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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
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 (show CTGF Proteins), and VEGF (show VEGFA Proteins) 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 (show CCNA2 Proteins)) promotes monocyte migration by upregulating monocyte chemoattractant protein-1 (CCL2 (show CCL2 Proteins)) expression in osteoblasts in rheumatoid arthritis (RA) disease. CCN1 (show CCNA2 Proteins) could serve as a potential target for RA treatment.
MiR (show MLXIP Proteins)-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 (show AKT1 Proteins)/NF-kappaB (show NFKB1 Proteins) pathway by up-regulating Bcl-2 (show BCL2 Proteins).
PPARgamma (show PPARG Proteins) agonists may have beneficial effects on the migration and invasion of rheumatoid arthritis-fibroblast-like synoviocytes via the downregulation of Cyr61.
CCN1 stimulates CCL20 prod (show CCNA2 Proteins)uction in vitro and in vivo, and thus supports the notion that overexpressed (show CCL20 Proteins)CCN1 in hyperproliferating k (show IL23A Proteins)eratinocyte 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.
Blocking or knockdown CCN1 (show CCNA2 Proteins) expression ameliorated skin inflammation and reduced the expression of CCL20 (show CCL20 Proteins) in both imiquimod and IL-23 (show IL23A Proteins)-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.
This study is the first to describe how CCN1 (show CCNA2 Proteins) promotes VEGF (show VEGFA Proteins) expression in osteoblasts and increased endothelial progenitor cells angiogenesis in rheumatoid arthritis disease.
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 (show LPAR1 Proteins)-CCN1 (show CCNA2 Proteins) axis may be the central control for SMC (show DYM Proteins) migration.
these data suggest that the WNT (show WNT2 Proteins)/beta-catenin (show CTNNB1 Proteins) 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.
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