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anti-Human Cathepsin K Antibodies:
anti-Mouse (Murine) Cathepsin K Antibodies:
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Chicken Polyclonal Cathepsin K Primary Antibody for IP, IHC - ABIN223282
López-Guisa, Cai, Collins, Yamaguchi, Okamura, Bugge, Isacke, Emson, Turner, Shankland, Eddy: Mannose receptor 2 attenuates renal fibrosis. in Journal of the American Society of Nephrology : JASN 2012
Show all 2 Pubmed References
Human Polyclonal Cathepsin K Primary Antibody for ELISA, WB - ABIN548113
Asagiri, Hirai, Kunigami, Kamano, Gober, Okamoto, Nishikawa, Latz, Golenbock, Aoki, Ohya, Imai, Morishita, Miyazono, Kato, Saftig, Takayanagi: Cathepsin K-dependent toll-like receptor 9 signaling revealed in experimental arthritis. in Science (New York, N.Y.) 2008
Human Monoclonal Cathepsin K Primary Antibody for IHC (p), ELISA - ABIN514786
Cordes, Bartling, Simm, Afar, Lautenschläger, Hansen, Silber, Burdach, Hofmann: Simultaneous expression of Cathepsins B and K in pulmonary adenocarcinomas and squamous cell carcinomas predicts poor recurrence-free and overall survival. in Lung cancer (Amsterdam, Netherlands) 2009
Sclerostin is degraded by cathepsin K in vitro. Cathepsin K degradation of sclerostin is affected by hypoxia.
Upregulation of CTSK seems to be associated with high incidence of lymphatic spread and poor survival in OSCC. CTSK could therefore serve as a predictive biomarker for OSCC.
expression of cathepsin B and X was detected in stromal cells and cancer cells throughout the glioblastoma (GBM) sections, whereas cathepsin K expression was more restricted to arteriole-rich regions in the GBM sections. Metabolic mapping showed that cathepsin B, but not cathepsin K is active in GSC niches.
our data showed that elevated Cathepsin K in epithelial ovarian cancer can potentiate the metastasis of epithelial ovarian cancer cells
results highlight the possibility that the interaction between GAGs and collagen under acidic conditions has a regulatory impact on cathepsin K-mediated bone degradation.
measurement of a periostin fragment resulting from in vivo cathepsin K digestion may help to identify subjects at high risk of fracture.
cathepsin K in the development of chronic subdural hematoma
Cathepsin K expression within the subchondral bone of the medial tibia plateau was not associated with osteoclast density or symptomatic knee osteoarthritis.
The enhanced invasion of carcinomas resulting from cathepsin K overexpression is probably due to the increased cell migration and adhesion. Thus, cathepsin K is implicated not only in protein degradation but also in invasion, migration and adhesion of oral squamous cell carcinomas.
positive expression of cathepsin K in melanoma of the skin is associated with other unfavorable prognostic factors
Patients affected by castration-resistant prostate carcinoma may be tested for cathepsin K, and a positive strong expression (2+) could be a useful predictive biomarker of response to targeted agents, aiding in the selection of patients eligible for these treatments.
Of 160 top compounds tested in enzymatic assays, 28 compounds showed blocking of the collagenase activity of Cathepsin K (CatK) at 100 muM.
Cathepsin K cleavage of SDF-1alpha inhibits its chemotactic activity towards glioblastoma stem-like cells.
Increased cathepsin K expression in skull base chordoma was associated with tumor invasion and reduced progression free survival.
Immunohistochemistry confirmed cathepsin K protein was expressed in lymphangioleiomyomatosis but not control lungs. Cathepsin K gene expression and protein and protease activity were detected in lymphangioleiomyomatosis -associated fibroblasts but not the LAM cell line 621-101.
The allosteric site of cathepsin K has been modified by site-directed mutagenesis, and it was shown that it is involved in specific regulation of the collagenolytic activity of cathepsin K.
Cathepsin K and osteocalcin plasma levels may be suggested as the significant markers of osteopoenia/osteoporosis. In addition, cathepsin K plasma level can be also a valuable marker of severe Coronary Atherosclerosis and Coronary Artery Calcification .
Six mutations in CTSK were identified in 33 families with pycnodysostosis. The high frequency of pycnodysostosis in Ceara State is the consequence of the high inbreeding in that region.
The above studies not only demonstrated that CTSK was widely expressed in tooth-related cells (including odonto- clasts, periodontal ligament cells, pulp cells and odonto- blasts), but also indicated that CTSK was closely related to the development of tissues in oral and maxillofacial region as well as occurrence and development of many oral diseases.
This mutation (c.480_481insT), (p.L160fsX173) is a novel frameshift mutation. The index case extends the phenotypic spectrum and the list of previously reported mutations in the CTSK gene.
