Ignet

Gene Information

Gene symbol: CYR61

Gene name: cysteine-rich, angiogenic inducer, 61

HGNC ID: 2654

Synonyms: GIG1, CCN1

Related Genes

#	Gene Symbol	Number of hits
1	AGT	1 hits
2	CLU	1 hits
3	COL1A1	1 hits
4	CTGF	1 hits
5	GAS6	1 hits
6	IGFBP2	1 hits
7	IGFBP6	1 hits
8	IGFBP7	1 hits
9	MMP2	1 hits
10	NOV	1 hits
11	TP53	1 hits
12	WISP1	1 hits
13	WISP2	1 hits
14	WISP3	1 hits

Related Sentences

#	PMID	Sentence
1	1725860	Identification and molecular characterization of insulin-like growth factor binding proteins (IGFBP-1, -2, -3, -4, -5 and -6).
2	1725860	Six different insulin-like growth factor binding proteins (IGFBPs) have been identified by molecular cloning of their cDNAs from rat and human tissues and designated as IGFBP-1, -2, -3, -4, -5 and -6.
3	1725860	The total number of amino acid residues for the mature rat BPs ranges from 201 for IGFBP-6 to 270 for IGFBP-2, while the human homologs range from 216 for IGFBP-6 to 289 for IGFBP-2.
4	1725860	One potential N-linked glycosylation site is located at the mid-region of rat and human IGFBP-4, whereas only human but not rat IGFBP-6 possesses one N-linked glycosylation site at the extreme C-terminal of the molecule.
5	1725860	An RGD sequence is found in the C-terminal of IGFBP-1 and -2.
6	12904165	The CCN family comprises cysteine-rich 61 (CYR61/CCN1), connective tIssue growth factor (CTGF/CCN2), nephroblastoma overexpressed (NOV/CCN3), and Wnt-induced secreted proteins-1 (WISP-1/CCN4), -2 (WISP-2/CCN5) and -3 (WISP-3/CCN6).
7	18187544	The matricellular proteins, cysteine-rich protein 61 (Cyr61) and connective tissue growth factor (CTGF), are aberrantly expressed in the retinal vasculature from the early stages of DR, but their effects on retinal pericytes are unknown.
8	18187544	We show herein that rat retinal pericytes (RRPs) exposed to advanced glycosylation-end products, an important injurious stimulus of diabetes, express increased levels of both Cyr61 and CTGF, and concomitantly undergo anoikis, a form of apoptosis by loss of cell-matrix interactions.
9	18187544	Adenovirus-mediated expression of Cyr61 and/or CTGF conferred an anoikis-prone phenotype to rat retinal pericytes, including decreased phosphotyrosine protein levels at focal adhesion points and formation of cortical actin rings.
10	18187544	When used as substrates for pericyte attachment and compared with other matrix proteins (e.g. type IV collagen), recombinant Cyr61 and CTGF proteins exhibited antiadhesive and apoptogenic activities.
11	18187544	Phosphatase inhibitors reversed these effects, suggesting that Cyr61 and CTGF promote dephosphorylation events.
12	18187544	Furthermore, Cyr61- and CTGF-induced apoptosis was mediated through the intrinsic pathway and involved the expression of genes that have been functionally grouped as p53 target genes.
13	18187544	Expression of the matrix metalloproteinase-2 gene, a known target of p53, was increased in pericytes overexpressing either Cyr61 or CTGF.
14	18187544	Inhibition of matrix metalloproteinase-2 had, at least in part, a protective effect against Cyr61- and CTGF-induced apoptosis.
15	18187544	Taken together, these findings support the involvement of Cyr61 and CTGF in pericyte detachment and anoikis, implicating these proteins in the pathogenesis of DR.
16	18187544	The matricellular proteins, cysteine-rich protein 61 (Cyr61) and connective tissue growth factor (CTGF), are aberrantly expressed in the retinal vasculature from the early stages of DR, but their effects on retinal pericytes are unknown.
17	18187544	We show herein that rat retinal pericytes (RRPs) exposed to advanced glycosylation-end products, an important injurious stimulus of diabetes, express increased levels of both Cyr61 and CTGF, and concomitantly undergo anoikis, a form of apoptosis by loss of cell-matrix interactions.
18	18187544	Adenovirus-mediated expression of Cyr61 and/or CTGF conferred an anoikis-prone phenotype to rat retinal pericytes, including decreased phosphotyrosine protein levels at focal adhesion points and formation of cortical actin rings.
19	18187544	When used as substrates for pericyte attachment and compared with other matrix proteins (e.g. type IV collagen), recombinant Cyr61 and CTGF proteins exhibited antiadhesive and apoptogenic activities.
20	18187544	Phosphatase inhibitors reversed these effects, suggesting that Cyr61 and CTGF promote dephosphorylation events.
21	18187544	Furthermore, Cyr61- and CTGF-induced apoptosis was mediated through the intrinsic pathway and involved the expression of genes that have been functionally grouped as p53 target genes.
22	18187544	Expression of the matrix metalloproteinase-2 gene, a known target of p53, was increased in pericytes overexpressing either Cyr61 or CTGF.
