrahydro-4H-pyrimido[1,2-a]pyrimidin-4-one, AZD3147, 5-[4-[(methanesulfonyl)methyl]-6-(morpholin-4-yl)pyrimidin-2-yl]-1H-indole, gedatolisib, 4'-(cyclopropylmethyl)-N2-(pyridin-4-yl)[4,5'-bipyrimidine]-2,2'-diamine, 1-([2-[(2-chloropyridin-4-yl)amino]-4'-(cyclopropylmethyl)[4,5'-bipyrimidin]-2'-yl]amino)-2-methylpropan-2-ol, SAR405, (2S)-2-amino-1-(4-[4-[2-(difluoromethyl)-1H-benzimidazol-1-yl]-6-(morpholin-4-yl)-1,3,5-triazin-2-yl]piperazin-1-yl)-3-phenylpropan-1-one, N-[4-(morpholin-4-yl)-2-[3-[(naphthalene-2-sulfonyl)amino]phenyl]quinazolin-6-yl]acetamide, N-[2-[3-[(benzenesulfonyl)amino]phenyl]-4-(morpholin-4-yl)quinazolin-6-yl]acetamide, N-(3-[[3-(2-chloro-5-methoxyanilino)quinoxalin-2-yl]sulfamoyl]phenyl)-2-methylalaninamide, N-[3-(3,5-dimethoxyanilino)quinoxalin-2-yl]-4-fluorobenzene-1-sulfonamide, 3-amino-N-[3-(3,5-dimethoxyanilino)pyrazin-2-yl]benzene-1-sulfonamide, and N-[3-(2-chloro-5-hydroxyanilino)pyrazin-2-yl]benzenesulfonamide
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additional information
no or poor inhibition by NVP-BYL719/buparlisib, 5-fluoro-3-phenyl-2-[(1S)-1-[(9H-purin-6-yl)amino]propyl]quinazolin-4(3H)-one, 3-[4-(morpholin-4-yl)pyrido[3',2':4,5]furo[3,2-d]pyrimidin-2-yl]phenol, (8S)-2-[(3R)-3-methylmorpholin-4-yl]-9-(3-methyl-2-oxobutyl)-8-(trifluoromethyl)-6,7,8,9-tetrahydro-4H-pyrimido[1,2-a]pyrimidin-4-one, AZD3147, 5-[4-[(methanesulfonyl)methyl]-6-(morpholin-4-yl)pyrimidin-2-yl]-1H-indole, gedatolisib, 4'-(cyclopropylmethyl)-N2-(pyridin-4-yl)[4,5'-bipyrimidine]-2,2'-diamine, 1-([2-[(2-chloropyridin-4-yl)amino]-4'-(cyclopropylmethyl)[4,5'-bipyrimidin]-2'-yl]amino)-2-methylpropan-2-ol, SAR405, (2S)-2-amino-1-(4-[4-[2-(difluoromethyl)-1H-benzimidazol-1-yl]-6-(morpholin-4-yl)-1,3,5-triazin-2-yl]piperazin-1-yl)-3-phenylpropan-1-one, N-[4-(morpholin-4-yl)-2-[3-[(naphthalene-2-sulfonyl)amino]phenyl]quinazolin-6-yl]acetamide, N-[2-[3-[(benzenesulfonyl)amino]phenyl]-4-(morpholin-4-yl)quinazolin-6-yl]acetamide, N-(3-[[3-(2-chloro-5-methoxyanilino)quinoxalin-2-yl]sulfamoyl]phenyl)-2-methylalaninamide, N-[3-(3,5-dimethoxyanilino)quinoxalin-2-yl]-4-fluorobenzene-1-sulfonamide, 3-amino-N-[3-(3,5-dimethoxyanilino)pyrazin-2-yl]benzene-1-sulfonamide, and N-[3-(2-chloro-5-hydroxyanilino)pyrazin-2-yl]benzenesulfonamide
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Acute Lung Injury
Involvement of phosphoinositide 3-kinases in neutrophil activation and the development of acute lung injury.
Arthritis, Rheumatoid
Discovery of N-{5-[3-(3-hydroxypiperidin-1-yl)-1,2,4-oxadiazol-5-yl]-4-methyl-1,3-thiazol-2-yl}acetamide (TASP0415914) as an orally potent phosphoinositide 3-kinase ? inhibitor for the treatment of inflammatory diseases.
Arthritis, Rheumatoid
Novel phosphoinositide 3-kinase ?,? inhibitor: potent anti-inflammatory effects and joint protection in models of rheumatoid arthritis.
Asthma
Comprehensive attenuation of IL-25-induced airway hyperresponsiveness, inflammation and remodelling by the PI3K inhibitor LY294002.
Asthma
Consensus model for identification of novel PI3K inhibitors in large chemical library.
Asthma
Phosphoinositide 3-kinase {delta} inhibitor suppresses IL-17 expression in a murine asthma model.
Asthma
PI3K, p38 and JAK/STAT signalling in bronchial tissue from patients with asthma following allergen challenge.
