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Validated All-in-One™ qPCR Primer for CXCL10(NM_001565.3) Search again
Product ID:
HQP009746
(click here to view gene annotation page)
Species:
Human
Symbol:
Alias:
C7, IFI10, INP10, IP-10, SCYB10, crg-2, gIP-10, mob-1
Gene Description:
C-X-C motif chemokine ligand 10
Target Gene Accession:
NM_001565.3(click here to view gene page)
Estimated Delivery:
Approximately 1-3 weeks, but may vary. Please email sales@genecopoeia.com or call 301-762-0888 to confirm ETA.
Important Note:
By default, qPCR primer pairs are designed to measure the expression level of the splice variant (accession number) you selected for this gene WITHOUT consideration of other possible variants of this gene. If this gene has multiple variants, and you would like to measure the expression levels of one particular variant, multiple variants, or all variants, please contact us for a custom service project at inquiry@genecopoeia.com.
Validated result:
Summary
This gene encodes a chemokine of the CXC subfamily and ligand for the receptor CXCR3. Binding of this protein to CXCR3 results in pleiotropic effects, including stimulation of monocytes, natural killer and T-cell migration, and modulation of adhesion molecule expression. [provided by RefSeq].
Gene References into function
- In a mouse model, this protein is expressed as a marker of hepatic inflammation and injury, suggesting a role in liver repair and regeneration.
- Production by endometrial stromal cells is regulated by inflammatory mediators; Level may regulate leukocyte trafficking in the endometrium
- synthesis was detected in human Leydig cells exposed to the Sendai virus, but not in human total germ cells
- These findings suggest that the CXCR3/CXCL10 axis may be involved in the T cell recruitment that occurs in peripheral airways of smokers with COPD and that these T cells may have a type-1 profile.
- bacterium-induced CXCL10(IP-10) secretion by osteoblast can be mediated in part through toll-like receptor 4
- Leishmania promastigotes release a granulocyte chemotactic factor and inhibit gamma-interferon-inducible protein 10 production by neutrophil granulocyte
- The IFN-gamma-inducible IP-10 protein was induced in human brain microvascular endothelial cells and astrocytes only after inflammatory stimuli.
- The structure of IP-10 has been solved by NMR spectroscopy and the surface of IP-10 that interacts with the N-terminus of the receptor CXCR3 has been defined.
- circulating IP-10 concentrations is increased in patients with Type I diabetes, but only during the early and subclinical stage of the disease.
- Gene expression is predictive for the individual response of children with chronic allograft nephropathy to mycophenolate mofetil.
- Increased levels of CXCL10 in cerebrospinal fluid were found in a subgroup of MS patients.
- IFNgamma stimulates the production of IP-10 and Mig in the SS ductal epithelium, and that IP-10 and Mig are involved in the accumulation of T cell infiltrates in the SS salivary gland.
- complex gene expression regulation for IP-10 in peripheral blood t lymphocytes, involving both calcineurin-dependent and -independent pathways, is demonstrated
- release is evoked by tumor necrosis factor-alpha and interferon-gamma in HaCaT cell line by interleukin-4
- highly expressed by mumps virus-infected Leydig cells and ribavirin does not block IP-10 production
- 17beta-estradiol inhibited interferon-gamma-induced interferon-induced protein of 10 kDa secretion, mRNA expression, and promoter activity in keratinocytes; effects may be mediated by cell surface receptors
- infection with cytomegalovirus was found to elicit the production of CXCL10 from primary microglial cells but not from astrocytes; CXCL10 production was regulated by human and viral interleukin-10
- This chemokine receptor stimulates HIV-1 replication.
- IP-10 expression and secretion in human monocytic cells is selectively induced by leptin
- Regulation of interferon-inducible cytokine IP-10 expression in rheumatoid arthritis.
- expression in serum and liver highest in chronic hepatitis C and correlates with accumulation of Il-18 and INFgamma mRNA in chronic hepatitis C, but not in hepatitis B nor in nonviral liver disorders
- Data suggest that in oral lichen planus, the presence of CCL5 and CXCL10 in the cytolytic granules of tissue-infiltrating CD8(+)T cells expressing CCR5 and CXCR3 reveals a potential self-recruiting mechanism involving activated effector cytotoxic T cells
- Cannot be related to islet autoimmune processes in IDDM.
