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Human CYR61 Protein expressed in Wheat germ - ABIN1351026
Jeansonne, Pacifici, Lassak, Reiss, Russo, Zabaleta, Peruzzi: Differential Effects of MicroRNAs on Glioblastoma Growth and Migration. in Genes 2014
Show all 16 Pubmed References
High CCN1 expression is associated with pancreatic cancer cell invasion.
Studied CYR61 genetic variants in osteosarcoma patients.
Results indicate that ATF3 up-regulates the expression of CYR61 through directly binding to an area near the transcriptional start site of CYR61, which contributes to the inhibition of hepatocellular carcinoma (HCC) progression.
CYR61 could be an adjuvant biomarker associated with the inflammatory activity of Graves' orbitopathy (GO).
Serum CCN1 concentrations in Acute Heart Failure patients were significantly increased compared with those in individuals without Acute Heart Failure (237 pg/ml vs. 124.8 pg/ml, p< 0.001).
Results show that mRNA and serum expression levels of Cyr61, CTGF, and VEGF in muscle tissues of patients with polymyositis (PM)/dermatomyositis (DM). These data suggest that these genes may be involved in the pathogenesis mainly by affecting the formation of blood vessels and promoting inflammatory response.
the CC genotype of CYR61significantly increased the risk of acute myeloid leukemia (AML) in the dominant inheritance and the recessive inheritance. Additionally, it was shown that the rs2297141 and rs6576776 genotypes were associated with AML-M5 and AML-M2, respectively. Our findings indicated that genetic polymorphisms in the CYR61 gene may be considered potential AML risk factors in the Han Chinese population
Study describes how cysteine-rich 61 (CCN1) promotes monocyte migration by upregulating monocyte chemoattractant protein-1 (CCL2) expression in osteoblasts in rheumatoid arthritis (RA) disease. CCN1 could serve as a potential target for RA treatment.
MiR-365 acts as a tumor suppressor in OS, partly, by targeting CYR61 expression.
CCN1 may be involved in the progression of the hepatic cirrhosishepatocellular carcinoma axis through regulating Hepatic stellate cells.
study is the first to reveal that Cyr61 is elevated in ALL and promotes cell survival through the AKT/NF-kappaB pathway by up-regulating Bcl-2.
PPARgamma agonists may have beneficial effects on the migration and invasion of rheumatoid arthritis-fibroblast-like synoviocytes via the downregulation of Cyr61.
CCN1 stimulates CCL20 production in vitro and in vivo, and thus supports the notion that overexpressed CCN1 in hyperproliferating keratinocyte is functionally involved in the recruitment of inflammatory cells to skin lesions affected by psoriasis.
Plasma Cyr61 concentration in pulmonary arterial hypertension (PAH)patients was highly increased. Cyr61 could promote pulmonary arterial smooth muscle cells proliferation via AKT pathway, indicating that Cyr61 may play a role in the pathogenesis of PAH.
Cyr61 and VEGF expressions were independent prognostic indicators of overall survival and may serve as important prognostic predictors in patients with osteosarcoma.
our study suggests that suppression of Cyr61 in cancer stem cell-like cells in PDAC may inhibit tumor cell metastasis after resection of the primary tumor.
CYR61 promotes breast cancer lung metastasis by facilitating tumor cell extravasation and protecting from anoikis during initial seeding to the lung.
Knockdown of CYR61 in gastric cancer AGS cells impairs the cancer cell migration and invasion, suggesting a driver role of CYR61 in metastasis.
This study is the first to describe how CCN1 promotes VEGF expression in osteoblasts and increased endothelial progenitor cells angiogenesis in rheumatoid arthritis disease.
Two interacting partners of urokinase-type plasminogen activator (uPA) receptor, the cysteine-rich angiogenic inducer 61 (Cyr61) and the Y-box-binding protein 1 (YB-1) were identified and their differential expression demonstrated in the triple-negative breast cancer (TNBC) cells as well as in tumors.
study provides evidence that CYR61 regulates adipocyte differentiation via multiple signaling pathways that involve at least the inactivation of mTORC1 signaling and the activation of canonical Wnt signaling.