23	18187544	Inhibition of matrix metalloproteinase-2 had, at least in part, a protective effect against Cyr61- and CTGF-induced apoptosis.
24	18187544	Taken together, these findings support the involvement of Cyr61 and CTGF in pericyte detachment and anoikis, implicating these proteins in the pathogenesis of DR.
25	18187544	The matricellular proteins, cysteine-rich protein 61 (Cyr61) and connective tissue growth factor (CTGF), are aberrantly expressed in the retinal vasculature from the early stages of DR, but their effects on retinal pericytes are unknown.
26	18187544	We show herein that rat retinal pericytes (RRPs) exposed to advanced glycosylation-end products, an important injurious stimulus of diabetes, express increased levels of both Cyr61 and CTGF, and concomitantly undergo anoikis, a form of apoptosis by loss of cell-matrix interactions.
27	18187544	Adenovirus-mediated expression of Cyr61 and/or CTGF conferred an anoikis-prone phenotype to rat retinal pericytes, including decreased phosphotyrosine protein levels at focal adhesion points and formation of cortical actin rings.
28	18187544	When used as substrates for pericyte attachment and compared with other matrix proteins (e.g. type IV collagen), recombinant Cyr61 and CTGF proteins exhibited antiadhesive and apoptogenic activities.
29	18187544	Phosphatase inhibitors reversed these effects, suggesting that Cyr61 and CTGF promote dephosphorylation events.
30	18187544	Furthermore, Cyr61- and CTGF-induced apoptosis was mediated through the intrinsic pathway and involved the expression of genes that have been functionally grouped as p53 target genes.
31	18187544	Expression of the matrix metalloproteinase-2 gene, a known target of p53, was increased in pericytes overexpressing either Cyr61 or CTGF.
32	18187544	Inhibition of matrix metalloproteinase-2 had, at least in part, a protective effect against Cyr61- and CTGF-induced apoptosis.
33	18187544	Taken together, these findings support the involvement of Cyr61 and CTGF in pericyte detachment and anoikis, implicating these proteins in the pathogenesis of DR.
34	18187544	The matricellular proteins, cysteine-rich protein 61 (Cyr61) and connective tissue growth factor (CTGF), are aberrantly expressed in the retinal vasculature from the early stages of DR, but their effects on retinal pericytes are unknown.
35	18187544	We show herein that rat retinal pericytes (RRPs) exposed to advanced glycosylation-end products, an important injurious stimulus of diabetes, express increased levels of both Cyr61 and CTGF, and concomitantly undergo anoikis, a form of apoptosis by loss of cell-matrix interactions.
36	18187544	Adenovirus-mediated expression of Cyr61 and/or CTGF conferred an anoikis-prone phenotype to rat retinal pericytes, including decreased phosphotyrosine protein levels at focal adhesion points and formation of cortical actin rings.
37	18187544	When used as substrates for pericyte attachment and compared with other matrix proteins (e.g. type IV collagen), recombinant Cyr61 and CTGF proteins exhibited antiadhesive and apoptogenic activities.
38	18187544	Phosphatase inhibitors reversed these effects, suggesting that Cyr61 and CTGF promote dephosphorylation events.
39	18187544	Furthermore, Cyr61- and CTGF-induced apoptosis was mediated through the intrinsic pathway and involved the expression of genes that have been functionally grouped as p53 target genes.
40	18187544	Expression of the matrix metalloproteinase-2 gene, a known target of p53, was increased in pericytes overexpressing either Cyr61 or CTGF.
41	18187544	Inhibition of matrix metalloproteinase-2 had, at least in part, a protective effect against Cyr61- and CTGF-induced apoptosis.
42	18187544	Taken together, these findings support the involvement of Cyr61 and CTGF in pericyte detachment and anoikis, implicating these proteins in the pathogenesis of DR.
43	18187544	The matricellular proteins, cysteine-rich protein 61 (Cyr61) and connective tissue growth factor (CTGF), are aberrantly expressed in the retinal vasculature from the early stages of DR, but their effects on retinal pericytes are unknown.
44	18187544	We show herein that rat retinal pericytes (RRPs) exposed to advanced glycosylation-end products, an important injurious stimulus of diabetes, express increased levels of both Cyr61 and CTGF, and concomitantly undergo anoikis, a form of apoptosis by loss of cell-matrix interactions.
45	18187544	Adenovirus-mediated expression of Cyr61 and/or CTGF conferred an anoikis-prone phenotype to rat retinal pericytes, including decreased phosphotyrosine protein levels at focal adhesion points and formation of cortical actin rings.
46	18187544	When used as substrates for pericyte attachment and compared with other matrix proteins (e.g. type IV collagen), recombinant Cyr61 and CTGF proteins exhibited antiadhesive and apoptogenic activities.
