3.4.22.38: cathepsin K
This is an abbreviated version!
For detailed information about cathepsin K, go to the full flat file.
Word Map on EC 3.4.22.38
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3.4.22.38
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resorption
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osteoporosis
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osteoclastogenesis
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rankl
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tartrate-resistant
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osteoblast
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collagen
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nfatc1
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rankl-induced
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multinucleated
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mmp-9
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c-fos
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fracture
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trabecular
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pi
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calcitonin
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osteocalcin
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osteoprotegerin
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osteolytic
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resorb
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m-csf
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collagenolytic
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bisphosphonates
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osteoclast-mediated
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trap-positive
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osteoclast-specific
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odanacatib
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oscar
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antiresorptive
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tracp
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lacuna
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ovariectomy-induced
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rankl-mediated
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dc-stamp
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bone-resorbing
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sclerostin
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osteoclast-related
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telopeptide
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osteoclast-like
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osteoclastogenic
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denosumab
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preosteoclasts
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teriparatide
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pharmacology
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anti-osteoclastogenic
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osteosclerosis
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anti-osteoporotic
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atp6v0d2
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medicine
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ranelate
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drug development
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deoxypyridinoline
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rankl-stimulated
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diagnostics
- 3.4.22.38
- resorption
- osteoporosis
-
osteoclastogenesis
- rankl
-
tartrate-resistant
- osteoblast
- collagen
- nfatc1
-
rankl-induced
-
multinucleated
- mmp-9
- c-fos
-
fracture
-
trabecular
- pi
- calcitonin
- osteocalcin
- osteoprotegerin
-
osteolytic
-
resorb
- m-csf
-
collagenolytic
- bisphosphonates
-
osteoclast-mediated
-
trap-positive
-
osteoclast-specific
- odanacatib
- oscar
-
antiresorptive
- tracp
- lacuna
-
ovariectomy-induced
-
rankl-mediated
-
dc-stamp
-
bone-resorbing
-
sclerostin
-
osteoclast-related
-
telopeptide
-
osteoclast-like
-
osteoclastogenic
-
denosumab
-
preosteoclasts
-
teriparatide
- pharmacology
-
anti-osteoclastogenic
- osteosclerosis
-
anti-osteoporotic
- atp6v0d2
- medicine
-
ranelate
- drug development
-
deoxypyridinoline
-
rankl-stimulated
- diagnostics
Reaction
Broad proteolytic activity. With small-molecule substrates and inhibitors, the major determinant of specificity is P2, which is preferably Leu, Met > Phe, and not Arg =
Synonyms
Cat K, Cat-K, cath K, cathepsin K, cathepsin O, Cathepsin O2, cathepsin-K, catK, Ctk, CTSK, Human osteoclast cathepsin K, More, OC-2 protein, rhCK
ECTree
3.4.22.38 cathepsin KAdvanced search results
results (
results (Engineering
Engineering on EC 3.4.22.38 - cathepsin K
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PROTEIN VARIANTS 
ORGANISM
UNIPROT
COMMENTARY 
LITERATURE
G243E
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the missense mutation is associated with autosomal recessive pycnodysostosis
K9E
the mutant shows decreased catalytic efficiencies towards Z-Leu-Arg-7-amido-4-methylcoumarin and Z-Gly-Pro-Arg-7-amido-4-methylcoumarin compared to the wild type enzyme
K9E/I171E/Q172S
the mutant shows decreased catalytic efficiency towards Z-Leu-Arg-7-amido-4-methylcoumarin and increased catalytic efficiency towards Z-Gly-Pro-Arg-7-amido-4-methylcoumarin compared to the wild type enzyme
K9E/I171E/Q172S/N190M/K191G/L195K
the mutant shows decreased catalytic efficiency towards Z-Leu-Arg-7-amido-4-methylcoumarin and increased catalytic efficiency towards Z-Gly-Pro-Arg-7-amido-4-methylcoumarin compared to the wild type enzyme
K9E/N190M/K191G/L195K
the mutant shows increased catalytic efficiency towards Z-Leu-Arg-7-amido-4-methylcoumarin and decreased catalytic efficiency towards Z-Gly-Pro-Arg-7-amido-4-methylcoumarin compared to the wild type enzyme
N190M/K191G/L195K
the mutant shows increased catalytic efficiencies towards Z-Leu-Arg-7-amido-4-methylcoumarin and Z-Gly-Pro-Arg-7-amido-4-methylcoumarin compared to the wild type enzyme
Q187P
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a naturally occurring mutant gene, the c.684 A-C point mutation in exon 5 of the CTSK gene results in the typical clinical features found in Chinese patients with pycnodysostosis
Y67L/L205A
Y61D/V157L
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corresponding to the amino acid at that position in human enzyme, yields an enzyme with kinetic constants and inhibitor specificity profiles equivalent to human ortholog
S134A
site-directed mutagenesis of the rat residue Ser to the correspondent Ala of the human sequence, the mutant looses the P2 Hyp specificity
S134A/V160L
site-directed mutagenesis of the rat residues Ser and Val to the correspondent Ala and Leu, respectively, of the human sequence, the mutant looses the P2 Hyp specificity
V160L
