Phospho-Bad (Ser112) Antibody (YA3099)
(Synonyms: BAD; BBC6; BCL2L8; Bcl2 antagonist of cell death; BAD; Bcl-2-binding component 6; Bcl-2-like protein 8; Bcl2-L-8; Bcl-XL/Bcl-2-associated death promoter)
Based on 1 Customer Validation
Phospho-Bad (Ser112) Antibody (YA3099) is a Rabbit-derived and non-conjugated IgG monoclonal antibody, targeting to Phospho-Bad (Ser112).
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Host:
Rabbit
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Isotype:
IgG
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Application:
WB, IP
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Reactivity :
Human, Mouse, Rat
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Formulation:
Supplied in rabbit IgG in 10mM PBS, pH 7.4, 150mM sodium chloride, 0.05% BSA, 0.02% sodium azide and 50% glycerol.
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Conjugation:
Non-conjugated
To place orders, for customer services and technical support, please contact: MedChemExpress USA
Tel: 609-228-6898 E-mail: [email protected] [email protected]
Applications
| Application |
WB
WB: Western Blot
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IP
IP: Immunoprecipitation
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|---|---|---|
| Dilution Ratio | 1:1000-1:2000 | 1:20 |
Product Details
Phospho-Bad (Ser112) Antibody (YA3099) is a Rabbit-derived and non-conjugated IgG monoclonal antibody, targeting to Phospho-Bad (Ser112).
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Host Rabbit
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Clonality Recombinant,Monoclonal
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Species ReactivityHuman, Mouse, Rat
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Observed Molecular WeightObserved band size: 23 kDa
Note: Due to possible protein modifications or aggregation, the molecular weight should be confirmed by actual measurement, and the predicted value is for reference only.
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Calculated Molecular Weight Predicted band size: 18 kDa
Entrez Gene: 572 Human ; 12015 Mouse ; 64639 Rat
SwissProt: Q92934 Human ; Q61337 Mouse ; O35147 Rat
OMIM: 603167 Human
A synthesized peptide derived from human Bad RHS-pS-YPA.
Endogenous
Affinity Chromatography
Non-conjugated
Phosphorylated
IgG
Product Properties
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Appearance
Solution
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Formulation
Supplied in rabbit IgG in 10mM PBS, pH 7.4, 150mM sodium chloride, 0.05% BSA, 0.02% sodium azide and 50% glycerol.
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Concentration
Batch-dependent, Please check the COA for the concentration of each lot. Check Lot Concentration
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Storage & Stability
Stored at -20°C for 1 year. Avoid repeated freeze / thaw cycles.
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Shipping
Shipping with blue ice.
Background
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Function
BAD is a pro-apoptotic BH3-only Bcl-2 family protein that promotes apoptosis by binding Bcl-xL and Bcl-2, displacing BAX, and reversing death-repressor activity[1]. Mechanistically, survival-factor signaling phosphorylates BAD, causing 14-3-3 binding rather than Bcl-xL binding, while Akt phosphorylation blocks BAD-induced neuronal death[2][3]. Therefore, BAD links growth-factor survival pathways to the intrinsic mitochondrial apoptosis machinery, where Bcl-2 family interactions control apoptotic commitment[3][4]. In disease-relevant metabolic models, BAD resides in a glucokinase-containing mitochondrial complex that integrates glycolysis and apoptosis, and BAD deficiency or non-phosphorylatable BAD mutants impair glucose homeostasis[5]. In pancreatic β-cells, BAD supports glucose-stimulated insulin secretion and β-cell survival, giving BAD practical value in diabetes-related apoptosis and metabolism studies[6]. Compared with activator isoforms such as BID, BIM, and PUMA, BAD functions mainly as a sensitizer that neutralizes anti-apoptotic Bcl-2 proteins rather than directly activating BAX-BAK[4]. For experimental applications, phospho-BAD BH3 helix mimetics activate glucokinase through a mechanism distinct from classical allosteric activators[7].
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Subcellular Localization
Mitochondrion outer membrane; Cytoplasm
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Expression
Tissue_specificity:Expression in multiple organizations -
Subunit
Forms heterodimers with the anti-apoptotic proteins, Bcl-X(L), Bcl-2 and Bcl-W.
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SwissProt ID
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Synonyms
BAD; BBC6; BCL2L8; Bcl2 antagonist of cell death; BAD; Bcl-2-binding component 6; Bcl-2-like protein 8; Bcl2-L-8; Bcl-XL/Bcl-2-associated death promoter
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Research Field
Cell Biology
Documentation
References
[1]. Yang E, et al. Bad, a heterodimeric partner for Bcl-XL and Bcl-2, displaces Bax and promotes cell death. Cell. 1995 Jan 27;80(2):285-91. [Content Brief]
[2]. Zha J, et al. Serine phosphorylation of death agonist BAD in response to survival factor results in binding to 14-3-3 not BCL-X(L). Cell. 1996 Nov 15;87(4):619-28. [Content Brief]
[3]. Datta SR, et al. Akt phosphorylation of BAD couples survival signals to the cell-intrinsic death machinery. Cell. 1997 Oct 17;91(2):231-41. [Content Brief]
[4]. Hongay CF, et al. Antisense transcription controls cell fate in Saccharomyces cerevisiae. Cell. 2006 Nov 17;127(4):735-45. [Content Brief]
[5]. Danial NN, et al. BAD and glucokinase reside in a mitochondrial complex that integrates glycolysis and apoptosis. Nature. 2003 Aug 21;424(6951):952-6. [Content Brief]
[6]. Danial NN, et al. Dual role of proapoptotic BAD in insulin secretion and beta cell survival. Nat Med. 2008 Feb;14(2):144-53. [Content Brief]
[7]. Szlyk B, et al. A phospho-BAD BH3 helix activates glucokinase by a mechanism distinct from that of allosteric activators. Nat Struct Mol Biol. 2014 Jan;21(1):36-42. [Content Brief]
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