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ATP + 1-phosphatidyl-1D-myo-inositol
ADP + 1-phosphatidyl-1D-myo-inositol 5-phosphate
ATP + 1-phosphatidyl-1D-myo-inositol 3-phosphate
ADP + 1-phosphatidyl-1D-myo-inositol 3,5-bisphosphate
ATP + 1-phosphatidyl-1D-myo-inositol 4-phosphate
ADP + 1-phosphatidyl-1D-myo-inositol 4,5-bisphosphate
additional information
?
-
ATP + 1-phosphatidyl-1D-myo-inositol

ADP + 1-phosphatidyl-1D-myo-inositol 5-phosphate
-
recombinant enzyme
-
-
?
ATP + 1-phosphatidyl-1D-myo-inositol
ADP + 1-phosphatidyl-1D-myo-inositol 5-phosphate
-
recombinant enzyme
-
-
?
ATP + 1-phosphatidyl-1D-myo-inositol 3-phosphate

ADP + 1-phosphatidyl-1D-myo-inositol 3,5-bisphosphate
-
-
-
-
?
ATP + 1-phosphatidyl-1D-myo-inositol 3-phosphate
ADP + 1-phosphatidyl-1D-myo-inositol 3,5-bisphosphate
-
-
-
?
ATP + 1-phosphatidyl-1D-myo-inositol 3-phosphate
ADP + 1-phosphatidyl-1D-myo-inositol 3,5-bisphosphate
-
-
-
-
?
ATP + 1-phosphatidyl-1D-myo-inositol 3-phosphate
ADP + 1-phosphatidyl-1D-myo-inositol 3,5-bisphosphate
-
-
-
?
ATP + 1-phosphatidyl-1D-myo-inositol 3-phosphate
ADP + 1-phosphatidyl-1D-myo-inositol 3,5-bisphosphate
-
the main function of PPK-3 is to mediate membrane retrieval from matured lysosomes through regulation of PtdIns(3,5)P2. Complete loss of ppk-3 function induces developmental defects characterized by embryonic lethality, whereas partial loss of function leads to growth retardation. At the cellular level, ppk-3 mutants display a striking enlargement of vacuoles positive for lysosome-associated membrane protein 1 in different tissues
-
-
?
ATP + 1-phosphatidyl-1D-myo-inositol 3-phosphate
ADP + 1-phosphatidyl-1D-myo-inositol 3,5-bisphosphate
-
-
-
-
?
ATP + 1-phosphatidyl-1D-myo-inositol 3-phosphate
ADP + 1-phosphatidyl-1D-myo-inositol 3,5-bisphosphate
-
-
-
-
?
ATP + 1-phosphatidyl-1D-myo-inositol 3-phosphate
ADP + 1-phosphatidyl-1D-myo-inositol 3,5-bisphosphate
-
-
-
-
?
ATP + 1-phosphatidyl-1D-myo-inositol 3-phosphate
ADP + 1-phosphatidyl-1D-myo-inositol 3,5-bisphosphate
Drosophila sp. (in: flies)
-
Fab1 phosphatidylinositol 3-phosphate 5-kinase controls trafficking but not silencing of endocytosed receptors. Drosophila fab1 mutants contain undetectable phosphatidylinositol 3,5-bisphosphate levels, show profound increases in cell and organ size, and die at the pupal stage
-
-
?
ATP + 1-phosphatidyl-1D-myo-inositol 3-phosphate
ADP + 1-phosphatidyl-1D-myo-inositol 3,5-bisphosphate
-
-
-
-
?
ATP + 1-phosphatidyl-1D-myo-inositol 3-phosphate
ADP + 1-phosphatidyl-1D-myo-inositol 3,5-bisphosphate
-
-
-
?
ATP + 1-phosphatidyl-1D-myo-inositol 3-phosphate
ADP + 1-phosphatidyl-1D-myo-inositol 3,5-bisphosphate
-
-
-
-
?
ATP + 1-phosphatidyl-1D-myo-inositol 3-phosphate
ADP + 1-phosphatidyl-1D-myo-inositol 3,5-bisphosphate
-
-
-
?