Study shows that the interplay between CYR61-CTGF-NOV1 (CCN1) and Wnt5a in endothelial cells and pericytes determines the angiogenic outcome in a model of ischemic retinopathy. Data highlight the significance of CCN1-EC and CCN1-pericyte communication signals in driving physiological and pathological angiogenesis.
Mechanical cyclic stretch led to increased Cyr61 mRNA and protein expression, mobilized NF-kappaB from the cytoplasm to the nucleus and increased IL-8 secretion in A549 cells.
Blocking or knockdown CCN1 expression ameliorated skin inflammation and reduced the expression of CCL20 in both imiquimod and IL-23-induced psoriasis-like mouse models.
refine the leukocyte recruitment cascade model by introducing endothelium-bound CCN1 as an inflammation mediator and by demonstrating a role for platelets and patrolling Ly6C(low) monocytes in acute vascular inflammation.
Data show that cysteine rich protein 61 protein (CCN1) critically mediates doxorubicin (DOX)-induced cardiotoxicity.
Our results not only reveal a novel mechanism illustrating the role of Cyr61 in epidermis pathogenesis but also suggest that therapies targeting Cyr61 may represent a novel strategy in the treatment of psoriasis vulgaris.
The LPA1-CCN1 axis may be the central control for SMC migration.
these data suggest that the WNT/beta-catenin signaling pathway enhances pancreatic cancer development and malignancy in part via up-regulation of CYR61.
Lysophosphatidic acid induced time-dependent phosphorylation of serum response factor and CRE-binding protein in in smooth muscle cells, inducing transcription of CCN1.
Data show that Cysteine-rich 61 (CYR61) acts as a tumor-promoting gene in pancreatic neuroendocrine tumors.
CCN1 is an important regulator of chondrocyte maturation during cartilage development and homeostasis.
CCN1 exacerbates tracheal obliterative bronchiolitis by enhancing fibroproliferation via an alphavbeta3-integrin-independent pathway.
Data show that RNA silencing of CCN family member 1 protein (CCN1) inhibits retinal neovascularization (RNV) by inhibiting phosphoinositide 3-kinase (PI3K)/AKT protein signaling in mouse pup model of oxygen-induced retinopathy (OIR).
CCN genes are activated in heart failure.
These findings reveal a critical role for CCN1 in restoring mucosal homeostasis after intestinal injury
CCN1 is an injury response protein that functions not only to restrict fibrosis in the liver, but also to suppress hepatocarcinogenesis by inhibiting EGFR-dependent hepatocyte compensatory proliferation
Both knockin mice expressing a mutant CCN1 that is unable to bind alphavbeta3/alphavbeta5 and mice with Ccn1 knockdown are defective in neutrophil efferocytosis, resulting in exuberant neutrophil accumulation and delayed healing.
The increased expression of CYR61 in the Day 4 corpus lutum (CL) and its transient increase by prostaglandin F2alpha in Day 6, Day 10, and Day 16 CL indicate that CYR61 may play a role in regulating angiogenesis over the life span of the CL.
Together, these results indicate that Cyr61 is an important determinant of the genetic reprogramming that occurs in mechanically challenged cells.
Mechanical regulation of the Cyr61 gene in smooth muscle cells
The secreted protein encoded by this gene is growth factor-inducible and promotes the adhesion of endothelial cells. The encoded protein interacts with several integrins and with heparan sulfate proteoglycan. This protein also plays a role in cell proliferation, differentiation, angiogenesis, apoptosis, and extracellular matrix formation.
CCN family member 1
, IGF-binding protein 10
, cysteine-rich heparin-binding protein 61
, cysteine-rich, anigogenic inducer, 61
, insulin-like growth factor-binding protein 10
, protein CYR61
, cysteine rich protein 61
, cysteine-rich, angiogenic inducer, 61
, cysteine-rich angiogenic inducer 61
, protein CYR61-like
, insulin-like growth factor binding protein 10
, intermediate early
, secreted cysteine-rich protein cyr61