BID Antibody (Antigen Affinity Purified)

BID Antibody ( Antigen Affinity Purified ) Datasheet

BID Antibody Product Information

• Immunogen: Recombinant Human BID protein (Catalog#10468-HNCE)
• Antibody Type: Rabbit Polyclonal Antibody ( Antibody Purification Platform )
• Ig Type: Rabbit IgG
• Formulation: 0.2 μm filtered solution in PBS with 5% trehalose
• Preparation: Produced in rabbits immunized with purified, recombinant Human BID (rh BID; Catalog#10468-HNCE; P55957-1; Met 1-Asp 195). BID specific IgG was purified by Human BID affinity chromatography.

BID Antibody Usage Guide

• Specificity: Human BID
• Western blot: This antibody can be used at 0.1-0.2 μg/mL with the appropriate secondary reagents to detect Human BID in WB. Using a DAB detection system, the detection limit for Human BID is approximately 0.5 ng/lane under non-reducing conditions and reducing conditions.
• Direct ELISA: This antibody can be used at 0.1-0.2 μg/mL with the appropriate secondary reagents to detect Human BID. The detection limit for Human BID is approximately 3 ng/well.
• Storage: This antibody can be stored at 2℃-8℃ for one month without detectable loss of activity. Antibody products are stable for twelve months from date of receipt when stored at -20℃ to -70℃. Preservative-Free.
  Sodium azide is recommended to avoid contamination (final concentration 0.05%-0.1%). It is toxic to cells and should be disposed of properly. Avoid repeated freeze-thaw cycles.

BID Antibody Background

BID, BH3-interacting domain death agonist, is a member of the Bcl-2 protein family. BID contains only the BH3 domain, which is required for its interaction with the Bcl-2 family proteins and for its pro-death activity. BID is susceptible to proteolytic cleavage by caspases, calpains, Granzyme B and cathepsins. It is an integrating key regulator of the intrinsic death pathway that amplifies caspase-dependent and caspase-independent execution of neuronal apoptosis. Therefore pharmacological inhibition of BID provides a promising therapeutic strategy in neurological diseases where programmed cell death is prominent, and also offer a new strategy for the treatment of acute renal failure associated with ischemia-reperfusion. BID receives direct inputs from a key regulator of the cell cycle arrest/DNA repair machinery (ATM), and therefore is an excellent candidate to coordinate genotoxic stress responses and apoptotic cell death. BID is a novel pro-apoptosis Bcl-2 family protein that is activated by caspase 8 in response to Fas/TNF-R1 death receptor signals. Activated BID is translocated to mitochondria and induces cytochrome c release, which in turn activates downstream caspases. Recent studies further indicate that BID may be more than just a killer molecule. Deletion of BID inhibits carcinogenesis in the liver, although this genetic alteration promotes tumorigenesis in the myeloid cells. This is likely related to the function of BID to promote cell cycle progression into S phase. BID could be also involved in the maintenance of genomic stability by engaging at mitosis checkpoint.

References

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4. Yin XM. 2006, Gene. 369: 7-19.
5. Yin XM. 2000, Cell Res. 10 (3): 161-7.