ATP + 1-phosphatidyl-1D-myo-inositol 3-phosphate
ADP + 1-phosphatidyl-1D-myo-inositol 3,5-bisphosphate
-
regulation of 1-phosphatidyl-1D-myo-inositol 3,5-bisphosphate synthesis involving osmotic stress, interleukins, UV radiation, and autophosphorylation, overview
-
-
?
ATP + 1-phosphatidyl-1D-myo-inositol 3-phosphate
ADP + 1-phosphatidyl-1D-myo-inositol 3,5-bisphosphate
-
-
-
-
?
ATP + 1-phosphatidyl-1D-myo-inositol 3-phosphate
ADP + 1-phosphatidyl-1D-myo-inositol 3,5-bisphosphate
-
-
-
?
ATP + 1-phosphatidyl-1D-myo-inositol 3-phosphate
ADP + 1-phosphatidyl-1D-myo-inositol 3,5-bisphosphate
-
-
-
?
ATP + 1-phosphatidyl-1D-myo-inositol 3-phosphate
ADP + 1-phosphatidyl-1D-myo-inositol 3,5-bisphosphate
-
-
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?
ATP + 1-phosphatidyl-1D-myo-inositol 3-phosphate
ADP + 1-phosphatidyl-1D-myo-inositol 3,5-bisphosphate
-
-
-
-
?
ATP + 1-phosphatidyl-1D-myo-inositol 3-phosphate
ADP + 1-phosphatidyl-1D-myo-inositol 3,5-bisphosphate
preferred substrate
-
-
?
ATP + 1-phosphatidyl-1D-myo-inositol 3-phosphate
ADP + 1-phosphatidyl-1D-myo-inositol 3,5-bisphosphate
-
stress-activated enzyme
-
?
ATP + 1-phosphatidyl-1D-myo-inositol 3-phosphate
ADP + 1-phosphatidyl-1D-myo-inositol 3,5-bisphosphate
-
essential for vacuole function
-
?
ATP + 1-phosphatidyl-1D-myo-inositol 3-phosphate
ADP + 1-phosphatidyl-1D-myo-inositol 3,5-bisphosphate
-
generation of 1-phosphatidyl-1D-myo-inositol 3,5-bisphosphate is regulated by Vac7 protein, whereas turnover of 1-phosphatidyl-1D-myo-inositol 3,5-bisphosphate is mediated in part by the Sac1 polyphosphoinositide phosphatase family member Fig4
-
?
ATP + 1-phosphatidyl-1D-myo-inositol 3-phosphate
ADP + 1-phosphatidyl-1D-myo-inositol 3,5-bisphosphate
-
reaction is essential for retrograde trafficking between the vacuole/lysosome and the late endosome and also for trafficking of some proteins into the vacuole via multivesicular bodies, enzyme synthesis is regulated by vac14 and vac7, 2 upstream activators, physiological roles of the enzyme and regulation mechnaism, overview
-
-
?
ATP + 1-phosphatidyl-1D-myo-inositol 3-phosphate
ADP + 1-phosphatidyl-1D-myo-inositol 3,5-bisphosphate
regulation of 1-phosphatidyl-1D-myo-inositol 3,5-bisphosphate synthesis involving osmotic stress, overview, enzymes hydrolyzing the product are counteracting, overview
-
-
?
ATP + 1-phosphatidyl-1D-myo-inositol 3-phosphate
ADP + 1-phosphatidyl-1D-myo-inositol 3,5-bisphosphate
-
Fab1p and AP-1 are required for trafficking of endogenously ubiquitylated cargoes to the vacuole lumen
-
-
?
ATP + 1-phosphatidyl-1D-myo-inositol 3-phosphate
ADP + 1-phosphatidyl-1D-myo-inositol 3,5-bisphosphate
-
-
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?
ATP + 1-phosphatidyl-1D-myo-inositol 3-phosphate
ADP + 1-phosphatidyl-1D-myo-inositol 3,5-bisphosphate
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-
-
-
?
ATP + 1-phosphatidyl-1D-myo-inositol 3-phosphate
ADP + 1-phosphatidyl-1D-myo-inositol 3,5-bisphosphate
-
-
-
?
ATP + 1-phosphatidyl-1D-myo-inositol 3-phosphate
ADP + 1-phosphatidyl-1D-myo-inositol 3,5-bisphosphate
-
phosphatidylinositol(3,5)bisphosphate is essential for cellular responses to various stresses and for the mating pheromone signalling under starvation conditions
-
?