Autoimmune Diseases
Furan-2-ylmethylene thiazolidinediones as novel, potent, and selective inhibitors of phosphoinositide 3-kinase gamma.
Autoimmune Diseases
PI3K inhibitors as potential therapeutics for autoimmune disease.
Autoimmune Diseases
Small molecule inhibitors of phosphoinositide 3-kinase (PI3K) delta and gamma.
Breast Neoplasms
Amplification of Chromosome 1q Genes Encoding the Phosphoinositide Signalling Enzymes PI4KB, AKT3, PIP5K1A and PI3KC2B in Breast Cancer.
Breast Neoplasms
Class II phosphoinositide 3-kinase C2? regulates a novel signaling pathway involved in breast cancer progression.
Breast Neoplasms
GDC-0941, a novel class I selective PI3K inhibitor, enhances the efficacy of docetaxel in human breast cancer models by increasing cell death in vitro and in vivo.
Breast Neoplasms
Identification and Kinetic Characterization of Serum- and Glucocorticoid-Regulated Kinase Inhibitors Using a Fluorescence Polarization-Based Assay.
Breast Neoplasms
PI3KCA mutations and/or PTEN loss in Her2-positive breast carcinomas treated with trastuzumab are not related to resistance to anti-Her2 therapy.
Burkitt Lymphoma
Dual inhibition of histone deacetylases and phosphoinositide 3-kinases: effects on Burkitt lymphoma cell growth and migration.
Carcinogenesis
Activation of phosphoinositide 3-kinase by the NBS1 DNA repair protein through a novel activation motif.
Carcinogenesis
Class IA phosphoinositide 3-kinase isoforms and human tumorigenesis: implications for cancer drug discovery and development.
Carcinogenesis
Identification and Kinetic Characterization of Serum- and Glucocorticoid-Regulated Kinase Inhibitors Using a Fluorescence Polarization-Based Assay.
Carcinogenesis
Phosphatidylinositol 3-kinase, class 2 beta (PI3KC2?) isoform contributes to neuroblastoma tumorigenesis.
Carcinogenesis
The recent progress and therapy in endometriosis-associated ovarian cancer.
Carcinogenesis
[Involvement of phosphoinositide 3-kinases and phosphoinositide phosphatases in immune responses, glucose metabolism and tumorigenesis]
Carcinoma
The recent progress and therapy in endometriosis-associated ovarian cancer.
Carcinoma, Hepatocellular
A class II phosphoinositide 3-kinase plays an indispensable role in hepatitis C virus replication.
Carcinoma, Hepatocellular
beta-estradiol stimulation of DNA synthesis requires different PKC isoforms in HepG2 and MCF7 cells.
Carcinoma, Squamous Cell
Phosphoinositide 3-Kinase C2beta Regulates Cytoskeletal Organization and Cell Migration via Rac-dependent Mechanisms.
Cardiovascular Diseases
Blockade of PI3Kgamma suppresses joint inflammation and damage in mouse models of rheumatoid arthritis.
Cardiovascular Diseases
Consensus model for identification of novel PI3K inhibitors in large chemical library.
Cardiovascular Diseases
PI3K Inhibitors in Cardiovascular Disease.
Cardiovascular Diseases
Progress in the Preclinical Discovery and Clinical Development of Class I and Dual Class I/IV Phosphoinositide 3-Kinase (PI3K) Inhibitors.
Cardiovascular Diseases
Progress in the preclinical discovery and clinical development of class I and dual class I/IV phosphoinositide 3-kinase (PI3K) inhibitors.
Colonic Neoplasms
Down-regulation of p110? expression increases chemosensitivity of colon cancer cell lines to oxaliplatin.
Colorectal Neoplasms
Identification and Kinetic Characterization of Serum- and Glucocorticoid-Regulated Kinase Inhibitors Using a Fluorescence Polarization-Based Assay.
Colorectal Neoplasms
PIK3C2G copy number is associated with clinical outcomes of colorectal cancer patients treated with oxaliplatin.
Diabetes Mellitus, Type 2
Association of the PIK3C2G gene polymorphisms with type 2 DM in a Japanese population.
Diabetes Mellitus, Type 2
Insulin-feedback via PI3K-C2{alpha} activated PKB{alpha}/Akt1 is required for glucose-stimulated insulin secretion.
Diabetic Cardiomyopathies
Phosphoinositide 3-kinases and Diabetic Cardiomyopathy.
Diphtheria
PI3KC2?, a class II PI3K, is required for dynamin-independent internalization pathways.
Encephalomyelitis
PI3-Kinase p110? Deficiency Modulates T Cell Homeostasis and Function and Attenuates Experimental Allergic Encephalitis in Mature Mice.
Encephalomyelitis, Autoimmune, Experimental
PI3-Kinase p110? Deficiency Modulates T Cell Homeostasis and Function and Attenuates Experimental Allergic Encephalitis in Mature Mice.
Epilepsy
Phosphoinositide 3-Kinases Upregulate System xc(-) via Eukaryotic Initiation Factor 2? and Activating Transcription Factor 4?-?A Pathway Active in Glioblastomas and Epilepsy.