Beta-catenin deletion in cathepsin K (CtsK)-expressing cells causes a severe loss of bone mass.
these data indicate that CatK not only plays a major role in bone remodeling but also modulates modeling-based cortical bone formation by degrading periostin and thereby moderating Wnt-beta-catenin signaling.
This study established a possible role of CatK in TLR7 proteolytic activation, Treg immunosuppressive activity, and lupus autoimmunity and pathology.
catK deficiency almost completely blunted the increased vascular remodeling response of apoE-/- mice to flow cessation, possibly by correcting hyperlipidemia-associated pro-inflammatory effects on the peripheral immune response
The effects of muscarinic receptor M3 knockout on cathepsin K expression, bone density and biomechanical properties of bone are reported.
Cathepsin K expression is increased in the bone of a diabetic mouse model.
Data suggest Ctsk gene, key gene upregulated during osteoclast differentiation, is transcriptionally activated during cell hypoxia-induced mitochondrial dysfunction/disruption; hnRNPA2 (heterogeneous ribonucleoprotein A2) is coactivator in this process.
cathepsin K knockout attenuates age-related decline in cardiac function via suppressing caspase-dependent and caspase-independent apoptosis
Data (including data from studies in knockout/transgenic mice) suggest that Ctsk is involved in inflammatory response and bone resorption in both rheumatoid arthritis and periodontitis; thus, Ctsk appears to play a role in osteoimmune responses.
In a mouse model of post-traumatic osteoarthritis, cathepsin K activity was significantly increased in injured knees relative to uninjured knees.
Gene deletion of cathepsin K in mice accelerated callus size resolution, significantly increased callus mineralized mass, and improved mechanical strength as compared to wild type mice.
synergism between HIV proteins and pro-atherogenic shear stress to increase endothelial cell expression of the powerful protease cathepsin K
in addition to its other effects, the absence of CatK in OCP limits their ability to engraft in a repairing fracture callus compared to WT OCP.
Cardiac mammalian target of rapamycin and extracellular signal-regulated kinases (ERK) signaling cascades were upregulated by pressure overload, the effects of which were attenuated by cathepsin K knockout.
The localization pattern of the intercellular junction proteins E-cadherin and occludin was altered in the colon of Ctsk-/- mice, suggesting potential impairment of the barrier function.
Targeted ablation of Ctsk in hematopoietic cells, or specifically in osteoclasts and cells of the monocyte-osteoclast lineage, resulted in increased bone volume and bone formation rate as well as osteoclast and osteoblast numbers.
cathepsin K contributes to the development of obesity-associated cardiac hypertrophy and may represent a potential target for the treatment to obesity-associated cardiac anomalies.
cathepsin K exocytosis is controlled by PKCdelta through modulation of the actin bundling protein myristoylated alanine-rich C-kinase substrate.
results raise significant concerns regarding in vivo bone phenotypes created using Ctsk(Cre/+) mice and warrant further investigation into the role of Cathepsin K in gametes as well as alternative tools for studying osteoclast-specific gene loss in vivo
CTK plays crucial direct roles in the early to intermediate stage of osteoarthritis development. CTK-positive chondrocytes and synovial cells may be a possible target to prevent disease progression in osteoarthritis.
The CTSK marker was associated with back fat thickness and lean cuts (P < 0.01), and average daily gain and feed:gain ratio (P < 0.05) estimated breeding values.
components of the large latent TGFss complex were identified as novel targets of cathepsin K at neutral pH.
The authors showed CTSK upregulation in human lung specimens and elevated serum CTSK levels of patients with tuberculosis, compared with controls.
Down-regulation of cathepsin K in synovium at the initial stage of osteoarthritis significantly accelerated cartilage degeneration.
CatK inhibition in horses did affect bone marrow nucleated cells other than mature osteoclasts rendering them hypo-responsive to both TLR4- and TLR9-induced inflammation, predicting a proteolytic activity for CatK within the MyD88 pathway and/or the following proteolytic events required for the cytokines secretion.
The protein encoded by this gene is a lysosomal cysteine proteinase involved in bone remodeling and resorption. This protein, which is a member of the peptidase C1 protein family, is predominantly expressed in osteoclasts. However, the encoded protein is also expressed in a significant fraction of human breast cancers, where it could contribute to tumor invasiveness. Mutations in this gene are the cause of pycnodysostosis, an autosomal recessive disease characterized by osteosclerosis and short stature.
, cathepsin O1
, cathepsin O2
, cathepsin X
, Cat K
, minisatellite 10q detected by probe MMS10
, cathepsin K
, cathepsin K preproprotein
, cathepsin K (pycnodysostosis)
, protein OC-2
, Cathepsin K