BAD Antibodies

BAD (BCL2 Associated Agonist Of Cell Death) is a Protein Coding gene. Diseases associated with BAD include B-Cell Lymphoma and Transient Cerebral Ischemia. Among its related pathways are Amyotrophic lateral sclerosis (ALS) and Immune response Fc epsilon RI pathway. Gene Ontology (GO) annotations related to this gene include protein heterodimerization activity and lipid binding.

CUSABIO produces high-quality anti-BAD 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 BAD 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 BAD antibodies custom service.

BAD Antibodies Catalog

BAD Antibodies for Homo sapiens (Human)

BAD Antibodies for Mus musculus (Mouse)

BAD Background

Bcl2-associated agonist of cell death (BAD) is a protein in humans that is encoded by a BAD gene. BAD belongs to a member of the BH3 ( Bcl-2 homology 3)-only family [1], a subfamily of the Bcl-2 family. BAD only contains the BH3 domain required for its induction of apoptosis [2][3] and lacks a C-terminal transmembrane domain for the outer mitochondrial membrane [4]. The sensitizer BH3-only protein BAD is abundantly expressed in many epithelial cells and acts in inducing apoptotic signals [2][5]. The pro-apoptotic functions of BAD are directly mediated through interaction of BAD with Bcl-2 and Bcl-xl via the BH3 domain of BAD and through subsequent ablation of the pro-apoptotic activity of Bcl-2 and Bcl-xl [3][6]. This ablation allows activation of downstream molecules, such as Bax and Bak, to induce the cell to apoptosis [7][8]. Li Jiang et al. demonstrated that BAD overexpression in non-small cell lung cancer (NSCLC) led cancer cells to undergo apoptosis through a mitochondrial pathway which is independent of Bax, Bcl-2, and Bcl-xl expression levels [9]. In addition to regulating apoptosis, BAD proteins also are associated with cell proliferation. But the effect of BAD on cell proliferation may be cell- type-specific. For example, increased BAD expression promotes the proliferation of prostate cancer cells [10]. And previous studies have reported that BAD contributes to tumorigenesis in several cancers [11-13]. Whereas, cell growth is inhibited by BAD overexpression in breast cancer cell MCF7 [14], lung adenocarcinoma cell line A549 [15], and NSCLC [9]. It suggests that BAD is a novel potential target for tumor interventions.

[1] Adachi M, Imai K . The proapoptotic BH3-only protein BAD transduces cell death signals independently of its interaction with Bcl-2 [J]. Cell Death Differ. 2002, 9 (11): 1240-7.
[2] Zha J, Harada H, et al. Serine phosphorylation of death agonist BAD in response to survival factor results in binding to 14-3-3 not BCL-XL [J]. Cell, 1996, 87: 619-628.
[3] Zha J, Harada H, et al. BH3 domain of BAD is required for heterodimerization [J]. J. Biol. Chem. 1997, 272: 24101-24104.
[4] K Wang, X M Yin, et al. BID: A Novel BH3 Domain-Only Death Agonist [J]. Genes Dev, 1996, 10 (22), 2859-69.
[5] Kitada S, Krajewska M, et al. Expression and location of pro-apoptotic Bcl-2 family protein BAD in normal human tissues and tumor cell lines Am [J]. J. Pathol. 1998, 152: 51–61.
[6] Yang E, Zha J, et al. Bad, a heterodimeric partner for Bcl-XL and Bcl-2, displaces Bax and promotes cell death [J]. Cell, 1995, 80: 285-291.
[7] Adams JM, Cory S. The Bcl-2 apoptotic switch in cancer development and therapy [J]. Oncogene. 2007 Feb 26; 26(9):1324-37.
[8] Sommer P, Cowen RL, et al. Glucocorticoid receptor over-expression promotes human small cell lung cancer apoptosis in vivo and thereby slows tumor growth [J]. Endocr Relat Cancer. 2010 Mar; 17 (1):203-13.
[9] Li Jiang, Man Luo, et al. BAD overexpression inhibits cell growth and induces apoptosis via mitochondrial-dependent pathway in non-small cell lung cancer [J]. Cancer Cell Int. 2013; 13: 53.
[10] Smith AJ, Karpova Y, et al. Expression of the Bcl-2 protein BAD promotes prostate cancer growth [J]. PLoS One. 2009 Jul 13; 4(7):e6224.
[11] Sinicrope FA, Rego RL, et al. Proapoptotic Bad and Bid protein expression predict survival in stages II and III colon cancers [J]. Clin Cancer Res. 2008 Jul 1; 14(13):4128-33.
[12] Al-Bazz YO, Underwood JC, et al. Prognostic significance of Akt, phospho-Akt and BAD expression in primary breast cancer [J]. Eur J Cancer. 2009 Mar; 45(4):694-704.
[13] Marchion DC, Cottrill HM, et al. BAD phosphorylation determines ovarian cancer chemosensitivity and patient survival [J]. Clin Cancer Res. 2011 Oct 1; 17(19):6356-66.  
[14] Fernando R, Foster JS, et al. Breast cancer cell proliferation is inhibited by BAD: regulation of cyclin D1 [J]. J Biol Chem. 2007 Sep 28; 282(39):28864-73.
[15] Huang N, Zhu J, et al. Overexpression of Bcl-2-associated death inhibits A549 cell growth in vitro and in vivo [J]. Cancer Biother Radiopharm. 2012 Mar; 27(2):164-8.

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