|Other Names||Suppression of tumorigenicity 5 protein, DENN domain-containing protein 2B, HeLa tumor suppression 1, ST5, DENND2B, HTS1|
|Target/Specificity||The synthetic peptide sequence used to generate the antibody AP6249a was selected from the C-term region of human ST5 . A 10 to 100 fold molar excess to antibody is recommended. Precise conditions should be optimized for a particular assay.|
|Format||The synthetic peptide was lyophilized with 100% acetonitrile and is supplied as a powder. Reconstitute with 0.1 ml deionized water for a final concentration of 1 mg/ml.|
|Storage||Maintain refrigerated at 2-8°C for up to 6 months. For long term storage store at -20°C.|
|Precautions||This product is for research use only. Not for use in diagnostic or therapeutic procedures.|
|Function||Guanine nucleotide exchange factor (GEF) which may activate RAB9A and RAB9B. Promotes the exchange of GDP to GTP, converting inactive GDP-bound Rab proteins into their active GTP- bound form. May be involved in cytoskeletal organization and tumorogenicity. Isoform 1 seems to be involved in a signaling transduction pathway leading to activation of MAPK1/ERK2. Isoform 3 may block ERK2 activation stimulated by ABL1. Isoform 3 may alter cell morphology and cell growth.|
|Tissue Location||Widely expressed with the exception of peripheral blood lymphocytes. Isoform 1 is expressed in several epithelial and fibroblast (including tumorigenic) but absent in lymphoid cell lines (at protein level). Isoform 3 is expressed in primary cell or weakly tumorigenic but not in tumorigenic cell lines (at protein level).|
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Provided below are standard protocols that you may find useful for product applications.
ST5 was identified by its ability to suppress the tumorigenicity of Hela cells in nude mice. The protein contains a C-terminal region that shares similarity with the Rab 3 family of small GTP binding proteins. This protein preferentially binds to the SH3 domain of c-Abl kinase, and acts as a regulator of MAPK1/ERK2 kinase, which may contribute to its ability to reduce the tumorigenic phenotype in cells.
Majidi, M., et al., J. Biol. Chem. 275(9):6560-6565 (2000).Hubbs, A.E., et al., Oncogene 18(15):2519-2525 (1999).Majidi, M., et al., J. Biol. Chem. 273(26):16608-16614 (1998).Lichy, J.H., et al., Nucleic Acids Res. 24(23):4700-4708 (1996).Lichy, J.H., et al., Cell Growth Differ. 3(8):541-548 (1992).
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