ATP + 1-phosphatidyl-1D-myo-inositol 3-phosphate
ADP + 1-phosphatidyl-1D-myo-inositol 3,5-bisphosphate
-
reaction is essential for retrograde trafficking between the vacuole/lysosome and the late endosome and also for trafficking of some proteins into the vacuole via multivesicular bodies, enzyme synthesis is regulated by vac14 and vac7, 2 upstream activators, physiological roles of the enzyme and regulation mechnaism, overview
-
-
?
ATP + 1-phosphatidyl-1D-myo-inositol 3-phosphate
ADP + 1-phosphatidyl-1D-myo-inositol 3,5-bisphosphate
-
regulation of 1-phosphatidyl-1D-myo-inositol 3,5-bisphosphate synthesis involving osmotic stress, overview
-
-
?
ATP + 1-phosphatidyl-1D-myo-inositol 3-phosphate
ADP + 1-phosphatidyl-1D-myo-inositol 3,5-bisphosphate
-
-
-
?
ATP + 1-phosphatidyl-1D-myo-inositol 3-phosphate
ADP + 1-phosphatidyl-1D-myo-inositol 3,5-bisphosphate
-
-
-
?
ATP + 1-phosphatidyl-1D-myo-inositol 3-phosphate
ADP + 1-phosphatidyl-1D-myo-inositol 3,5-bisphosphate
-
-
-
-
?
ATP + 1-phosphatidyl-1D-myo-inositol 4-phosphate

ADP + 1-phosphatidyl-1D-myo-inositol 4,5-bisphosphate
-
recombinant enzyme
-
-
?
ATP + 1-phosphatidyl-1D-myo-inositol 4-phosphate
ADP + 1-phosphatidyl-1D-myo-inositol 4,5-bisphosphate
recombinant enzyme
-
-
?
ATP + 1-phosphatidyl-1D-myo-inositol 4-phosphate
ADP + 1-phosphatidyl-1D-myo-inositol 4,5-bisphosphate
-
recombinant enzyme
-
-
?
additional information

?
-
TLC measurement of phospholipids in wild-type and FAB1A-GFP-expressing plants, overview
-
-
?
additional information
?
-
-
PIKfyve participates in the SGK1-dependent regulation of the Na+, glucose cotransporter SGLT1 (SLC5A1)
-
-
?
additional information
?
-
-
substrate specificity in descending order: 1-phosphatidyl-1D-myo-inositol 3-phosphate, 1-phosphatidyl-1D-myo-inositol 4-phosphate, and 1-phosphatidyl-1D-myo-inositol, the enzyme also shows lipid kinase activity
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?
additional information
?
-
physiological roles of the catalyzed reaction, overview
-
-
?
additional information
?
-
substrate specificity, the enzyme also shows lipid kinase activity
-
-
?
additional information
?
-
-
Fab1p activators, Vac7p and Vac14p, independently regulate Fab1p activity. A maximal increase in the levels of PI3,5P2 requires both Vac7p and the Vac14pFig4p complex
-
-
?
additional information
?
-
-
physiological roles of the catalyzed reaction, overview
-
-
?
additional information
?
-
-
substrate specificity in descending order: 1-phosphatidyl-1D-myo-inositol 3-phosphate, 1-phosphatidyl-1D-myo-inositol 4-phosphate, and 1-phosphatidyl-1D-myo-inositol
-
-
?
Please wait a moment until the data is sorted. This message will disappear when the data is sorted.
ATP + 1-phosphatidyl-1D-myo-inositol 3-phosphate
ADP + 1-phosphatidyl-1D-myo-inositol 3,5-bisphosphate
additional information
?
-
ATP + 1-phosphatidyl-1D-myo-inositol 3-phosphate

ADP + 1-phosphatidyl-1D-myo-inositol 3,5-bisphosphate
-
-
-
-
?
ATP + 1-phosphatidyl-1D-myo-inositol 3-phosphate
ADP + 1-phosphatidyl-1D-myo-inositol 3,5-bisphosphate
-
-
-
?