site-directed mutagenesis of the rat residue Val to the correspondent Leu of the human sequence, the mutant looses the P2 Hyp specificity
additional information
Y67L/L205A
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10fold lower interaction with inhibitor stefin B (Ki: 0.0000000008) suggesting that Tyr67 and Leu205 are critical for interaction with stefin B. Inhibitor cystatin C Ki: 0.0000000087, inhibitor L-kininogen Ki: 0.0000000135, inhibitor H-kininogen Ki: 0.0000000145
Y67L/L205A
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this mutant fails to degrade bradykinin, indicating that Tyr67 and Leu205 are key active site residues for the kinin degrading activity of cathepsin
Y67L/L205A
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2-aminobenzoyl-RP-PGFSPFR-(3-nitrotyrosine) is not cleaved by the the mutant enzyme
additional information
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determination of six naturally occuring mutations in cathepsin K: an A-G transition at cDNA position 1095, a G-C transition at nucleotide 541, a C-T transition at nucleotide, a C-T transition at nucleotide 935, a G-A transition at nucleotide 236, and a T-C transition at nucleotide 926, overview
additional information
site-directed mutagenesis of the rat residues Ser and Val to the correspondent Ala and Leu, respectively, of the human sequence causes a loss of the P2 Hyp specificity, overview
additional information
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site-directed mutagenesis of the rat residues Ser and Val to the correspondent Ala and Leu, respectively, of the human sequence causes a loss of the P2 Hyp specificity, overview
additional information
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targeted disruption of cathepsin K results in defective Toll-like receptor 9 signaling in dendritic cells in response to unmethylated CpG DNA, which in turn leads to an attenuated induction of T helper 17 cells, without affecting the antigen-presenting ability of dendritic cells
additional information
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the effects of cathepsin K deficiency (ctsK-/-) on atherosclerotic plaque formation in brachiocephalic arteries in an aggressive atherosclerosis model using apoE-deficient mice on cholate-containing high fat diet is examined. Cathepsin K deficiency appears to increase lesion stability in brachiocephalic arteries by maintaining the integrity of the tunica media and by decreasing plaque vulnerability to rupture
additional information
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10-week-old male cathepsin K-deficient knockout mice show bones that are mechanically more brittle, while both osteoclasts and osteoblasts show impaired activity relative to the wild type, phenotype with significant hypercalcification of the calcified cartilage and cortices, overview
additional information
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bone marrow transplantation for selective disruption of CatK in the haematopoietic system, usage of total bone marrow progenitor cells from CatK-/-, CatK-/+, and CatK+/+, and low-density lipoprotein receptor knockout mice. Silencing of leucocyte CatK results in phenotypic changes in bone formation with an increased total bone mineral density in the CatK2/2 chimeras, effect of leucocyte cathepsin K deficiency on bone remodelling, overview
additional information
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catK-deficient cells show a similar suppression of actin rings as wild-type osteoclasts treated with inhibitor LHVS
additional information
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construction of male and female wild-type, heterozygous, and homozygous CatK null mice, phenotypes in young mice, bone mass, strength, resorption, and formation, overview. CatK-/- mice show higher bone mineral density at the central and distal femur. Central femur ultimate load is positively influenced by genotype, and is positively correlated with both cortical area and bone mineral content. Lumbar vertebral body ultimate load is also positively correlated to bone mineral content. Genotype does not influence the relationship of ultimate load to bone mineral content in either the central femur or vertebral body
additional information
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construction of transgenic UTU17 mice, overexpression of cathepsin K accelerates the resorption cycle and osteoblast differentiation in vitro, cathepsin K overexpression enhances osteogenesis and induces the formation of exceptionally small, actively resorbing osteoclasts from their bone marrow precursors in vitro, intracellular mechanisms, overview. The number of cathepsin K-containing vesicles in UTU17+/+ osteoclasts is highly increased
additional information
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enzyme deficiency leads to blocked adipogenesis in 3T3-L1 preadipocytes, while CatK overexpression leads to enhanced adipogenesis, phenotypes, overview
additional information
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overexpression of cathepsin K in mice decreases collagen deposition and lung resistance in response to bleomycin-induced pulmonary fibrosis, overview. Cathepsin K protein levels are strongly increased in alveolar macrophages and lung parenchymal tissue of mock-treated cathepsin K transgenic mice relative to wild-type mice
additional information
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phenotype comparisons of C57BL/6 mice either wild-type for cathepsin K, CK+/+, heterozygous for cathepsin K, CK+/-, or deficient in cathepsin K, CK-/-, no influence of cathepsin K deficiency on the severity of inflammation in arthritic knee joints, overview, Maintenance of the osteopetrosis phenotype of cathepsin K-deficient mice in arthritic mice
additional information
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catK-deficient cells show a similar suppression of actin rings as wild-type osteoclasts treated with inhibitor LHVS
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additional information
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10-week-old male cathepsin K-deficient knockout mice show bones that are mechanically more brittle, while both osteoclasts and osteoblasts show impaired activity relative to the wild type, phenotype with significant hypercalcification of the calcified cartilage and cortices, overview
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additional information
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overexpression of cathepsin K in mice decreases collagen deposition and lung resistance in response to bleomycin-induced pulmonary fibrosis, overview. Cathepsin K protein levels are strongly increased in alveolar macrophages and lung parenchymal tissue of mock-treated cathepsin K transgenic mice relative to wild-type mice
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additional information
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the single nucleotide polymorphism G15A in intron 4 of the porcine cathepsin K gene is associated with back fat thickness and production traits in Italian Duroc pigs, but not in Italian Large White pigs
