|Calculated MW||86.0 kDa|
|Other Names||FGR, Gardner-Rasheed feline sarcoma viral (v-fgr) oncogene homolog, Gardner-Rasheed feline sarcoma viral (v-fgr) oncogene homolog, Proto-oncogene c-Fgr, p55-Fgr, p58-Fgr, p58c-Fgr|
|Source||Baculovirus (Sf9 insect cells)|
|Storage||-80°C; Recombinant protein in storage buffer (50 mM Tris-HCl, pH 7.5, 150 mM NaCl, 0.25 mM DTT, 0.1 mM EGTA, 0.1 mM EDTA, 0.1 mM PMSF, 25% glycerol).|
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Fgr is a protooncogene that is a unique member of the tyrosine kinase gene family. It is localized to the distal portion of the short arm of human chromosome 1 at p36.1-36.2 by in situ hybridization (1). Certain lymphomas (but not sarcomas or carcinomas) express fgr-related messenger RNA. This transcript is detected in Burkitt's lymphoma cell lines naturally infected with Epstein-Barr virus (EBV), but not in EBV-negative Burkitt's lymphoma cells (2). Normal umbilical cord or peripheral blood lymphocyte lines established in vitro by EBV infection also contain detectable c-fgr mRNA. Moreover, a 50-fold increase of the steady-state c-fgr mRNA concentration is observed when uninfected Burkitt's lymphoma cell lines are deliberately infected with EBV demonstrating the induction of a proto-oncogene in response to infection by a DNA tumour virus. Fgr expression is limited to normal peripheral blood granulocytes, monocytes, and alveolar macrophages, all of which contain 50 to 100 copies of c-fgr mRNA per cell (3). The c-fgr RNA molecules in these cells consisted of partially spliced transcripts containing intron 7 and completely spliced molecules capable of encoding the predicted p55 c-fgr protein. The level of fgr transcripts begin to increase 2 to 4 h after TPA addition, peak at 8 h, and subsequently declined suggesting transient transcriptional activation of fgr during TPA-induced differentiation. Cycloheximide also causes accumulation of c-fgr transcripts in U937 cells. Thus, c-fgr gene is expressed in a tissue- and development-specific fashion and constitutive expression of c-fgr in U937 cells is regulated by a labile transcriptional repressor.
Katamine S.,et al.Mol. Cell. Biol. 8:259-266(1988).
Gregory S.G.,et al.Nature 441:315-321(2006).
Mural R.J.,et al.Submitted (SEP-2005) to the EMBL/GenBank/DDBJ databases.
Brickell P.M.,et al.Br. J. Cancer 58:704-709(1988).
Inoue K.,et al.Oncogene 1:301-304(1987).
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