ATP + 1-phosphatidyl-1D-myo-inositol 3-phosphate
ADP + 1-phosphatidyl-1D-myo-inositol 3,5-bisphosphate
-
-
-
-
?
ATP + 1-phosphatidyl-1D-myo-inositol 3-phosphate
ADP + 1-phosphatidyl-1D-myo-inositol 3,5-bisphosphate
-
-
-
?
ATP + 1-phosphatidyl-1D-myo-inositol 3-phosphate
ADP + 1-phosphatidyl-1D-myo-inositol 3,5-bisphosphate
-
the main function of PPK-3 is to mediate membrane retrieval from matured lysosomes through regulation of PtdIns(3,5)P2. Complete loss of ppk-3 function induces developmental defects characterized by embryonic lethality, whereas partial loss of function leads to growth retardation. At the cellular level, ppk-3 mutants display a striking enlargement of vacuoles positive for lysosome-associated membrane protein 1 in different tissues
-
-
?
ATP + 1-phosphatidyl-1D-myo-inositol 3-phosphate
ADP + 1-phosphatidyl-1D-myo-inositol 3,5-bisphosphate
-
-
-
-
?
ATP + 1-phosphatidyl-1D-myo-inositol 3-phosphate
ADP + 1-phosphatidyl-1D-myo-inositol 3,5-bisphosphate
-
-
-
-
?
ATP + 1-phosphatidyl-1D-myo-inositol 3-phosphate
ADP + 1-phosphatidyl-1D-myo-inositol 3,5-bisphosphate
-
-
-
-
?
ATP + 1-phosphatidyl-1D-myo-inositol 3-phosphate
ADP + 1-phosphatidyl-1D-myo-inositol 3,5-bisphosphate
Drosophila sp. (in: flies)
-
Fab1 phosphatidylinositol 3-phosphate 5-kinase controls trafficking but not silencing of endocytosed receptors. Drosophila fab1 mutants contain undetectable phosphatidylinositol 3,5-bisphosphate levels, show profound increases in cell and organ size, and die at the pupal stage
-
-
?
ATP + 1-phosphatidyl-1D-myo-inositol 3-phosphate
ADP + 1-phosphatidyl-1D-myo-inositol 3,5-bisphosphate
-
-
-
-
?
ATP + 1-phosphatidyl-1D-myo-inositol 3-phosphate
ADP + 1-phosphatidyl-1D-myo-inositol 3,5-bisphosphate
-
-
-
?
ATP + 1-phosphatidyl-1D-myo-inositol 3-phosphate
ADP + 1-phosphatidyl-1D-myo-inositol 3,5-bisphosphate
-
-
-
?
ATP + 1-phosphatidyl-1D-myo-inositol 3-phosphate
ADP + 1-phosphatidyl-1D-myo-inositol 3,5-bisphosphate
-
regulation of 1-phosphatidyl-1D-myo-inositol 3,5-bisphosphate synthesis involving osmotic stress, interleukins, UV radiation, and autophosphorylation, overview
-
-
?
ATP + 1-phosphatidyl-1D-myo-inositol 3-phosphate
ADP + 1-phosphatidyl-1D-myo-inositol 3,5-bisphosphate
-
-
-
-
?
ATP + 1-phosphatidyl-1D-myo-inositol 3-phosphate
ADP + 1-phosphatidyl-1D-myo-inositol 3,5-bisphosphate
-
-
-
?
ATP + 1-phosphatidyl-1D-myo-inositol 3-phosphate
ADP + 1-phosphatidyl-1D-myo-inositol 3,5-bisphosphate
-
stress-activated enzyme
-
?
ATP + 1-phosphatidyl-1D-myo-inositol 3-phosphate
ADP + 1-phosphatidyl-1D-myo-inositol 3,5-bisphosphate
-
essential for vacuole function
-
?
ATP + 1-phosphatidyl-1D-myo-inositol 3-phosphate
ADP + 1-phosphatidyl-1D-myo-inositol 3,5-bisphosphate
-
generation of 1-phosphatidyl-1D-myo-inositol 3,5-bisphosphate is regulated by Vac7 protein, whereas turnover of 1-phosphatidyl-1D-myo-inositol 3,5-bisphosphate is mediated in part by the Sac1 polyphosphoinositide phosphatase family member Fig4
-
?
