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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.
Pifithrin-μ is a potent inhibitor of? p53 binding and p53-mediated apoptosis with Kd value of 0.82 mM in vitro[1].The p53 is encoded in humans by the TP53 gene. The molecular mass of p53 is 53 KD. The p53 has the function of regulating the cell cycle, thus, it functions as preventing cancer, a tumor suppressor. The p53 plays an important role in apoptosis, inhibition of angiogenesis and genomic stability by activating DNA repair proteins, arresting cell growth though holding the cell cycle and initiating apoptosis. p53 becomes activated in response to DNA damage, osmotic shock, oxidative stress or other myriad stressors. Activated p53 activates the expression of several genes by binding DNA including p21. p21 binds to the G1-S/CDK complexes which is an important molecules for the G1/S transition, then causes cell cycle arrest. The increasing amount of p53 may be a solution for prevention of tumors spreading or treatment of them[1]. Pifithrin-μis a cell-permeable inhibitor of p53-binding and p53-mediated apoptosis. Pifithrin-μdirectly inhibits that p53 binds to mitochondria. Pifithrin-μ also inhibits p53 binds to Bcl-2 and Bcl-xL proteins. PFT-μbinds both Bcl-xL and p53 with Kd = 0.80 mM and 0.82 mM respectively.[1] Pifithrin-μ reduces apoptosis which triggered by nutlin-3 in ML-1 cells at 25μM [2]. Pifithrin-μ also selectively inhibits heat shock protein 70 (HSP 70) activity.Pre-treatment with Pifithrin-μcan rescue primary thymocytes from γ-irradiation? or DNA damaging agents in mice.[2]?? ?References: [1].?? ?Hagn F, Klein C, Demmer O, Marchenko N, Vaseva A, Moll UM, Kessler H: BclxL changes conformation upon binding to wild-type but not mutant p53 DNA binding domain. J Biol Chem 2010, 285(5):3439-3450.[2].?? ?Vaseva AV, Marchenko ND, Moll UM: The transcription-independent mitochondrial p53 program is a major contributor to nutlin-induced apoptosis in tumor cells. Cell Cycle 2009, 8(11):1711-1719.
