Rabbit BAD Polyclonal Antibody | anti-BAD antibody
Rabbit anti BAD
IHC-Paraffin: 1:50-1:200
WB: 1:500-1:2000
Storage in frost-free freezers is not recommended. This product should be stored undiluted.
Avoid repeated freezing and thawing as this may denature the antibody. Should this product contain a precipitate we recommend microcentrifugation before use. Shelf Life: 12 months from date of despatch
Testing Data
(Rabbit anti BAD antibody detects a band of approximately 18 kDa in PC3 cell lysate under reducing conditions)
Immunohistochemistry (IHC)
(Immunohistochemistry of paraffin-embedded rat kidney using Rabbit anti BAD antibody at a dilution of 1/200)
The precise role of BAD in apoptosis signaling depends on BAD's post-translational modification status. Nonphosphorylated BAD forms heterodimers with the two anti-apoptotic Bcl-2 protein family members, Bcl-xL and Bcl-2 (Zha et al. 1996). The binding of BAD to Bcl-xL promotes apoptosis by inhibiting the apoptosis repressor function of Bcl-xL (Yang et al. 1995). Once serine phosphorylated, BAD is unable to heterodimerize with Bcl-xL and interacts with 14-3-3 proteins instead (Masters et al. 1995). This binding retains BAD in the cytoplasm and thereby enables Bcl-xL to suppress apoptosis (Zha et al. 1996).
NCBI and Uniprot Product Information
NCBI Description
The protein encoded by this gene is a member of the BCL-2 family. BCL-2 family members are known to be regulators of programmed cell death. This protein positively regulates cell apoptosis by forming heterodimers with BCL-xL and BCL-2, and reversing their death repressor activity. Proapoptotic activity of this protein is regulated through its phosphorylation. Protein kinases AKT and MAP kinase, as well as protein phosphatase calcineurin were found to be involved in the regulation of this protein. Alternative splicing of this gene results in two transcript variants which encode the same isoform. [provided by RefSeq, Jul 2008]
Uniprot Description
Promotes cell death. Successfully competes for the binding to Bcl-X(L), Bcl-2 and Bcl-W, thereby affecting the level of heterodimerization of these proteins with BAX. Can reverse the death repressor activity of Bcl-X(L), but not that of Bcl-2 (). Appears to act as a link between growth factor receptor signaling and the apoptotic pathways.