ATP + 1-phosphatidyl-1D-myo-inositol 3-phosphate
ADP + 1-phosphatidyl-1D-myo-inositol 3,5-bisphosphate
-
reaction is essential for retrograde trafficking between the vacuole/lysosome and the late endosome and also for trafficking of some proteins into the vacuole via multivesicular bodies, enzyme synthesis is regulated by vac14 and vac7, 2 upstream activators, physiological roles of the enzyme and regulation mechnaism, overview
-
-
?
ATP + 1-phosphatidyl-1D-myo-inositol 3-phosphate
ADP + 1-phosphatidyl-1D-myo-inositol 3,5-bisphosphate
regulation of 1-phosphatidyl-1D-myo-inositol 3,5-bisphosphate synthesis involving osmotic stress, overview, enzymes hydrolyzing the product are counteracting, overview
-
-
?
ATP + 1-phosphatidyl-1D-myo-inositol 3-phosphate
ADP + 1-phosphatidyl-1D-myo-inositol 3,5-bisphosphate
-
Fab1p and AP-1 are required for trafficking of endogenously ubiquitylated cargoes to the vacuole lumen
-
-
?
ATP + 1-phosphatidyl-1D-myo-inositol 3-phosphate
ADP + 1-phosphatidyl-1D-myo-inositol 3,5-bisphosphate
-
-
-
?
ATP + 1-phosphatidyl-1D-myo-inositol 3-phosphate
ADP + 1-phosphatidyl-1D-myo-inositol 3,5-bisphosphate
-
phosphatidylinositol(3,5)bisphosphate is essential for cellular responses to various stresses and for the mating pheromone signalling under starvation conditions
-
?
ATP + 1-phosphatidyl-1D-myo-inositol 3-phosphate
ADP + 1-phosphatidyl-1D-myo-inositol 3,5-bisphosphate
-
reaction is essential for retrograde trafficking between the vacuole/lysosome and the late endosome and also for trafficking of some proteins into the vacuole via multivesicular bodies, enzyme synthesis is regulated by vac14 and vac7, 2 upstream activators, physiological roles of the enzyme and regulation mechnaism, overview
-
-
?
ATP + 1-phosphatidyl-1D-myo-inositol 3-phosphate
ADP + 1-phosphatidyl-1D-myo-inositol 3,5-bisphosphate
-
regulation of 1-phosphatidyl-1D-myo-inositol 3,5-bisphosphate synthesis involving osmotic stress, overview
-
-
?
ATP + 1-phosphatidyl-1D-myo-inositol 3-phosphate
ADP + 1-phosphatidyl-1D-myo-inositol 3,5-bisphosphate
-
-
-
?
ATP + 1-phosphatidyl-1D-myo-inositol 3-phosphate
ADP + 1-phosphatidyl-1D-myo-inositol 3,5-bisphosphate
-
-
-
?
ATP + 1-phosphatidyl-1D-myo-inositol 3-phosphate
ADP + 1-phosphatidyl-1D-myo-inositol 3,5-bisphosphate
-
-
-
-
?
additional information

?
-
TLC measurement of phospholipids in wild-type and FAB1A-GFP-expressing plants, overview
-
-
?
additional information
?
-
-
PIKfyve participates in the SGK1-dependent regulation of the Na+, glucose cotransporter SGLT1 (SLC5A1)
-
-
?
additional information
?
-
physiological roles of the catalyzed reaction, overview
-
-
?
additional information
?
-
-
Fab1p activators, Vac7p and Vac14p, independently regulate Fab1p activity. A maximal increase in the levels of PI3,5P2 requires both Vac7p and the Vac14pFig4p complex
-
-
?
additional information
?
-
-
physiological roles of the catalyzed reaction, overview
-
-
?
Please wait a moment until the data is sorted. This message will disappear when the data is sorted.
Please wait a moment until the data is sorted. This message will disappear when the data is sorted.
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1-phosphatidylinositol-3-phosphate 5-kinase deficiency
Cell-Wall-Degrading Enzymes Required for Virulence in the Host Selective Toxin-Producing Necrotroph Alternaria alternata of Citrus.