47	18187544	Phosphatase inhibitors reversed these effects, suggesting that Cyr61 and CTGF promote dephosphorylation events.
48	18187544	Furthermore, Cyr61- and CTGF-induced apoptosis was mediated through the intrinsic pathway and involved the expression of genes that have been functionally grouped as p53 target genes.
49	18187544	Expression of the matrix metalloproteinase-2 gene, a known target of p53, was increased in pericytes overexpressing either Cyr61 or CTGF.
50	18187544	Inhibition of matrix metalloproteinase-2 had, at least in part, a protective effect against Cyr61- and CTGF-induced apoptosis.
51	18187544	Taken together, these findings support the involvement of Cyr61 and CTGF in pericyte detachment and anoikis, implicating these proteins in the pathogenesis of DR.
52	18187544	The matricellular proteins, cysteine-rich protein 61 (Cyr61) and connective tissue growth factor (CTGF), are aberrantly expressed in the retinal vasculature from the early stages of DR, but their effects on retinal pericytes are unknown.
53	18187544	We show herein that rat retinal pericytes (RRPs) exposed to advanced glycosylation-end products, an important injurious stimulus of diabetes, express increased levels of both Cyr61 and CTGF, and concomitantly undergo anoikis, a form of apoptosis by loss of cell-matrix interactions.
54	18187544	Adenovirus-mediated expression of Cyr61 and/or CTGF conferred an anoikis-prone phenotype to rat retinal pericytes, including decreased phosphotyrosine protein levels at focal adhesion points and formation of cortical actin rings.
55	18187544	When used as substrates for pericyte attachment and compared with other matrix proteins (e.g. type IV collagen), recombinant Cyr61 and CTGF proteins exhibited antiadhesive and apoptogenic activities.
56	18187544	Phosphatase inhibitors reversed these effects, suggesting that Cyr61 and CTGF promote dephosphorylation events.
57	18187544	Furthermore, Cyr61- and CTGF-induced apoptosis was mediated through the intrinsic pathway and involved the expression of genes that have been functionally grouped as p53 target genes.
58	18187544	Expression of the matrix metalloproteinase-2 gene, a known target of p53, was increased in pericytes overexpressing either Cyr61 or CTGF.
59	18187544	Inhibition of matrix metalloproteinase-2 had, at least in part, a protective effect against Cyr61- and CTGF-induced apoptosis.
60	18187544	Taken together, these findings support the involvement of Cyr61 and CTGF in pericyte detachment and anoikis, implicating these proteins in the pathogenesis of DR.
61	18187544	The matricellular proteins, cysteine-rich protein 61 (Cyr61) and connective tissue growth factor (CTGF), are aberrantly expressed in the retinal vasculature from the early stages of DR, but their effects on retinal pericytes are unknown.
62	18187544	We show herein that rat retinal pericytes (RRPs) exposed to advanced glycosylation-end products, an important injurious stimulus of diabetes, express increased levels of both Cyr61 and CTGF, and concomitantly undergo anoikis, a form of apoptosis by loss of cell-matrix interactions.
63	18187544	Adenovirus-mediated expression of Cyr61 and/or CTGF conferred an anoikis-prone phenotype to rat retinal pericytes, including decreased phosphotyrosine protein levels at focal adhesion points and formation of cortical actin rings.
64	18187544	When used as substrates for pericyte attachment and compared with other matrix proteins (e.g. type IV collagen), recombinant Cyr61 and CTGF proteins exhibited antiadhesive and apoptogenic activities.
65	18187544	Phosphatase inhibitors reversed these effects, suggesting that Cyr61 and CTGF promote dephosphorylation events.
66	18187544	Furthermore, Cyr61- and CTGF-induced apoptosis was mediated through the intrinsic pathway and involved the expression of genes that have been functionally grouped as p53 target genes.
67	18187544	Expression of the matrix metalloproteinase-2 gene, a known target of p53, was increased in pericytes overexpressing either Cyr61 or CTGF.
68	18187544	Inhibition of matrix metalloproteinase-2 had, at least in part, a protective effect against Cyr61- and CTGF-induced apoptosis.
69	18187544	Taken together, these findings support the involvement of Cyr61 and CTGF in pericyte detachment and anoikis, implicating these proteins in the pathogenesis of DR.
70	18676994	Proteins related to cell growth (CYR61, protein NOV, and clusterin) were increased, whereas growth arrest-specific 6 (GAS6) and growth/differentiation factor 6 were decreased by Ang II stimulation.
71	18676994	Ang II-stimulated changes of plasminogen activator inhibitor-1, GAS6, cathepsin B, and periostin were validated by Western blot.