Fibrosarcoma
3-Methyladenine suppresses cell migration and invasion of HT1080 fibrosarcoma cells through inhibiting phosphoinositide 3-kinases independently of autophagy inhibition.
Glioblastoma
Identification and Kinetic Characterization of Serum- and Glucocorticoid-Regulated Kinase Inhibitors Using a Fluorescence Polarization-Based Assay.
Glioblastoma
Phosphoinositide 3-Kinases Upregulate System xc(-) via Eukaryotic Initiation Factor 2? and Activating Transcription Factor 4?-?A Pathway Active in Glioblastomas and Epilepsy.
Hepatitis C
A class II phosphoinositide 3-kinase plays an indispensable role in hepatitis C virus replication.
Hypotension
Class II phosphoinositide 3-kinase alpha-isoform regulates Rho, myosin phosphatase and contraction in vascular smooth muscle.
Immune System Diseases
Class I PI 3-kinases signaling in platelet activation and thrombosis: PDK1/Akt/GSK3 axis and impact of PTEN and SHIP1.
Infections
iTRAQ-based proteomic profile analysis of ISKNV-infected CPB cells with emphasizing on glucose metabolism, apoptosis and autophagy pathways.
Insulin Resistance
Discovery of phosphoinositide 3-kinases (PI3K) p110? isoform inhibitor 4-[2-hydroxyethyl(1-naphthylmethyl)amino]-6-[(2S)-2-methylmorpholin-4-yl]-1H-pyrimidin-2-one, an effective antithrombotic agent without associated bleeding and insulin resistance.
Insulinoma
Class II phosphoinositide 3-kinase regulates exocytosis of insulin granules in pancreatic beta cells.
Leukemia
Class I phosphoinositide 3-kinases in normal and pathologic hematopoietic cells.
Leukemia
Inhibition of class I phosphoinositide 3-kinase activity impairs proliferation and triggers apoptosis in acute promyelocytic leukemia without affecting atra-induced differentiation.
Leukemia, Lymphocytic, Chronic, B-Cell
The pan phosphoinositide 3-kinase/mammalian target of rapamycin inhibitor SAR245409 (voxtalisib/XL765) blocks survival, adhesion and proliferation of primary chronic lymphocytic leukemia cells.
Leukemia, Myeloid, Acute
Class I phosphoinositide 3-kinases in normal and pathologic hematopoietic cells.
Leukemia, Promyelocytic, Acute
Inhibition of class I phosphoinositide 3-kinase activity impairs proliferation and triggers apoptosis in acute promyelocytic leukemia without affecting atra-induced differentiation.
Lymphadenopathy
Clinical and immunologic phenotype associated with activated phosphoinositide 3-kinase ? syndrome 2: A cohort study.
Lymphoma
Roles for phosphoinositide 3-kinases, Bruton's tyrosine kinase, and Jun kinases in B lymphocyte chemotaxis and homing.
Lymphoma, Follicular
miR-31 and miR-17-5p levels change during transformation of follicular lymphoma.
Multiple Myeloma
Targeting phosphoinositide 3-kinases and histone deacetylases in multiple myeloma.
Multiple Sclerosis
PI3-Kinase p110? Deficiency Modulates T Cell Homeostasis and Function and Attenuates Experimental Allergic Encephalitis in Mature Mice.
Myopathies, Structural, Congenital
Tamoxifen prolongs survival and alleviates symptoms in mice with fatal X-linked myotubular myopathy.
Neoplasms
A high-avidity biosensor reveals plasma membrane PI(3,4)P2 is predominantly a class I PI3K signaling product.
Neoplasms
A Novel Prognostic Signature of Transcription Factors for the Prediction in Patients With GBM.
Neoplasms
A synthetic peptide hijacks the catalytic subunit of class I PI3K to suppress the growth of cancer cells.
Neoplasms
Alkylsulfonamide-containing quinazoline derivatives as potent and orally bioavailable PI3Ks inhibitors.
Neoplasms
Analyses of FGFR3 and PIK3CA mutations in neuroblastomas and the effects of the corresponding inhibitors on neuroblastoma cell lines.
Neoplasms
Blockade of PI3Kgamma suppresses joint inflammation and damage in mouse models of rheumatoid arthritis.
Neoplasms
Calpain interacts with class IA phosphoinositide 3-kinases regulating their stability and signaling activity.
Neoplasms
Cellular function of phosphoinositide 3-kinases: implications for development, homeostasis, and cancer.
Neoplasms
Characterisation of the PTEN inhibitor VO-OHpic.
Neoplasms
Chemical interrogation of FOXO3a nuclear translocation identifies potent and selective inhibitors of phosphoinositide 3-kinases.
Neoplasms
Class (I) Phosphoinositide 3-Kinases in the Tumor Microenvironment.
Neoplasms
Class I phosphoinositide 3-kinases in normal and pathologic hematopoietic cells.
Neoplasms
Class I PI 3-kinases signaling in platelet activation and thrombosis: PDK1/Akt/GSK3 axis and impact of PTEN and SHIP1.