1-phosphatidylinositol-3-phosphate 5-kinase deficiency
Class III PI 3-kinase is the main source of PtdIns3P substrate and membrane recruitment signal for PIKfyve constitutive function in podocyte endomembrane homeostasis.
1-phosphatidylinositol-3-phosphate 5-kinase deficiency
Deletion of PIKfyve alters alveolar macrophage populations and exacerbates allergic inflammation in mice.
1-phosphatidylinositol-3-phosphate 5-kinase deficiency
PIKfyve deficiency in myeloid cells impairs lysosomal homeostasis in macrophages and promotes systemic inflammation in mice.
1-phosphatidylinositol-3-phosphate 5-kinase deficiency
Transcription factor STE12alpha has distinct roles in morphogenesis, virulence, and ecological fitness of the primary pathogenic yeast Cryptococcus gattii.
Acquired Immunodeficiency Syndrome
Trehalose limits opportunistic mycobacterial survival during HIV co-infection by reversing HIV-mediated autophagy block.
Adenocarcinoma
Combined Inhibition of p38MAPK and PIKfyve Synergistically Disrupts Autophagy to Selectively Target Cancer Cells.
Albuminuria
Nephron specific knockin of the PIKfyve binding deficient Vac14L156R mutant results in albuminuria and mesangial expansion.
Alzheimer Disease
A cell-permeable tool for analysing APP intracellular domain function and manipulation of PIKfyve activity.
Alzheimer Disease
APP controls the formation of PI(3,5)P(2) vesicles through its binding of the PIKfyve complex.
Alzheimer Disease
The amyloid precursor protein (APP) binds the PIKfyve complex and modulates its function.
Arthritis
Inhibition of c-Rel DNA binding is critical for the anti-inflammatory effects of novel PIKfyve inhibitor.
Autoimmune Diseases
Structure-activity relationship study, target identification, and pharmacological characterization of a small molecular IL-12/23 inhibitor, APY0201.
Autoimmune Diseases
The Phosphoinositide Kinase PIKfyve Promotes Cathepsin-S-Mediated Major Histocompatibility Complex Class II Antigen Presentation.
Breast Neoplasms
The PIKfyve-ArPIKfyve-Sac3 triad in human breast cancer: Functional link between elevated Sac3 phosphatase and enhanced proliferation of triple negative cell lines.
Carcinogenesis
Elevated levels of PtdIns5P in NPM-ALK transformed cells: implication of PIKfyve.
Carcinogenesis
The phosphoinositide kinase PIKfyve mediates epidermal growth factor receptor trafficking to the nucleus.
Carcinoma
The phosphoinositide kinase PIKfyve mediates epidermal growth factor receptor trafficking to the nucleus.
Carcinoma, Hepatocellular
Akebia saponin E, as a novel PIKfyve inhibitor, induces lysosome-associated cytoplasmic vacuolation to inhibit proliferation of hepatocellular carcinoma cells.
Carcinoma, Non-Small-Cell Lung
The effects of PIKfyve inhibitor YM201636 on claudins and malignancy potential of nonsmall cell cancer cells.
Cardiomyopathies
Inhibition of PIKfyve prevents myocardial apoptosis and hypertrophy through activation of SIRT3 in obese mice.
Corneal Dystrophies, Hereditary
A novel mutation (p.Glu1389AspfsX16) of the phosphoinositide kinase, FYVE finger containing gene found in a Japanese patient with fleck corneal dystrophy.
Corneal Dystrophies, Hereditary
A novel PIKFYVE mutation in fleck corneal dystrophy.
Corneal Dystrophies, Hereditary
Characterization of pip5k3 fleck corneal dystrophy-linked gene in zebrafish.
Corneal Dystrophies, Hereditary
Corneal dystrophies.
Corneal Dystrophies, Hereditary
Endosomal phosphoinositides and human diseases.
Corneal Dystrophies, Hereditary
Identification of novel PIKFYVE gene mutations associated with Fleck corneal dystrophy.
Corneal Dystrophies, Hereditary
Mutations in PIP5K3 are associated with François-Neetens mouchetée fleck corneal dystrophy.
COVID-19
PIKfyve: a lipid kinase target for COVID-19, cancer and neurodegenerative disorders.
