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CTHRC1 interacts with integrin beta3 and accelerates the FAK (show PTK2 Proteins) phosphorylation to promote ovarian cancer cell adhesion, migration and invasion in vitro and in vivo.
CTHRC1 plays a pivotal role in a great many fields, including increases bone mass, prevents myelination, reverses collagen synthesis in keloid fibroblasts, and increases fibroblast-like synoviocytes migration speed and abundant production of arthritic pannus in rheumatoid arthritis
CTHRC1, negatively regulated by miR (show MLXIP Proteins)-30c, promoted cell proliferation, invasion and migration and suppressed cell apoptosis in breast cancer, which might be by activating GSK-3beta/beta-catenin (show CTNNB1 Proteins) signaling and inhibiting Bax (show BAX Proteins)/Caspase-9 (show CASP9 Proteins)/Caspase-3 (show CASP3 Proteins) signaling respectively.
Our data suggest that CTHRC1 may act as an oncogenic driver in progression and metastasis of ESCC, and may serve as a potential biomarker for prognosis and personalized therapy.
The negative and sensitivity-predictive values of CTHRC1 staining were excellent for both lymph node and peritoneal metastases.
High CTHRC1 expression is associated with metastatic melanomas.
CTHRC1 was established as a novel marker of activated synoviocytes in murine experimental arthritis and rheumatoid arthritis
ANOS1 and its co-expression partner, CTHRC1, promote the development and metastasis of colorectal cancer.
Expression of CTHRC1 was significantly higher in Wilms' tumor compared to the expression in the adjacent non-cancerous tissues. High tumor expression of CTHRC1 was associated with tumor size, clinical stage, histopathological type, and vascular invasion/metastasis. Patients with high CTHRC1 expression also exhibited a shorter survival.
CTHRC1 expression is significantly upregulated in human masticatory mucosa during wound healing.
CTHRC1 secreted from osteocytes and osteoblasts functions as an inhibitor of osteoclast differentiation via inhibition of NFkappaB-dependent signaling.
These data suggest Cthrc1 reduces fibrotic tissue formation in bleomycin-induced lung fibrosis and the effect is potent enough to limit the decline in lung function.
CTHRC1 is an osteoclast-secreted coupling factor that regulates bone remodeling.
This study demonstrated that Cthrc1 plays a negative regulatory role, fine-tuning the onset of peripheral myelination.
this is the first demonstration of Cthrc1 as a marker of the severity of the disease progression in the dystrophic muscles.
Hormonal functions of Cthrc1 include regulation of lipid storage and cellular glycogen (show GYS1 Proteins) levels with potentially broad implications for cell metabolism and physiology.
Data show a dramatic discrepancy between ROSA26 reporter activity and Pdgfrb (show PDGFRB Proteins) promoter driven Cre dependent myc (show MYC Proteins)-tagged Cthrc1 transgene expression.
Downregulated by dietary beta-carotene in lungs of knockout Bcmo1 (show BCMO1 Proteins)-deficient mice.
Cthrc1 expression overlaps considerably with those reported for TGF-beta (show TGFB1 Proteins) family members and interstitial collagens.
This locus encodes a protein that may play a role in the cellular response to arterial injury through involvement in vascular remodeling. Mutations at this locus have been associated with Barrett esophagus and esophageal adenocarcinoma. Alternatively spliced transcript variants have been described.
collagen triple helix repeat containing 1
, collagen triple helix repeat-containing protein 1