Neoplasms
Class IA phosphoinositide 3-kinase isoforms and human tumorigenesis: implications for cancer drug discovery and development.
Neoplasms
Class II phosphoinositide 3-kinase C2? regulates a novel signaling pathway involved in breast cancer progression.
Neoplasms
Consensus model for identification of novel PI3K inhibitors in large chemical library.
Neoplasms
Critical signaling pathways in bone sarcoma: candidates for therapeutic interventions.
Neoplasms
Defining How Oncogenic and Developmental Mutations of PIK3R1 Alter the Regulation of Class IA Phosphoinositide 3-Kinases.
Neoplasms
Different PI 3-kinase inhibitors have distinct effects on endothelial permeability and leukocyte transmigration.
Neoplasms
Disease-related mutations in PI3K? disrupt regulatory C-terminal dynamics and reveal a path to selective inhibitors.
Neoplasms
Down-regulation of class II phosphoinositide 3-kinase alpha expression below a critical threshold induces apoptotic cell death.
Neoplasms
Downregulation of class II phosphoinositide 3-kinase PI3K-C2? delays cell division and potentiates the effect of docetaxel on cancer cell growth.
Neoplasms
Dual HDAC and PI3K Inhibitor CUDC-907 Downregulates MYC and Suppresses Growth of MYC-dependent Cancers.
Neoplasms
Effects of novel isoform-selective phosphoinositide 3-kinase inhibitors on natural killer cell function.
Neoplasms
Effects of PI3K and FGFR inhibitors alone and in combination, and with/without cytostatics in childhood neuroblastoma cell lines.
Neoplasms
ETP-46321, a dual p110?/? class IA phosphoinositide 3-kinase inhibitor modulates T lymphocyte activation and collagen-induced arthritis.
Neoplasms
Extended treatment with selective PI 3-kinase and mTOR inhibitors has effects on metabolism, growth, behaviour and bone strength.
Neoplasms
Genetic and epigenetic regulation of phosphoinositide 3-kinase Isoforms.
Neoplasms
Germline mutations in apoptosis pathway genes in ovarian cancer; the functional role of a TP53I3 (PIG3) variant in ROS production and DNA repair.
Neoplasms
Identification and Kinetic Characterization of Serum- and Glucocorticoid-Regulated Kinase Inhibitors Using a Fluorescence Polarization-Based Assay.
Neoplasms
Isoform-selective phosphoinositide 3'-kinase inhibitors inhibit CXCR4 signaling and overcome stromal cell-mediated drug resistance in chronic lymphocytic leukemia: a novel therapeutic approach.
Neoplasms
Mechanism of constitutive phosphoinositide 3-kinase activation by oncogenic mutants of the p85 regulatory subunit.
Neoplasms
Multi-kinase inhibitors, AURKs and cancer.
Neoplasms
Nitric oxide and protein phosphatase 2A provide novel therapeutic opportunities in ER-negative breast cancer.
Neoplasms
Phosphoinositide 3-Kinase C2beta Regulates Cytoskeletal Organization and Cell Migration via Rac-dependent Mechanisms.
Neoplasms
Phosphoinositide 3-kinases as drug targets in cancer.
Neoplasms
Phytochemicals and Gastrointestinal Cancer: Cellular Mechanisms and Effects to Change Cancer Progression.
Neoplasms
PI3K at the crossroads of tumor angiogenesis signaling pathways.
Neoplasms
PI3K/AKT signaling pathway and cancer: an updated review.
Neoplasms
PIK3CA and PIK3CB expression and relationship with multidrug resistance in colorectal carcinoma.
Neoplasms
Present and Future of PI3K Pathway Inhibition in Cancer: Perspectives and Limitations.
Neoplasms
Present and future of PI3K pathway inhibition in cancer: perspectives and limitations.
Neoplasms
Progress in the Preclinical Discovery and Clinical Development of Class I and Dual Class I/IV Phosphoinositide 3-Kinase (PI3K) Inhibitors.
Neoplasms
Progress in the preclinical discovery and clinical development of class I and dual class I/IV phosphoinositide 3-kinase (PI3K) inhibitors.
Neoplasms
Recent Developments of Small Molecule PI3K/mTOR Dual Inhibitors.
Neoplasms
Regioselective synthesis of 5- and 6-methoxybenzimidazole-1,3,5-triazines as inhibitors of phosphoinositide 3-kinase.
Neoplasms
Regulation of lipid binding underlies the activation mechanism of class IA PI3-kinases.
Neoplasms
Signal Transduction Pathways as Therapeutic Targets. 25-28 January 2004, Luxembourg.
Neoplasms
Stromal cell protein kinase C-? inhibition enhances chemosensitivity in B cell malignancies and overcomes drug resistance.
Neoplasms
Structure and ligand-based design of mTOR and PI3-kinase inhibitors leading to the clinical candidates VS-5584 (SB2343) and SB2602.
Neoplasms
Targeting p110gamma in gastrointestinal cancers: attack on multiple fronts.
