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VSIG4 encodes a v-set and immunoglobulin-domain containing protein that is structurally related to the B7 family of immune regulatory proteins. Additionally we are shipping VSIG4 Proteins (18) and VSIG4 Kits (3) and many more products for this protein.
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The VSIG4 upregulation by LMP1 (show PDLIM7 Antibodies) was regulated at the transcriptional level via the NF-kB signaling axis.
VSIG4 expression is significantly upregulated in human masticatory mucosa during wound healing
we concluded that let-7g-5p inhibits epithelial-mesenchymal transition (EMT (show ITK Antibodies)) consistent with reduction of glioma stem cell (GSC (show GSC Antibodies)) phenotypes by targeting VSIG4 in glioblastoma.
Data indicate that rotein kinase calpha (show PRKACA Antibodies) (PKCalpha (show PKCa Antibodies)) plays a role in downregulating complement receptor Ig (CRIg coded by V-set and Ig domain-containing protein 4 VSIG4) expression.
complement receptor of the immunoglobulin superfamily-L-factor H (show CFH Antibodies) protects glomerular mesangial cells from complement-mediated injury and proliferative lesions
we identified VSIG4 as a potential diagnostic marker of severe preeclampsia. The determination of this gene may improve the prognostic assessment of severe preeclampsia.
Data indicate that massive V-set and Ig domain-containing 4 VSIG4(+) cell infiltration throughout the non-small-cell lung cancer samples.
we showed that a complement receptor of the Ig superfamily (CRIg, also known as Z39Ig), a receptor for complement fragments (C3b and iC3b), was expressed on a subset of intestinal macrophages in murine and human large intestine
These results suggest that T cells can opposite T cell hyporesponsiveness through dampening Z39Ig inhibitory signals from macrophages and thus maintain their anti-viral function in chronic hepatitis B.
Results report the identification and characterization of a Complement Receptor of the Immunoglobulin superfamily, CRIg, that binds complement fragments C3b and iC3b.
These findings reveal a pattern recognition role for CRIg in the direct capture of circulating Gram-positive bacteria from the bloodstream via binding to bacterial teichoic acid.
The macrophage-expressed VSIG4 may act to alleviate renal tubulointerstitial injury via inhibition of T cell infiltration and secretion of inflammation related factors.
CRIg signals induce anti-intracellular bacterial phagosome activity in a chloride intracellular channel 3 (show CLIC3 Antibodies)-dependent manner.
CRIg plays an important role in regulating virus-induced Kupffer cell death and depletion of these cells from the liver sinusoidal lumen
The interstitial inflammatory cell infiltration and tubular lesion of VSIG4(-/-); urethral obstruction operation mice were increased, with the expression of TGF-beta1 (show TGFB1 Antibodies) increased and MMP-2 (show MMP2 Antibodies) reduced. VSIG4 may play a role in inhibiting interstitial fibrosis.
The specific expression of VSIG4 on resting macrophages suggests that VSIG4 may be important for the maintenance of T cell unresponsiveness in healthy tissues.
A soluble form of complement receptor of the immunoglobulin superfamily (CRIg) reversed inflammation and bone loss in two experimental models of arthritis by inhibiting the alternative pathway of complement in the joint.
This gene encodes a v-set and immunoglobulin-domain containing protein that is structurally related to the B7 family of immune regulatory proteins. The encoded protein may be a negative regulator of T-cell responses. This protein is also a receptor for the complement component 3 fragments C3b and iC3b. Alternate splicing results in multiple transcript variants.
V-set and immunoglobulin domain containing 4
, V-set and immunoglobulin domain-containing protein 4
, Ig superfamily protein
, complement receptor of the immunoglobulin superfamily
, protein Z39Ig