COVID-19
Synergistic block of SARS-CoV-2 infection by combined drug inhibition of the host entry factors PIKfyve kinase and TMPRSS2 protease.
COVID-19
The Global Phosphorylation Landscape of SARS-CoV-2 Infection.
COVID-19
The PIKfyve Inhibitor Apilimod: A Double-Edged Sword against COVID-19.
Dystonia
Altered homodimer formation and increased iron accumulation in VAC14-related disease: Case report and review of the literature.
Endometrial Hyperplasia
Autophagy in the physiological endometrium and cancer.
Endometrial Neoplasms
Autophagy in the physiological endometrium and cancer.
Glucose Intolerance
Muscle-specific Pikfyve gene disruption causes glucose intolerance, insulin resistance, adiposity, and hyperinsulinemia but not muscle fiber-type switching.
Glucose Intolerance
Unexpected severe consequences of Pikfyve deletion by aP2- or Aq-promoter-driven Cre expression for glucose homeostasis and mammary gland development.
Hyperinsulinism
Muscle-specific Pikfyve gene disruption causes glucose intolerance, insulin resistance, adiposity, and hyperinsulinemia but not muscle fiber-type switching.
Hypopigmentation
PIKfyve complex regulates early melanosome homeostasis required for physiological amyloid formation.
Infections
An STE12 gene identified in the mycorrhizal fungus Glomus intraradices restores infectivity of a hemibiotrophic plant pathogen.
Infections
fost12, the Fusarium oxysporum homolog of the transcription factor Ste12, is upregulated during plant infection and required for virulence.
Infections
Inhibition of PIKfyve kinase prevents infection by EBOV and SARS-CoV-2.
Infections
Inhibition of PIKfyve kinase prevents infection by Zaire ebolavirus and SARS-CoV-2.
Infections
Loss of PIKfyve drives the spongiform degeneration in prion diseases.
Infections
PIKfyve/Fab1 is required for efficient V-ATPase and hydrolase delivery to phagosomes, phagosomal killing, and restriction of Legionella infection.
Infections
Proteoglycan-Dependent Endo-Lysosomal Fusion Affects Intracellular Survival of Salmonella Typhimurium in Epithelial Cells.
Infections
Relevance of the transcription factor PdSte12 in Penicillium digitatum conidiation and virulence during citrus fruit infection.
Infections
Ste12 transcription factor homologue CpST12 is down-regulated by hypovirus infection and required for virulence and female fertility of the chestnut blight fungus Cryphonectria parasitica.
Infections
Synergistic block of SARS-CoV-2 infection by combined drug inhibition of the host entry factors PIKfyve kinase and TMPRSS2 protease.
Infections
The phosphatidylinositol-3-phosphate 5-kinase inhibitor apilimod blocks filoviral entry and infection.
Infections
The role of mitogen-activated protein (MAP) kinase signalling components and the Ste12 transcription factor in germination and pathogenicity of Botrytis cinerea.
Infections
Transcription Factor CfSte12 of Colletotrichum fructicola Is a Key Regulator of Early Apple Glomerella Leaf Spot Pathogenesis.
Infections
Vaccinia Virus Infection Requires Maturation of Macropinosomes.
Infertility
A dominant truncation allele identifies a gene, STE20, that encodes a putative protein kinase necessary for mating in Saccharomyces cerevisiae.
Infertility
Isolation of suppressor mutants of phosphatidylinositol 3-phosphate 5-kinase deficient cells in Schizosaccharomyces pombe.
Infertility
Role of STE genes in the mating factor signaling pathway mediated by GPA1 in Saccharomyces cerevisiae.
Infertility
Rst1 and Rst2 are required for the a/alpha diploid cell type in yeast.
Insulin Resistance
Muscle-specific Pikfyve gene disruption causes glucose intolerance, insulin resistance, adiposity, and hyperinsulinemia but not muscle fiber-type switching.
Insulin Resistance
Unexpected severe consequences of Pikfyve deletion by aP2- or Aq-promoter-driven Cre expression for glucose homeostasis and mammary gland development.
Liver Neoplasms
Inhibition of PIKfyve using YM201636 suppresses the growth of liver cancer via the induction of autophagy.
Lung Neoplasms
The effects of PIKfyve inhibitor YM201636 on claudins and malignancy potential of nonsmall cell cancer cells.
