|Application ||WB, IHC, IF|
|Calculated MW||20132 Da|
|Other Names||Bcl-2-related protein A1, Bcl-2-like protein 5, Bcl2-L-5, Hemopoietic-specific early response protein, Protein BFL-1, Protein GRS, BCL2A1, BCL2L5, BFL1, GRS, HBPA1|
|Target/Specificity||A synthetic peptide corresponding to residues in the N-term of human Bcl-2 related protein A1 was used as immunogen.|
|Format||50 mM Tris-Glycine (pH 7.4), 0.15 M NaCl, 40% Glycerol, 0.01% sodium azide and 0.05% BSA.|
|Storage||Maintain refrigerated at 2-8°C for up to 6 months. For long term storage store at -20°C in small aliquots to prevent freeze-thaw cycles.|
|Precautions||Bcl-2 A1/Bfl1 Antibody (N-term) is for research use only and not for use in diagnostic or therapeutic procedures.|
|Synonyms||BCL2L5, BFL1, GRS, HBPA1|
|Function||Retards apoptosis induced by IL-3 deprivation. May function in the response of hemopoietic cells to external signals and in maintaining endothelial survival during infection (By similarity). Can inhibit apoptosis induced by serum starvation in the mammary epithelial cell line HC11 (By similarity).|
|Tissue Location||Seems to be restricted to the hematopoietic compartment. Expressed in peripheral blood, spleen, and bone marrow, at moderate levels in lung, small intestine and testis, at a minimal levels in other tissues. Also found in vascular smooth muscle cells and hematopoietic malignancies|
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Provided below are standard protocols that you may find useful for product applications.
Bcl-2 related protein A1; also known as Bcl2A1 and Bfl1, is an anti-apoptotic Bcl-2 family member preferentially expressed in hematopoietic and endothelial cells (1). Bfl1 is involved in a variety of cellular activities such as embryonic development, homeostasis and tumorigenesis. Expression of Bfl1 is stimulated by NF-kB in response to inflammatory stimuli and up-regulated by TNF-alpha, IL1-beta, IGF1, GMC-SF, CD40 and phorbol ester (2-3). Bfl1 has also been shown to reduce the release of pro-apoptotic cytochrome c from mitochondria, block caspase activation and suppress apoptosis induced by p53 (4-5).
1. Lin, E. Y.; Orlofsky, A.; Berger, M. S.; Prystowsky, M. B.: J. Immun. 151: 1979-1988, 1993.
2. Lee, H. H., Dadgostar, H., Cheng, Q., Shu, J., and Cheng, G. (1999) Proc. Natl. Acad. Sci. U. S. A. 96, 9136-9141
3. Zong, W.-X., Edelstein, L. C., Chen, C., Bash, J., and Gelinas, C. (1999) Genes Dev. 13, 382-387
4. D'Sa-Eipper, C.; Subramanian, T.; Chinnadurai, G. : Cancer Res. 56: 3879-3882, 1996.
5. Arlette B. Werner, Evert de Vries, Stephen W. G. Tait, Ilja Bontjer, and Jannie Borst; J. Biol. Chem., Vol. 277, Issue 25, 22781-22788, June 21, 2002
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