- A higher amount of IP-10 mRNA is expressed after exposure of keratinocytes to interferon-gamma, leading to migration of T cells from the dermis to the epidermis and representing a second step of chemotaxis following T cell recruitment from blood.
- CCR3 functional responses are regulated by both CXCR3 and its ligands CXCL9, CXCL10 and CXCL11.
- Constitutive NF-kappaB activity is required for the induced gene expression of CXCL10 in tumour cell lines in response to IFNgamma.
- Peak of expression of CXCL9 and CXCL10 occurred 4 days before CD8+ T cells infiltrated infected tissues. CXCL9 and CXCL10 may play role early during immune response against rickettsial infections.
- MIG and IP-10 are cleaved by gelatinase B and neutrophil collagenase
- In restinosis, increased plasma concentrations of IP10 were accompanied by a compensatory decrease in the CXCR3 expression on lymphocytes, but not monocytes, suggesting that a high plasma concentration of IP10 strongly induces monocytes signaling.
- both at molecular and protein levels CXCL10 and CXCL12 significantly increased only when cells were differentiated on calcium phosphate-coated slides
- furin is a novel chemokine-modifying enzyme in vitro and most probably also in vivo, generating a C-terminally truncated CXCL10, which fully retains its (inverse) agonistic properties.
- Nitric oxide suppressed IP-10 expression.
- Chronic production of CXCL10 does not alter synaptic plasticity in CXCL10 transgenic (TG)mouse hippocampal slices. By contrast, exogenous recombinant CXCL10 significantly inhibits long-term potentiation in slices from normal C57Bl/6J and CXCL10 TG mice.
- The chemokine CXCL10, usually associated with Th1 cells, is elevated in serum of patients with acute Syndenham's chorea.
- CXCL9, CXCL10, and CXCL11 functions are mediated by intracellular domains of CXCR3
- Pretransplant serum CXCL10 levels might represent a clinically useful parameter to identify subjects who are at high risk of severe rejection and graft failure.
- TRAIL pretreatment of endothelial cells down-modulated mRNA steady-state levels of several TNF-alpha-induced chemokines, and it abrogated the TNF-alpha-mediated up-regulation of CCL8 and CXCL10, modulating leukocyte/endothelial cell adhesion
- These data indicate that IFN-gamma mediates the recruitment of lymphocytes into the lung via production of the chemokine CXCL10, resulting in Tc1-cell alveolitis and granuloma formation.
- increased CXCL10 especially in hypothyroid patients with a more aggressive disorder, and normal CCL2 serum levels in autoimmune thyroiditis
- recruitment might enhance the sequestration of T cells in infected lymphoid organs and the spread of infection between cells, contributing to the immunopathology of AIDS
- IP-10/CXCR3 signaling is associated with the pathogenesis of human myasthenia gravis.
- These results suggest that inhibition of the CXCL10/CXCR3 axis offers a novel target for the treatment of asthma.
- Pretransplant serum CXCL10 levels greater than 150 pg/mL confer an increased risk of early, severe, acute rejection.
- CXCL10 creates a chemokine gradient between the cerebrospinal fluid (CSF) and serum and recruits CXCR3-expressing memory CD4+ T-cells into the CSF of neuroborreliosis patients.
- expression induced in macrophages by SARS-CoV infection
- Elevated bronchial mucosal expression of IP-10/CXCL10 is implicated in asthma pathogenesis; its action is partly through selective development and retention, or recruitment of T helper type 2, not Th1, receptor-bearing cells.
- IP10 inhibits viral replication through the induction of host cell death via a p53-mediated apoptotic pathway.
- Increase in serum CXCL10 with advancing age.
- IP-10 was increased in lung tissue from patients who died of SARS
- Increased expression of the interferon-induced angiostatic ELR- CXC chemokines is a feature of juvenile DM that parallels the degree of vasculopathy in patients with the disease.
- This CXCR3 ligand has the ability to activate biochemical (e.g., PtdIns 3-kinase and MAP kinase activation) and functional events in intestinal myofibroblasts.
- Increased plasma IP-10 levels in daughters and sisters of primary biliary cirrhosis (PBC) patients demonstrates involvement of IP-10 interaction with its receptor CXCR3 as a familial risk factor for PBC.
- Poly IC enhanced the expression of IP-10 mRNA and protein in concentration- and time-dependent manners. Overexpression of RIG-I or IRF-3 potentiated the poly-IC-induced upregulation of IP-10.
- High levels of CXCL10 are present in synovial fluid of children with juvenile idiopathic arthritis.
