BID Antibodies

BID (BH3 Interacting Domain Death Agonist) is a Protein Coding gene. Diseases associated with BID include Bladder Transitional Cell Papilloma and Colon Adenocarcinoma. Among its related pathways are Direct p53 effectors and Amyotrophic lateral sclerosis (ALS). Gene Ontology (GO) annotations related to this gene include ubiquitin protein ligase binding and death receptor binding.

CUSABIO produces high-quality anti-BID antibodies (includes polyclonal antibodies, monoclonal antibodies, recombinant antibodies) in house with strict quality control. And they can help you discover more in your research.
These BID antibodies are validated in multiple tissues with various applications and covering a broad range of life science research and drug development. They are featured with high specificity, multiple epitopes recognition, and wide species reactivity. Moreover, CUSABIO provides various options on sizes, excellent technical support and BID antibodies custom service.

BID Antibodies Catalog

BID Antibodies for Homo sapiens (Human)

BID Background

The BID gene encodes the BH3-interacting domain death agonist (BID), a pro-apoptotic member of the Bcl-2 protein family [1]. BID possesses a single BH3 (Bcl-2 homology 3) domain and lacks a C-terminal transmembrane domain for the outer mitochondrial membrane[1]. BID is localized in the cytosolic or on the plasma membrane. BID is inactive, but becomes activated after Caspase-8 cleavage [2][3][4]. Truncated BID (tBID) may expose the BH3 motif buried in the uncleaved molecule. Protease-cleaved BID subsequently translocates to mitochondria where it induces permeabilization of the mitochondrial outer membrane (MOM) dependent on the pro-apoptotic proteins Bax and/or Bak. BID, therefore, acts as a sentinel for protease-mediated death signals [7]. Mutagenesis study indicated that the BH3 domain is required for the apoptotic activity of BID since BID with an intact BH3 domain may retain interaction with BAX [4][5]. Cells generate pro-apoptotic proteins with a single active domain called BH3 in stress or damage. BID acts as an activator to induce the overexpression of effector pro-apoptotic proteins such as BAX (BCL2-associated X) and BAK (BCL2 antagonist/killer 1) [6]. The production of BAX and BAK further leads to cytochrome c release into the cytoplasm, following caspase activation and apoptosis [6].

[1] Wang K, Yin XM, et al. BID: a novel BH3 domain-only death agonist [J]. Genes Dev. 1996, 10 (22): 2859-9.
[2] Gross A., Yin X.-M., et al. Caspase cleaved BID targets mitochondria and is required for cytochrome c release, while BCL-XL prevents this release but not TNF-R1/Fas death [J]. J. Biol. Chem. 1999; 274: 1156-1163.
[3] Li H., Zhu H., et al. Cleavage of BID by caspase 8 mediates the mitochondrial damage in the Fas pathway of apoptosis [J]. Cell. 1998; 94: 491-501.
[4] Luo X., Budihardjo I. et al. Bid, a Bcl2 interacting protein, mediates cytochrome c release from mitochondria in response to activation of cell surface death receptors [J]. Cell. 1998; 94: 481-490.
[5] Wang K., Gross A., et al. Mutagenesis of the BH3 domain of BAX identifies residues critical for dimerization and killing [J]. Mol. Cell. Biol. 1998; 18: 6083-6089.
[6] Korsmeyer SJ, Wei MC, et al. Pro-apoptotic cascade activates BID, which oligomerizes BAK or BAX into pores that result in the release of cytochrome c [J]. Cell Death Differ 2001; 7: 1166-173.


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