Ignet

Gene Information

Gene symbol: CXCL2

Gene name: chemokine (C-X-C motif) ligand 2

HGNC ID: 4603

Synonyms: SCYB2, GROb, MIP-2a, MGSA-b, CINC-2a

Related Genes

#	Gene Symbol	Number of hits
1	APLP2	1 hits
2	CCL11	1 hits
3	CCL2	1 hits
4	CCL20	1 hits
5	CCL24	1 hits
6	CCL3	1 hits
7	CCL4	1 hits
8	CCL5	1 hits
9	CCL8	1 hits
10	CCR5	1 hits
11	CSF3	1 hits
12	CXCL1	1 hits
13	CXCL10	1 hits
14	CXCL13	1 hits
15	CXCL5	1 hits
16	CXCL9	1 hits
17	CXCR4	1 hits
18	DDIT3	1 hits
19	IAPP	1 hits
20	IFNG	1 hits
21	IL10	1 hits
22	IL1B	1 hits
23	IL6	1 hits
24	MMP9	1 hits
25	TLR2	1 hits
26	TLR4	1 hits
27	TNF	1 hits
28	XCL1	1 hits

Related Sentences

#	PMID	Sentence
1	15191547	Similar results were noted at the molecular level by the persistent expression of tumor necrosis factor-alpha (TNF-alpha) and the chemokines MCP-1 and MIP-2.
2	15601743	The results showed that inflammatory cytokine stimulation of islets induced de novo expression of CCL2, CCL5/RANTES, CXCL9/MIG, and CXCL10/IP-10 and increased expression of CXCL2/macrophage-inflammatory protein-2.
3	15601743	Transplantation of islets with high levels of CCL2 into syngeneic recipients led to a significantly greater influx of CCR2(+) cells and higher expression of monocyte/macrophage-associated inflammatory cytokines compared with low CCL2-donor islets.
4	15601743	A direct toxic effect of CCL2 on islets was excluded by assessing cell viability and insulin release in vitro.
5	15826373	When injected into connective tissue of the scalp, purified FimA protein induced TNF-alpha and MIP-2 expression confirming that it is pro-inflammatory.
6	16132691	MCP-1 and MIP-2 expression and production in BB diabetic rat: effect of chronic hypoxia.
7	16132691	The aim was to investigate whether production of MIP-2 and MCP-1 are implicated in the pathogenesis of diabetes, and if the regulatory effects of these chemokines are affected by hypoxia.
8	16132691	Our data point to MCP-1 and MIP-2 as important components in the pathophysiology of diabetes, and hypoxia is an important and potent environmental stimulus capable of modulating the expression and production of these chemokines.
9	16132691	MCP-1 and MIP-2 expression and production in BB diabetic rat: effect of chronic hypoxia.
10	16132691	The aim was to investigate whether production of MIP-2 and MCP-1 are implicated in the pathogenesis of diabetes, and if the regulatory effects of these chemokines are affected by hypoxia.
11	16132691	Our data point to MCP-1 and MIP-2 as important components in the pathophysiology of diabetes, and hypoxia is an important and potent environmental stimulus capable of modulating the expression and production of these chemokines.
12	16132691	MCP-1 and MIP-2 expression and production in BB diabetic rat: effect of chronic hypoxia.
13	16132691	The aim was to investigate whether production of MIP-2 and MCP-1 are implicated in the pathogenesis of diabetes, and if the regulatory effects of these chemokines are affected by hypoxia.
14	16132691	Our data point to MCP-1 and MIP-2 as important components in the pathophysiology of diabetes, and hypoxia is an important and potent environmental stimulus capable of modulating the expression and production of these chemokines.
15	16844399	The worsening of sepsis and arthritis was associated with a significant increase in systemic and local production of IL-6, IL-1 beta, TNF-alpha, IL-10, macrophage inflammatory protein 1 alpha (MIP-1alpha), and MIP-2 and with a decrease in IFN-gamma production.
16	20848181	Over time, the normal non-ESWT treated wounds exhibited varying patterns of elevated expression of 25-30 genes, whereas wounds with impaired healing displayed prolonged elevated expression of only a few genes (CXCL2, CXCL5, CSF3, MMP9, TGF-α).
17	21813778	IL-1 blockade attenuates islet amyloid polypeptide-induced proinflammatory cytokine release and pancreatic islet graft dysfunction.
18	21813778	We sought to determine whether human islet amyloid polypeptide (hIAPP), the main component of islet amyloid, might contribute to islet inflammation by recruiting and activating macrophages.
19	21813778	Early aggregates of hIAPP, but not nonamyloidogenic rodent islet amyloid polypeptide, caused release of CCL2 and CXCL1 by islets and induced secretion of TNF-α, IL-1α, IL-1β, CCL2, CCL3, CXCL1, CXCL2, and CXCL10 by C57BL/6 bone marrow-derived macrophages. hIAPP-induced TNF-α secretion was markedly diminished in MyD88-, but not TLR2- or TLR4-deficient macrophages, and in cells treated with the IL-1R antagonist (IL-1Ra) anakinra.
20	21813778	Our results suggest that hIAPP-induced islet chemokine secretion promotes macrophage recruitment and that IL-1R/MyD88, but not TLR2 or TLR4 signaling is required for maximal macrophage responsiveness to prefibrillar hIAPP.
21	21859958	In response to M. tuberculosis infection, db/db mice exhibited disorganized granulomas, neutrophilia, and reduced B cell migration to the lungs, correlating with dysfunctional lung chemokine responses that include XCL1, CCL2, CXCL1, CXCL2, and CXCL13.
22	23235477	Unexpectedly, while Toll-like receptor 4 (TLR4) expression levels were comparable in kidneys of CHOP(-/-) and wild-type (WT) mice, CHOP(-/-) mice developed more severe AKI after LPS injection.
23	23235477	Additionally, the kidneys of LPS-treated CHOP(-/-) mice had a more prominent increase in NF-κB activation and further upregulation of proinflammatory genes, i.e., c-x-c motif ligand 1 (CXCL-1), macrophage inflammatory protein-2 (MIP-2), and IL-6.
24	23262028	CCL4 were examined in fracture calluses by immunohistochemistry and the role of TNF in diabetes-enhanced expression was investigated by treatment of animals with the TNF-specific inhibitor, pegsunercept.
25	23262028	Diabetes significantly upregulated mRNA levels of several chemokines in vivo including CCL4, CCL8, CCL6, CCL11, CCL20, CCL24, CXCL2, CXCL5 and chemokine receptors CCR5 and CXCR4.
26	23262028	Chondrocytes were identified as a significant source of CCL4 and its expression in diabetic fractures was dependent on TNF (P<0.05).