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The fibroblast-specific deletion of Basigin did not influence the growth, fertility and the general condition of the mice. No obvious differences were found in the size, morphology, and histological structure of the major organs, including heart, liver, spleen, lung and kidney, between the knockout mice and the control mice. The deletion of Basigin in fibroblasts did not induce apoptosis in the tissues of the major organs
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ectopic CD147-polarized distribution on basolateral membrane promotes hepatocyte depolarization by activation of the CD147-integrin alpha5beta1-E-cadherin ubiquitination-partitioning defective 3 decrease and beta-catenin translocation signaling cascade, replenishing a molecular pathway in hepatic carcinogenesis
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CD147 deletion in hepatic stellate cells alleviated CCl4-induced liver fibrosis and inhibited HSCs activation. Overexpression of CD147 upregulated the secretion of CXCL1.
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A new molecular mechanism for high angiogenic capacity, whereby microglia cells release basigin via up-regulation of PI3K-AKT and IGF-1 pathway to induce angiogenesis is unveiled.
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EMMPRIN inhibited bFGF-induced IL-6 secretion by reducing the p65 subunit phosphorylation, it might be concluded that bFGF and EMMPRIN crosstalk in their respective signaling pathways.
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protein-protein interaction studies on TRAF6 and BSG to get molecular level insights of the reactions.
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This study has highlighted basigin as a common essential molecule for various stimuli-induced impairment of retinal vascular barrier, which can be a target for strategies to establish a curative treatment of diabetic retinopathy
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Deletion of N-linked glycosylation at Asn152 on CD147 significantly suppressed in situ tumor metastasis in hepatocellular carcinoma.
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MCT1 and Basigin variant-2, but not Basigin variant-1, are expressed within the mouse pineal gland.
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this study provided a new mechanistic concept that CD147 can be a target for lymphocyte lineage reprogramming.
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these results suggested that CD147 plays a key role in reducing extrinsic apoptosis in spermatocytes, but not spermatogonia, through modulating NFkappaB signaling pathway.
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results establish neuroplastin and basigin as obligatory auxiliary subunits of native Plasma Membrane Calcium Atpases and key regulators of intracellular Ca2+ concentration.
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Data show that caveolin-3 binds to low glycosylated extracellular matrix metalloproteinase inducer (LG-EMMPRIN) in cardiac cells and in the hearts of healthy mice.
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These results suggest that basigin has a functional role as a binding partner with MCT2 in testicular and epididymal spermatozoa.
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both caveolin-1 and EMMPRIN mRNA levels increased gradually with progression of developmental stages, and peaked at day two postnatal. The current finding suggests that both caveolin-1 and EMMPRIN take part in mouse tooth development, especially in the differentiation and organization of odontogenic tissues.
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knockdown of CD147 on Hepa1-6 cells resulted in significantly increased T cells chemotaxis induced by CypA both in vivo and in vitro.
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These findings indicate that TGF-beta1-CD147 loop plays a key role in regulating the HSC activation and combination of TGF-beta receptor inhibitor and anti-CD147 antibody might be promised to reverse fibrogenesis.
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Decreased CD147 expression inhibited osteoclast formation and bone resorption, inhibited RANKL-induced nuclear translocation of the nuclear factor of activated T cells NFATc1.
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EMMPRIN promotes tumor growth and metastasis by recruitment of bone marrow-derived cells through controlling secretion and paracrine signaling of SDF-1 and VEGF.
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Results indicate the crucial roles of intracellular and extracellular Bsg in the pathogenesis of cardiac hypertrophy, fibrosis, and failure.