Neoplasms
Targeting PI3K in neuroblastoma.
Neoplasms
The Essential Role of Phosphoinositide 3-Kinases (PI3Ks) in Regulating Pro-Inflammatory Responses and the Progression of Cancer.
Neoplasms
The lipid products of phosphoinositide 3-kinase isoforms in cancer and thrombosis.
Neoplasms
The relation between PI3K/AKT signalling pathway and cancer.
Neoplasms
The transforming functions of PI3-kinase-gamma are linked to disruption of intercellular adhesion and promotion of cancer cell invasion.
Neoplasms
Theoretical studies on the selectivity mechanisms of PI3K? inhibition with marketed idelalisib and its derivatives by 3D-QSAR, molecular docking, and molecular dynamics simulation.
Neoplasms
TSC1 Activates TGF-?-Smad2/3 Signaling in Growth Arrest and Epithelial-to-Mesenchymal Transition.
Neoplasms
Uncovering the PI3Ksome: phosphoinositide 3-kinases and counteracting PTEN form a signaling complex with intrinsic regulatory properties.
Neoplasms
Whole Genome Resequencing of Arkansas Progressor and Regressor Line Chickens to Identify SNPs Associated with Tumor Regression.
Neuroblastoma
Phosphatidylinositol 3-kinase, class 2 beta (PI3KC2?) isoform contributes to neuroblastoma tumorigenesis.
Neuroblastoma
Targeting PI3K in neuroblastoma.
Primary Immunodeficiency Diseases
Conformational disruption of PI3K? regulation by immunodeficiency mutations in PIK3CD and PIK3R1.
Prostatic Neoplasms
Downregulation of class II phosphoinositide 3-kinase PI3K-C2? delays cell division and potentiates the effect of docetaxel on cancer cell growth.
Prostatic Neoplasms
Identification and Kinetic Characterization of Serum- and Glucocorticoid-Regulated Kinase Inhibitors Using a Fluorescence Polarization-Based Assay.
Prostatic Neoplasms
Novel roles for class II Phosphoinositide 3-Kinase C2? in signalling pathways involved in prostate cancer cell invasion.
Psoriasis
Hypoxia-inducible factor-1: A potential pharmacological target to manage psoriasis.
Sarcoma
The landscape of gene mutations and clinical significance of tumor mutation burden in patients with soft tissue sarcoma who underwent surgical resection and received conventional adjuvant therapy.
Sarcoma
Xenograft tumors derived from malignant pleural effusion of the patients with non-small-cell lung cancer as models to explore drug resistance.
Sepsis
In Search of a Cure for Sepsis: Taming the Monster in Critical Care Medicine.
Squamous Cell Carcinoma of Head and Neck
The PI3K/Akt/mTORC signaling axis in head and neck squamous cell carcinoma: Possibilities for therapeutic interventions either as single agents or in combination with conventional therapies.
Thrombosis
Membrane grease eases platelet maturation.
Thrombosis
Phosphoinositide 3-kinases in platelets, thrombosis and therapeutics.
Thrombosis
Resistance to thromboembolism in PI3Kgamma-deficient mice.
Thrombosis
The lipid products of phosphoinositide 3-kinase isoforms in cancer and thrombosis.
Uterine Cervical Neoplasms
Downregulation of class II phosphoinositide 3-kinase PI3K-C2? delays cell division and potentiates the effect of docetaxel on cancer cell growth.
Whooping Cough
The CC chemokine monocyte chemotactic peptide-1 activates both the class I p85/p110 phosphatidylinositol 3-kinase and the class II PI3K-C2alpha.