Lymphoma, Non-Hodgkin
B-cell non-Hodgkin lymphoma: Selective vulnerability to PIKFYVE inhibition.
Lymphoma, Non-Hodgkin
Identification of apilimod as a first-in-class PIKfyve kinase inhibitor for treatment of B-cell non-Hodgkin lymphoma.
Multiple Myeloma
Identification of PIKfyve kinase as a target in multiple myeloma.
Neoplasms
A Family of PIKFYVE Inhibitors with Therapeutic Potential Against Autophagy-Dependent Cancer Cells Disrupt Multiple Events in Lysosome Homeostasis.
Neoplasms
Autophagy in the physiological endometrium and cancer.
Neoplasms
B-cell non-Hodgkin lymphoma: Selective vulnerability to PIKFYVE inhibition.
Neoplasms
Combined Inhibition of p38MAPK and PIKfyve Synergistically Disrupts Autophagy to Selectively Target Cancer Cells.
Neoplasms
Elevated levels of PtdIns5P in NPM-ALK transformed cells: implication of PIKfyve.
Neoplasms
Inhibition of PIKfyve using YM201636 suppresses the growth of liver cancer via the induction of autophagy.
Neoplasms
PIKfyve inhibitor cytotoxicity requires AKT suppression and excessive cytoplasmic vacuolation.
Neoplasms
PIKfyve, MTMR3 and their product PtdIns5P regulate cancer cell migration and invasion through activation of Rac1.
Neoplasms
PIKfyve: a lipid kinase target for COVID-19, cancer and neurodegenerative disorders.
Neoplasms
Small molecule PIKfyve inhibitors as cancer therapeutics: Translational promises and limitations.
Neoplasms
The effects of PIKfyve inhibitor YM201636 on claudins and malignancy potential of nonsmall cell cancer cells.
Neoplasms
The Phosphoinositide Kinase PIKfyve Promotes Cathepsin-S-Mediated Major Histocompatibility Complex Class II Antigen Presentation.
Neurodegenerative Diseases
PIKfyve: a lipid kinase target for COVID-19, cancer and neurodegenerative disorders.
Obesity
Inhibition of PIKfyve prevents myocardial apoptosis and hypertrophy through activation of SIRT3 in obese mice.
Osteosarcoma
TRIM68, PIKFYVE, and DYNLL2: The Possible Novel Autophagy- and Immunity-Associated Gene Biomarkers for Osteosarcoma Prognosis.
Pancreatitis
Early to Late Endosome Trafficking Controls Secretion and Zymogen Activation in Rodent and Human Pancreatic Acinar Cells.
phosphatidylinositol 3-kinase deficiency
Active vacuolar H+ ATPase and functional cycle of Rab5 are required for the vacuolation defect triggered by PtdIns(3,5)P2 loss under PIKfyve or Vps34 deficiency.
Pneumonia
Deletion of PIKfyve alters alveolar macrophage populations and exacerbates allergic inflammation in mice.
Precursor Cell Lymphoblastic Leukemia-Lymphoma
Transcriptional Regulation of PIK3CD and PIKFYVE in T-Cell Acute Lymphoblastic Leukemia by IKAROS and Protein Kinase CK2.
Precursor T-Cell Lymphoblastic Leukemia-Lymphoma
Transcriptional Regulation of PIK3CD and PIKFYVE in T-Cell Acute Lymphoblastic Leukemia by IKAROS and Protein Kinase CK2.
Prion Diseases
Loss of PIKfyve drives the spongiform degeneration in prion diseases.
Severe Acute Respiratory Syndrome
Inhibition of PIKfyve kinase prevents infection by Zaire ebolavirus and SARS-CoV-2.
Starvation
AMPK-activated ULK1 phosphorylates PIKFYVE to drive formation of PtdIns5P-containing autophagosomes during glucose starvation.
Starvation
An AMPK-ULK1-PIKFYVE signaling axis for PtdIns5P-dependent autophagy regulation upon glucose starvation.
Starvation
Candida glabrata STE12 is required for wild-type levels of virulence and nitrogen starvation induced filamentation.
Starvation
Genomewide mechanisms of chronological longevity by dietary restriction in budding yeast.