- Furthermore, hyaluronan, by inducing IL-8 and IP-10 by distinct pathways, provides a unique target for differential regulation of key inflammatory chemokines.
- Increased sCXCL10 is not associated with Hyper or Hypo per se, but is specifically sustained by the autoimmune inflammatory event occurring in both Graves disease and autoimmune thyroiditis
- CXCL10 is up-regulated in bronchoalveolar lavage fluid taken from human lungs 24 h after lung transplantation.
- Results suggest that MCP-1/CCL2 and IP-10/CXCL10 produced by astrocytes may activate astrocytes in an autocrine or paracrine manner and direct reactive gliosis followed by migration and activation of microglia/macrophages in demyelinating lesions.
- Elevated systemic levels of the chemokines MCP-1, IL-8, and IP-10 precede coronary heart disease but do not represent independent risk factors.
- M. bovis BCG-infected human epithelial cells can have an active role in a local inflammatory immune response via the secretion of IL-4, CXCL-8 and CXCL-10, which can be selectively regulated by Th2-derived cytokines
- inhibitory effect of CXCL10/IP-10 on the binding of dengue virus to cells may represent a novel contribution of this chemokine to the host defense against viral infection
- IP-10 mRNA is stabilized by RNA-binding proteins in monocytes treated with S100b
- These results indicated that CXCL10 inhibited LNCaP cell proliferation and decreased PSA production by up-regulation of CXCR3 receptor. CXCL10 may be potentially useful in the treatment of prostate cancer.
- Uregulation of IP-10 during infection of the islets in vivo is the first step towards destructive insulitis.
- Activation of Ras plays a critical role in modulating the expression of both CXCL10 and CXCR3-B, which may have important consequences in the development of breast tumors through cancer cell proliferation.
- IP-10 may play an important role in regulating lymphocytes into the lung and ENA-78 may be associated with lung parenchymal disease in pulmonary sarcoidosis.
- The early induction of IP-10 and IL-2, as well as the subsequent over-production of IL-6 and lack of IL-10 production, probably contribute to the main immuno-pathological processes involved in lung injury in SARS.
- Activation of CXCL10 transcription in response to interferon gamma was paralleled by a decrease in histone H4 acetylation and an increase in recruitment of the STAT1 complex to the CXCL10 interferon-stimulated response element locus.
- Preterm infants have the ability to induce a robust chemokine and cytokine response during sepsis, and IP-10 is a sensitive early marker of infection.
- The reduction of CXCL10 levels after 131I treatment in Graves disease shows that the thyroid gland itself is the main source of circulating CXCL10.
- GGTT haplotype of CXCL10 gene is not susceptibility factor for development of multiple sclerosis(MS), but is probably to influence the course of MS, possibly contributing to slow down disease progression.
- prolactin may enhance IFN-gamma-induced CXCL9, CXCL10, and CXCL11 production in keratinocytes
- A study of CXCL10 transport across vascular endothelial cells was done.
- PA increase in IP-10 gene expression (and 2- to 4-fold increases in IL-8, MCP-1, COX-2, and MIG). PA also induced an approximately 2-fold increase (p<0.05) in active NF-kappaB.
- IP-10 levels significantly reverse-correlated with vascular endothelial growth factor (VEGF) levels in uterine cervical cancers.
- The Th1 cytokine IFN stimulated the expression of IP-10.
- IP-10 release is specific to acute virus-induced asthma
- HO-1 can regulate the expression of the anti-angiogenic CXCL-10 and may alter a critical balance between angiogenic vs. anti-angiogenic factors that are important to maintain renal microvasculature during injury.
- synergy observed between lipopolysaccharides(LPS) and Interferon-gamma toward CXCL10 gene expression likely reflects the cooperative induction of the NF-kappaB and STAT1 transcription factors by LPS and Interferon-gamma, respectively
- Pyelonephritis in pregnant women is associated with an increased maternal serum concentration of the chemokine CXCL10.
- Elevated IP-10 levels are associated with and may contribute to liver damage in both HCV-monoinfected and HCV/HIV-coinfected patients.
- CXCL10 plays a central role in the pathogenesis of skin aGVHD by the recruitment of CXCR3(+) T cells to the sites of inflammation.