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PI3KC2gamma
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PI3KC2gamma
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moderate expression of PI3K-C2alpha andPI3K-C2beta
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moderate expression of PI3K-C2alpha
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isozyme PI3K-C2beta is overexpressed in human breast cancer cell lines
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low amount of isozyme p85, isozyme PI3K-C2beta and isozyme PI3K-C2alpha in bronchial epithelium
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moderate expression of PI3K-C2alpha and PI3K-C2beta
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of Fallopian tube, moderate expression of PI3K-C2alpha and weak expression of PI3K-C2beta
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PI3K-C2alpha
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moderate expression of PI3K-C2alpha and weak expression of PI3K-C2beta
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high expression level of PI3KC2beta
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isozyme PI3K-C2alpha, high amount of isozyme p85, and low amount of isozyme PI3K-C2beta
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isozyme PI3K-C2alpha in smooth muscle layer, mononuclear cells, and lining epithelium, isozyme p85 and isozyme PI3K-C2beta in lining epithelium and mononuclear cells
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strong expression of PI3K-C2alpha
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strong expression of PI3K-C2alpha and moderate expression of PI3K-C2beta
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isozyme PI3K-C2alpha in bile ducts, no isozyme PI3K-C2beta and isozyme p85
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isozyme p85, isozyme PI3K-C2beta and isozyme PI3K-C2alpha in alveolar macrophages
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moderate expression of PI3K-C2alpha
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non-myelinated, moderate expression of PI3K-C2beta
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moderate expression of PI3K-C2alpha and PI3K-C2beta
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expression at low level
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fibromuscular stroma, moderate expression of PI3K-C2alpha
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isozyme PI3K-C2alpha inbasal epithelium and fibromuscular stroma, no isozyme PI3K-C2beta and isozyme p85
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expression at low level
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isozyme p85 in Langerhans cells, dermal macrophages, and in low amounts in sebaceous glands, hair follicles, and sweat gland, isozyme PI3K-C2beta and isozyme PI3K-C2alpha in dermal macrophages, low amount of isozyme PI3K-C2alpha in sweat gland
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different cell lines overexpress different isozymes, e.g. cell lines H-69, HC-33, H-510, H-1045, and H-209
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strong expression of PI3K-C2beta
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isozyme PI3K-C2beta and isozyme PI3K-C2alpha, and high amount of isozyme p85 in peptic cells
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monocyte
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isozyme PI3K-C2alpha in cervical smooth muscle, no isozyme PI3K-C2beta and isozyme p85
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isozyme p85 in proliferative endometrium and in low amounts in secretory endometrium, isozyme PI3K-C2alpha in myometrium, no isozyme PI3K-C2beta
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PI3KC2gamma
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carcinoma-derived cell
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low amount of isozyme PI3K-C2alpha in myoepithelial cells and lactiferous ducts, no isozyme PI3K-C2beta and isozyme p85
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non-neoplastic breast tissues
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isozyme p85, isozyme PI3K-C2beta and isozyme PI3K-C2alpha in colonocytes
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glomerular, PI3K-C2alpha
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strong expression of PI3K-C2beta
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high amounts of isozyme p85 and isozyme PI3K-C2beta
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expression at low level
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mRNA is undetectable in kidney
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isozyme p85 in glomerular macrophages, macula densa, and collecting tubules, high amount of isozyme PI3K-C2alpha in glomerular tuft, low amount of isozyme PI3K-C2beta and isozyme PI3K-C2alpha in proximal, distal, and collecting tubules
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weak expression of PI3K-C2alpha and PI3K-C2beta in germinal centre mononuclear cells, moderate expression of PI3K-C2alpha and PI3K-C2beta in tissue macrophages, strong expression of PI3K-C2alpha in polymorphonuclear leucocytes, weak expression of PI3K-C2alpha and moderate expression of PI3K-C2beta in medulla mononuclear cells, no expression in lymphoid follicles
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isozyme p85 in medulla, germinal centre mononuclear cells, low amount in polymorphnuclear leucocytes, and high amount in tissue macrophages, isozyme PI3K-C2alpha and isozyme PI3K-C2beta in medulla, tissue macrophages, and germinal centre mononuclear cells, high amount of isozyme PI3K-C2alpha in polymorphnuclear leucocytes
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PI3K-C2beta is highly expressed in lymph-nodes metastases compared to matching primary tumors
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dermal, moderate expression of PI3K-C2alpha and PI3K-C2beta
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glomerular, moderate expression of PI3K-C2beta
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PI3K-C2alpha and PI3K-C2beta
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isozyme PI3K-C2beta
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moderate expression of PI3K-C2alpha and strong expression of PI3K-C2beta
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all isozymes
