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In vitro transcription of capped mRNA with modified nucleotides and Poly(A) tail
TSA (Tyramide Signal Amplification), used for signal amplification of ISH, IHC and IC etc.
Separation of phosphorylated and non-phosphorylated proteins without phospho-specific antibody
A convenient and sensitive way for cell proliferation assay and cytotoxicity assay
Protect the integrity of proteins from multiple proteases and phosphatases for different applications.
GSK 525768A is the inactive stereoisomer of I-BET-762 which is a selective inhibitor of BET family with IC50 value of 35 nM [1].BET (bromodomain and extra-terminal domain) has 4 members, BRD2, BDR3, BRD4 and BRDT and plays an important role in regulating transcription. It has been shown that BET involves in the process of suppressing proinflammatory cytokines production by macrophages and has potent anti-proliferative effects on tumor cells [2]. I-BET-762 is a potent BET inhibitor and suppresses macrophage-derived proinflammatory cytokines production [1]. When tested with naïve CD4+ T cells, I-BET-762 treatment for short 2-d up-regulated anti-inflammatory cytokines production (IL-10, Lag 3 and Egr2) and down-regulated proinflammatory cytokines production (GM-CSF and IL-17) constantly [3]. When tested with LPS-treated C57BL/6 mice, administration with I-BET-762 (5 mg per kg, i.p.) significantly suppressed LPS-induced acute inflammation compared with control GSK 525768A treated group [1]. In adoptive transfer of EAE mouse model with 2D2 T cell receptor that producing IL-17, pretreated T cells with I-BET-762 suppressed T cell mediated inflammation and decreased macrophages recruitment compared with GSK 525768A treatment [3]. References: [1]. Nicodeme, E., et al., Suppression of inflammation by a synthetic histone mimic. Nature, 2010. 468(7327): p. 1119-23.[2]. Bartholomeeusen, K., et al., Bromodomain and extra-terminal (BET) bromodomain inhibition activate transcription via transient release of positive transcription elongation factor b (P-TEFb) from 7SK small nuclear ribonucleoprotein. J Biol Chem, 2012. 287(43): p. 36609-16.[3]. Bandukwala, H.S., et al., Selective inhibition of CD4+ T-cell cytokine production and autoimmunity by BET protein and c-Myc inhibitors. Proc Natl Acad Sci U S A, 2012. 109(36): p. 14532-7.