- serum IP-10 and MIG levels were significantly higher in lymphoproliferative disease of granular lymphocytes patients than in healthy donors, and MIG expression was associated with the number of circulating LGLs
- The existence of CXCL10 and CXCR3 with other CXC/CC chemokine signature in chronic pancreatitis is suggestive of their vital role in the progression of chronic inflammation.
- Patients with preeclampsia have significantly higher serum concentrations of chemokine (C-X-C motif) ligand 10(CXCL10/IP-10) than both normal pregnant women and mothers who have SGA neonates
- 3 markers in chemokine (C-X-C motif) ligand 10 (CXCL10, 4q21, 11,101 C>T, P=.007; 1642 C
- The serum IP-10 level was increased in AMI, and a higher level of serum IP-10 before PCI may be informative regarding infarct size.
- IP-10 expression in epithelial cell/PBMC co-cultures is regulated by multiple factors, such as intercellular interactions in addition to IFN-gamma and IL-12 levels.
- CXCL10 was detected in macrophages, endothelial cells, and fibroblasts in inflamed dental pulp.
- In colonic epithelial cells, depending on the cellular context and utilizing the NF-kappaB pathway, IL-1beta alone and/or in synergism with IFN-gamma may play a major role in the induction of CXCL10.
- Serum IP-10 levels reflected ulcerative colitis disease activity, and the source of IP-10 was granulocytes and monocytes.
- Chemokine IP-10 may play an important role in trafficking inflammatory cells to the local focus in the liver and induce the development of the chronicity of hepatitis B
- Cytokine treatment (TNF-alpha, IL-1beta and IFN-gamma) increased IP-10 and IL-8 protein and mRNA levels. Fluticasone (0.1 nM to 1 microM) increased IP-10 but reduced IL-8 protein release without changing IP-10 mRNA levels assessed by real time RT-PCR.
- DP8 cleavage of the N-terminal two residues of IP10 (CXCL10), ITAC (CXCL11) and SDF-1 (CXCL12), is reported.
- Low serum and peritoneal fluid concentration of interferon-gamma-induced protein-10 (CXCL10) in women with endometriosis.
- Data demonstrate high serum levels of CXCL10 in mixed cryoglobulinemia (MC) and that CXCL10 in MC+autoimmune thyroiditis patients are significantly higher compared to MC patients.
- Polymorphism G-210A in the promoter of CXCL10 gene could be a part of the genetic variation underlying the susceptibility of individuals to disease progression of chronic hepatitis B infection.
- CXCL-10 could play an important role in the intra-thyroid angiogenesis modulation, explaining, at least partiality, color Doppler ultrasound findings typical of thyroid autoimmune diseases.
- CXCL10 levels were lower in patients with Graves' disease, but the difference was statistically significant only when compared with patients with Hashimoto's thyroiditis.
- Significantly decreased interferon-gamma-inducible protein 10 expression is associated with angiogenesis in uterine endometrial cancers
- expression of chemokine receptor/ligand pairs such as CXCR3/CXCL10 have an important role in the proliferation of glioma cells
- These data provide new structure-function dimensions for chemokines in leukocyte mobilization, disclosing an anti-inflammatory role for PAD.
- Candida albicans-derived PGE(2) may impair IFN-gamma-induced IP-10 expression in human keratinocytes and may play a role in the pathogenesis of cutaneous candidiasis.
- IP-10 and il-2 are expressed in high levels in children with tuberculosis and may be used as a diagnostic tool.
- High CXCL10 and CCL2 serum levels in patients with mixed cryoglobulinemia and chronic hepatitis c(MC); CXCL10 in MC + autoimmune thyroiditis is significantly higher than that in MC.
- IFN-alpha2b possibly controls chemotaxis by regulating the interaction between CXCL10 and CXCR3A
- CXCL10 play an important role in the development of necroinflammation and fibrosis in the liver.
- NO inhibits HRV-16-induced production of CXCL10 by inhibiting viral activation of nuclear factor kappaB and of IRFs, including IRF-1, through a cGMP-independent pathway
- Like IFNgamma, IP-10 also does not distinguish between active tuberculosis (TB) and latent TB infection.
- Report downmodulatory effect of the antihistaminic drug bepotastine on CXCL10 expression in human keratinocytes.
- Measurement of pretransplant CXCL10 serum levels could be a clinically useful tool for predicting cardiac acute rejection, especially in the early posttransplant period.
- CXCL10 protein may serve as a marker for beta cell destruction and a potential mechanism for the switch from proliferation into apoptosis in insulin-secreting cells.