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PI3K class IIbeta (PI3KC2beta) and its regulator intersectin 1 (ITSN1) are highly expressed in primary neuroblastoma tumors and cell lines
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isozyme p85, low amount of isozyme PI3K-C2beta and isozyme PI3K-C2alpha in follicular cells
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moderate expression of PI3K-C2alpha and PI3K-C2beta
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low enzyme expression
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high amount of isozyme p85 in acini, isozyme PI3K-C2alpha in acini and ducts, no isozyme PI3K-C2beta
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highest expression in thymus and placenta
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moderate expression of PI3K-C2alpha and weak expression of PI3K-C2beta
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isozyme PI3K-C2alpha, high amount of isozyme p85, and low amount of isozyme PI3K-C2beta in enterocytes, isozyme p85 in Paneth cells
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bronchial and cervical, moderate expression of PI3K-C2alpha
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isozyme PI3K-C2alpha
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strong expression of PI3K-C2alpha in red pulp splenic sinusoids, weak expression of PI3K-C2alpha and moderate expression of PI3K-C2beta in red pulp mononuclear cells, no expression in white pulp
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isozyme p85, isozyme PI3K-C2beta and isozyme PI3K-C2alpha in red pulp
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high content of isozyme p85 and isozyme PI3K-C2beta in spermatogenic cells, high content of isozyme PI3K-C2alpha in Leydig cells, isozyme p85 and PI3K-C2beta in Leydig cells
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highest expression in thymus and placenta
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high activity of PI3KC2beta
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monocyte
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monocyte
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HUVEC
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moderate expression of PI3K-C2alpha and weak expression of PI3K-C2beta
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isozyme PI3K-C2alpha in muscularis and transitional epithelium, isozyme p85 and isozyme PI3K-C2beta in transitional epithelium
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additional information
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immunohistological analysis, no expression of isozymes in endocrine pancreas, thyroid, or parathyroid, topographical expression of class IA and class II isozymes in normal human tissues is consistent with a role in differentiation
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additional information
widely expressed, but not ubiquitous
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widely expressed, but not ubiquitous
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widely expressed, but not ubiquitous
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additional information
PI3KC2alpha is broadly expressed in human cells
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additional information
PI3KC2alpha is broadly expressed in human cells
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additional information
PI3KC2alpha is broadly expressed in human cells
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physiological function
PIK3C2G, the gene encoding PI3KC2gamma, acts mainly as a tumor suppressor gene. Low PI3KC2gamma expression influences colorectal cancer (CRC) development, with low copy number of PIK3C2G associated with a 2.5fold increase in the risk of death
evolution
three enzymes belong to the class II subfamily, PI3K-C2alpha, beta, and gamma
metabolism
knockdown studies of endogenous PI3K isoforms and clathrin heavy chain (CHC) mediated by small interfering RNA (siRNA) demonstrate that the class II PI3K PI3K-C2alpha and PI3K-C2beta, but not the class I or III PI3K, are required for pinocytosis, based on an evaluation of fluorescein-5-isothiocyanate (FITC)-dextran uptake in endothelial cells. Pinocytosis is partially dependent on both clathrin and dynamin, and both PI3K-C2alpha and PI3K-C2beta are required for clathrin-mediated, but not clathrin-nonmediated, FITC-dextran uptake at the step leading up to its delivery to early endosomes. PI3K-C2alpha and PI3K-C2beta play differential, indispensable roles in clathrin-mediated pinocytosis
malfunction
downregulation of PI3K-C2beta in breast cancer cell lines reduces colony formation, induces cell cycle arrest and inhibits tumor growth, in particular in an estrogen-dependent in vivo xenograft. PI3K-C2beta inhibits breast cancer cell invasion in vitro and breast cancer metastasis in vivo
malfunction
inhibition of MEK/ERK activation as well as downregulation of PI3K-C2beta does not affect cell proliferation while specifically inhibiting cell invasion
malfunction
PI3KC2beta-silencing inhibits early stages of neuroblastoma tumorigenic growth, but does not alter apoptotic or endocytic pathways, and silencing of the enzyme's regulator intersectin 1, ITSN1, also dramatically reduces the tumorigenic potential of neuroblastoma cells. Overexpression of PI3KC2beta rescues the anchorage-independent growth of ITSN1-silenced cells suggesting that PI3KC2beta mediates ITSN1's function in neuroblastoma cells. Silencing ITSN1 or PI3KC2beta decreases AKT activation in neuroblastoma cells
malfunction
TGFbeta1 stimulated nuclear accumulation of p-Smad2 is markedly suppressed by PI3K-C2alpha knockdown. Effect of PI3K-C2alpha knockdown on the co-localization of TGFbeta1 receptors and SARA. PI3K-C2alpha knockdown does not affect the numbers of either SARA-positive or EEA1-positive vesicles in nonstimulated cells but abolished TGFbeta1-induced increase in SARA- and EEA1-double positive early endosomes
malfunction
downregulation of PI3KC2beta results the inhibition of early stage neuroblastoma formation. Serum-dependent lamellipodia formation has been significantly reduced in cells lacking PI3KC2beta. Selective inhibition of PI3KC2beta with ceramide has been shown to diminish PI3KC2beta-dependent lamellipodia formation, reducing ovarian cancer cell mobility. Blocking of PI3KC2? pathway results in the impairment of SKOV3 cell migration. Depletion of PI3KC2beta can increase resistance of cells to chemotherapeutics
malfunction
