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Recombinant Mouse VEGF164 (P.pastoris-expressed)
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| 性狀 | Recombinant Mouse VEGF164 (P.pastoris-expressed), 一種血管內(nèi)皮生長(zhǎng)因子亞型剪接變體,在通過 VEGFR-2 誘導(dǎo)內(nèi)皮細(xì)胞間黏附分子-1的表達(dá)、VEGFR-1 誘導(dǎo)白細(xì)胞的遷移以及在成人角膜中炎癥和血管生成方面更有效。
Synonyms rMuVEGF164; VEGF-A; VPF ; 重組小鼠血管內(nèi)皮生長(zhǎng)因子 164 (P.Pastoris 表達(dá)) Species Mouse Source P. pastoris Accession Q00731 Gene ID 22339 Molecular Weight Approximately 39 kDa AA Sequence MAPTTEGEQK SHEVIKFMDV YQRSYCRPIE TLVDIFQEYP DEIEYIFKPS CVPLMRCAGC CNDEALECVP TSESNITMQI MRIKPHQSQH IGEMSFLQHS RCECRPKKDR TKPEKHCEPC SERRKHLFVQ DPQTCKCSCK NTDSRCKARQ LELNERTCRC DKPRR Biological Activity The ED50 is <6 ng/mL as measured by HUVEC cells, corresponding to a specific activity of >1.7 × 105 units/mg. Appearance Lyophilized powder. Formulation Lyophilized after extensive dialysis against 25 mM HEPES and 150 mM NaCl, pH 7.0. Endotoxin Level <1.0 EU/μg, determined by LAL method. Reconstitution Reconstitute the lyophilized recombinant Mouse VEGF164 (P.pastoris-expressed) (rMuVEGF164) to 100 μg/mL using ddH2O. Storage & Stability Lyophilized recombinant Mouse VEGF164 (P.pastoris-expressed) (rMuVEGF164) is stored at -20°C. After reconstitution, it is stable at 4°C for 4 weeks or -20°C for longer. It is recommended to freeze aliquots at -20°C or -80°C for extended storage. Shipping Room temperature in continental US; may vary elsewhere. Background VEGF164 (165) is a proinflammatory isoform. VEGF164 was found to be significantly more potent at inducing inflammation. In vivo blockade of VEGF receptor (VEGFR)-1 significantly suppressed VEGF164-induced corneal inflammation. In vitro, VEGF164 more potently stimulated intracellular adhesion molecule (ICAM)-1 expression on endothelial cells, an effect that was mediated by VEGFR2. VEGF164 was also more potent at inducing the chemotaxis of monocytes, an effect that was mediated by VEGFR1. In an immortalized human leukocyte cell line, VEGF164 was found to induce tyrosine phosphorylation of VEGFR1 more efficiently[1]. VEGF164 is an important isoform in the pathogenesis of early diabetic retinopathy[2]. |
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