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GloboZymes/c-Jun GST/5μg/GLO127G-005
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产品说明
c-Jun GSTSource: Recombinant human produced in E. coliPurity: > 90% by SDS-PAGE, apparent Mr ~ 68-kDaSupplied: In 50 μl of 50 mM Tris-HCl pH 7.0 buffer containing 14 mM β-mercaptoethanol, 1 mM benzamidine, 0.1 mM phenylmethanesulfonyl fluoride, 1 mM EDTA and 10% glycerol. Maintain in aliquots at -70° C. Avoid repeated thawing.GloboZymes c-Jun preparations are suitable for studies on the kinetics, enzymology and regulation of the phosphorylation of this important proto-oncogene. The purified preparations are effective as substrate for JNK/SAPK, MAPK, GSK-3 and CK-2 among other protein kinases. The GST-tagged preparations are also used for binding and pull down studies.Background: The proto-oncogene c-Jun is an important transactivating factor. It is a component of the AP-1 and ATF-2 transcription factors. A wide variety of cellular signals regulate c-Jun acutely via modulation of its phosphorylation state. Phosphorylation can both inhibit and activate the proto-oncogene. GSK-3 phosphorylates c-Jun at a region proximal to the highly basic DNA binding domain (Thr239/Ser243/Ser249). This phosphorylation prevents DNA association with c-Jun homodimers, but not with c-Jun-c-Fos heterodimers. In contrast, phosphorylation by JNK/SAPK at Ser63 and Ser73, in a region proximal to the transactivation domain, activates the c-Jun/AP-1 and c-Jun/ATF2 transcriptional activator complexes to induce a number of genes. The MAP kinases ERK1 and ERK2  phosphorylate c-Jun at Thr91/Thr93/Thr95. However, the significance of these phosphorylations is uncertain.References:  Al-Murrani SW et al (1999)  Biochem J 341, 293-298  Karin M (1995)  J Biol Chem 270, 16483-16486  Woodgett JR et al (1996) Phil Trans R Soc Lond 351, 135-141  Kyriakis JM & Avruch J (2001)  Physiol Rev 81, 807-869

GloboZymesDEK蛋白

来源:在大肠杆菌中生产的带有GST标签的重组人肾脏。


纯度:通过SDS-PAGE> 90%,表观先生〜70-kDa。


提供:在50μl50 mM Tris-HCl pH 7.0缓冲液中1μg,该缓冲液包含14 mMβ-巯基乙醇,1 mM苯甲idine,0.1 mM苯基甲磺酰氟,1 mM EDTA和10%甘油。将制剂分装在-70°C下。避免反复融化。


别名:DEK-GST癌蛋白


背景:DEK是一种明显的Mr〜43 kDa的核磷酸蛋白,由于急性髓性白血病和骨髓增生异常综合症的一部分发生复发性(6; 9)染色体易位,与核孔蛋白CAN融合。DEK还可以在青少年类风湿关节炎和其他风湿性疾病中充当自身免疫抗原。DEK与转录共抑制子Human Daxx,SRm160剪接共激活子和HIV-2增强子相关。它通过将约束的正超螺旋引入无蛋白和染色质相关的DNA中来改变DNA的拓扑。DEK与I2PP2A / SET具有某些结构相似性,在急性未分化白血病中也与CAN融合蛋白出现。但是,DEK确实会直接影响PP2A的活性。 


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