ITSN1 knockdown dramatically reduces the localization of PI3K-C2beta at actin patches and at clathrin-coated structures
malfunction
knockdown of PI3K-C2alpha inhibits internalization of cell surface molecules
malfunction
PI3KC2alpha mRNA is downregulated in islets from type 2 diabetic patients compared to nondiabetic individuals. PI3KC2alpha plays a sex-dependent role in the modulation of hypothalamic leptin action and systemic glucose homeostasis
physiological function
class II phosphoinositide 3-kinase C2beta regulates a novel signaling pathway involved in breast cancer progression. Isozyme PI3K-C2beta regulates breast cancer cell growth in vitro and in vivo, PI3K-C2beta expression in breast tissues is correlated with the proliferative status of the tumor. Analsis of the mechanism of the PI3K-C2beta-dependent regulation of cell cycle progression and cell growth revealed that PI3K-C2beta regulates cyclin B1 protein levels through modulation of microRNA miR-449a levels. PI3K-C2beta may represent a key molecular switch that regulates a rate-limiting step in breast tumor progression and therefore it may be targeted to limit breast cancer spread. PI3K-C2beta regulates cyclin B1 expression through modulation of miR-449a, miR-449a levels are downregulated in primary human breast cancer samples, and cyclin B1/miR-449a expression through modulation of LEF1/beta catenin pathway in MDA-MB-231 cells. PI3K-C2beta regulates senescence via miR-449 regulation
physiological function
isozyme phosphatidylinositol 3-kinase class II alpha is required for transforming growth factor beta-induced Smad signaling in endothelial cells, but not in smooth muscle cells or epithelial cells. TGFbeta1-induced phosphorylation and nuclear translocation of Smad2/3 are dependent on class II PI3K-C2alpha. C2alpha is required for SARA-Smad2/3 complex formation
physiological function
isozyme PI3K-C2beta regulates mitogen-activated protein kinase kinase (MEK1/2) and extracellular signal-regulated kinase (ERK1/2) activation in prostate cancer (PCa) cells. MEK/ERK and isozyme PI3K-C2beta are required for PCa cell invasion but not proliferation. MEK/ERK and PI3K-C2beta are not required for PCa cell proliferation. PI3K-C2beta but not MEK/ERK regulates PCa cell migration as well as expression of the transcription factor Slug. PI3K-C2beta regulates FBS-induced PCa cell migration in a mechanism that does not appear to involve MEK/ERK activation
physiological function
phosphatidylinositol 3-kinase class 2 beta isoform, PI3KC2beta, contributes to neuroblastoma tumorigenesis. Activation of the PI3K target AKT is frequent in neuroblastoma and correlates with poor prognosis
physiological function
class II phosphoinositide 3-kinases PI3K-C2alpha and PI3K-C2beta differentially regulate clathrin-dependent pinocytosis in human vascular endothelial cells. Pinocytosis is partially dependent on both clathrin and dynamin, and both PI3K-C2alpha and PI3K-C2beta are required for clathrin-mediated, but not clathrin-nonmediated, FITC-dextran uptake at the step leading up to its delivery to early endosomes. PI3K-C2alpha and PI3K-C2beta play differential, indispensable roles in clathrin-mediated pinocytosis
physiological function
class II phosphoinositide 3-kinases PI3K-C2alpha and PI3K-C2beta differentially regulate clathrin-dependent pinocytosis in human vascular endothelial cells. Pinocytosis is partially dependent on both clathrin and dynamin, and both PI3K-C2alpha and PI3K-C2beta are required for clathrin-mediated, but not clathrin-nonmediated, FITC-dextran uptake at the step leading up to its delivery to early endosomes. PI3K-C2alpha and PI3K-C2beta play differential, indispensable roles in clathrin-mediated pinocytosis. Endogenous ITSN1 is required for the formation of actin patches and recruitment of PI3K-C2beta to the clathrin-coated structures. mCherry-C2beta overexpression stimulates pinocytosis through the mechanisms involving GFP-ITSN1-mediated recruitment of mCherry-C2beta
physiological function
PI3KC2alpha has a role in glucose transport and secretion. Possible role of PI3KC2alpha in carcinogenesis, possible involvement of PI3KC2alpha in breast cancer development, and potential involvement of PI3KC2alpha in tumor angiogenesis favoring lung cancer and melanoma. Role for PI3KC2alpha in platelet function. PI3KC2alpha regulates a basal pool of PtdIns3P in platelets that may lead to impaired regulation of the platelet's cytoskeletal-membrane system
physiological function
PI3KC2beta plays an essential role in neuroblastoma development by mediating functions of ITSN1 and by stabilizing metylocytomatosis viral oncogene (MYCN), an oncogene found in 20% of neuroblastoma cases and a marker for poor prognosis. Correlation between PI3KC2beta expression levels and esophageal squamous-cell carcinoma (ESCC) metastasis. PI3KC2beta is involved in the regulation of cell invasion in PCa cells, partly by activation of MEK/ERK pathways and partly by regulation of cell migration through regulation of Slug protein. This protein is essential for epithelial-mesenchymal transition (EMT), a process which enables cells to gain migratory and invasive properties. PI3KC2beta has no influence on PCa cell proliferation. But it plays crucial roles in cell motility, migration, and invasion. PI3KC2beta is involved in the regulation of cell migration and invasion in different cancers. Implication of PI3KC2beta in metastasis has been demonstrated in breast, prostate, and ovarian cancers. The enzyme has a key role in lamellipodia formation in ovarian cancer SKOV3 cells, allowing for the increase in cell motility. A specific role for this enzyme in ovarian cancer cell motility and, as a consequence, in cancer metastasis. Importance of PI3KC2beta in ovarian cancer cell migration. Overexpression of PI3KC2beta has been also found to enhance migration of A-431 epidermoid carcinoma cells, HeLa and ovarian cancer cells, whereas overexpression of the negative PI3KC2beta is able to reduce this process. Possible mechanism of contribution of PI3KC2beta in cancer cell migration and metastasis included PIK3C2B is regulated by miR-515-5p, which plays a role in the control of cancer cell migration and metastasis. Overexpression of miR-515-5p downregulates PIK3C2B, among others, binding directly to its 3'-UTR region
additional information
PI3KC2beta catalytic site structure, overview
additional information
PI3KC2beta catalytic site structure, overview
additional information
PI3KC2beta catalytic site structure, overview
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