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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

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 Hydrolases
         3.4 Acting on peptide bonds (peptidases)
             3.4.22 Cysteine endopeptidases
                3.4.22.38 cathepsin K

Expression

Expression on EC 3.4.22.38 - cathepsin K

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EXPRESSION
ORGANISM
UNIPROT
LITERATURE
a marked increase in cathepsin K expression is seen in the lungs of patients with emphysema compared to normal subjects
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cathepsin K becomes up-regulated in its cerebral expression by neuroleptic treatment
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cathepsin K expression level is decreased in all tissues at 12 h post-infection with Aeromonas hydrophila
cathepsin K gene and protein expression is significantly up-regulated in synovium at the initial stage of osteoarthritis in rabbits
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cathepsin K levels decrease after nonsurgical treatment of periodontitis
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cathepsins K is elevated in endothelial cells by tumor necrosis factor-alpha stimulation
CtK expression is significantly increased in the muscle and gill at 3-24 h post-injection with bacterial lipopolysaccharide
CTSK expression is stimulated by nuclear factor kappaB ligand. Both, nuclear factor kappaB ligand treatment and overexpression of nuclear factor of activated T-cells c1 dramatically enhances CTSK promoter activity. Proximal nuclear factor of activated T-cells binding sites play a significant role in the nuclear factor of activated T-cells c1-mediated stimulation of CTSK gene expression by nuclear factor kappaB ligand
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expression of cathepsin K is significantly increased (2.7-1.6fold) in the low-energy laser irradiated group on days 2-7 compared with those in the non-irradiated group
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free cholesterol accumulation in macrophage membranes induces cathepsin K
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gingival crevicular fluid cathepsin K levels increase in periodontitis
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in fibroblasts, interleukin-1alpha and cellular confluence upregulate cathepsin K expression
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in osteosarcoma cells, tissue growth factor beta1 induces the secretion of cathepsin K by about 3fold
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increased expression of cathepsin K in tumors and tumor-associated cells may be a direct result of transcriptional regulation by ETS family members
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induction of cathepsin K expression in fibroblasts from young donors but not from old donors is observed both in vitro and in vivo after exposure to longwave UV-A (100-500 kJ/m2) in a time-dependent manner with a maximum 2 days after exposure. Induction of active cathepsin K is also seen 1 day after irradiation with UV-B and less so after exposure to ionizing radiation followed by decreased levels on the following days
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inhibiting calcineurin or chelation of intracellular Ca2+, prevents the stimulation of CTSK expression by nuclear factor kappaB ligand
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ligand of receptor activator of nuclear factor-kappaB does not induce cathepsin K expression in fibroblasts
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receptor activator of nuclear factor-kappaB or small GTPase Rab do not mediate cathepsin K induction
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serum cathepsin K decreases gradually after alendronate treatment (17% at 3 months, 22% at 6 months and 41% at 12 months)
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serum cathepsin K levels are higher in postmenopausal women with osteoporosis compared with healthy postmenopausal women and premenopausal women
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significantly down-regulated in intestine following Gram-negative bacteria Vibrio anguillarum immersion challenge
SM934-testosterone inhibits proliferation and metastasis ability of breast cancer cells via inhibiting the expression of cathepsin K followed by the inhibition of Bcl-xL
the levels of Cath K in serum of non-small cell lung cancer are comparable to those in controls
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there is a 3fold increase in cathepsin K activity in the lungs of guinea pigs after 12 weeks smoke exposure
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upregulated in three tissues (gill, skin and intestine) following Gram-positive bacteria Streptococcus iniae immersion challenge
vasoprotective shear stress inhibits cathepsin K protein expression and activation downstream of TNFalpha stimulation via reduced NF-kappaB activation and expression. TNFalpha stimulation activates JNK/c-jun phosphorylation, but reduction of NF-kappaB protein prevents induction of cathepsin K transcription under vasoprotective shear stress conditions