c-Jun, Proto-Oncogene
Source: Recombinant human produced in E. coli
Purity: > 90% by SDS-PAGE, apparent Mr ~ 39-kDa
Supplied: 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, functional significance 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.
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.
Figure: A purified preparation of recombinant human c-Jun was subjected to SDS-PAGE. The gel was stained with Coomassie Blue.
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
