Recombinant Rat Bcl2 antagonist of cell death(Bad)

Code CSB-YP002528RA
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Source Yeast
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Code CSB-EP002528RA
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Source E.coli
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Code CSB-EP002528RA-B
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Source E.coli
Conjugate Avi-tag Biotinylated
E. coli biotin ligase (BirA) is highly specific in covalently attaching biotin to the 15 amino acid AviTag peptide. This recombinant protein was biotinylated in vivo by AviTag-BirA technology, which method is BriA catalyzes amide linkage between the biotin and the specific lysine of the AviTag.
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Code CSB-BP002528RA
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Source Baculovirus
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Code CSB-MP002528RA
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Source Mammalian cell
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Product Details

Purity >85% (SDS-PAGE)
Target Names Bad
Uniprot No. O35147
Alternative Names BadBcl2-associated agonist of cell death; BAD; Bcl-2-binding component 6; Bcl-xL/Bcl-2-associated death promoter; Bcl2 antagonist of cell death
Species Rattus norvegicus (Rat)
Expression Region 1-205
Protein Length Full length protein
Tag Info The following tags are available.
N-terminal His-tagged
The tag type will be determined during production process. If you have specified tag type, please tell us and we will develop the specified tag preferentially.
Form Lyophilized powder
Buffer before Lyophilization Tris/PBS-based buffer, 6% Trehalose, pH 8.0
Reconstitution We recommend that this vial be briefly centrifuged prior to opening to bring the contents to the bottom. Please reconstitute protein in deionized sterile water to a concentration of 0.1-1.0 mg/mL.We recommend to add 5-50% of glycerol (final concentration) and aliquot for long-term storage at -20℃/-80℃. Our default final concentration of glycerol is 50%. Customers could use it as reference.
and FAQs
Protein FAQs
Storage Condition Store at -20°C upon receipt, aliquoting is necessary for mutiple use. Avoid repeated freeze-thaw cycles.
Shelf Life The shelf life is related to many factors, storage state, buffer ingredients, storage temperature and the stability of the protein itself.
Generally, the shelf life of liquid form is 6 months at -20°C/-80°C. The shelf life of lyophilized form is 12 months at -20°C/-80°C.
Lead Time Delivery time may differ from different purchasing way or location, please kindly consult your local distributors for specific delivery time.
Note: All of our proteins are default shipped with normal blue ice packs, if you request to ship with dry ice, please communicate with us in advance and extra fees will be charged.
Notes Repeated freezing and thawing is not recommended. Store working aliquots at 4°C for up to one week.
Datasheet Please contact us to get it.

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Target Background

(From Uniprot)
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 (By similarity). Appears to act as a link between growth factor receptor signaling and the apoptotic pathways.
Gene References into Functions
  1. Chrysin prevents apoptosis by upregulating the Bcl-2 mRNA expression and downregulating the pro-apoptotic (Bax, Bad) mRNAs in 3-nitropropionic acid induced behavioral despair/mitochondrial dysfunction/striatal apoptosis. PMID: 27690136
  2. By downregulating ATX-induced activation of Akt/Bad. PMID: 25072152
  3. OEC transplantation could effectively improve neurological deficits in TBI rats; the underlying mechanism may be related with their effects on neuroprotection and regeneration induction PMID: 24582457
  4. p38MAPK suppresses chronic pancreatitis by upregulating HSP27 expression and downregulating BAD expression. PMID: 22549003
  5. The protective mechanisms of fused combination FNK protein therapy might involve the inhibition of apoptotic pathways through caspase-12, but not through Bcl-2. PMID: 22099262
  6. The decrease in DA content in the striatum may correlate with the abnormal behavior in elderly rats, which could be ascribed to the variations in Bad and Bcl-2. PMID: 21818658
  7. deltaPKC initiates cytochrome c release via phosphorylation of PP2A and subsequent dephosphorylation of Bad. PMID: 21789211
  8. NRG-1 may be involved in regulating the expression of Bcl-2 and p-Bad through the PI3K/Akt pathway after transient focal cerebral ischemia. PMID: 20651836
  9. testosterone induced down-regulation of the Akt pathway in male hearts following ischemia reperfusion, thereby mediating cardiac injury through decreased p-Bad, reduced ratio of Bcl-2/Bax in the cytoplasm, and increased FOXO3a in the nucleus PMID: 20850791
  10. The expression of Bad led to the loss of retinal ganglion cells following optic nerve crush. PMID: 17080661
  11. Findings suggests that EGb 761 prevents cell death against ischemic brain injury and EGb 761 neuroprotection is affected by preventing the injury-induced increase of Bad and Bcl-X(L) interaction. PMID: 19885947
  12. Signaling pathways converging at BAD phosphorylation are key to growth factor-mediated attenuation of stretch-induced apoptosis in vitro and in vivo. PMID: 12472766
  13. Results indicate that neuronal ER stress is associated with an apoptotic cascade involving the mitochondria, a rapid dephosphorylation of BAD and decreased expression of Bcl-2. PMID: 12531534
  14. Akt is phosphorylated by PDGF, and activated Akt prevents apoptotic changes via activation of NF-kappa B and phosphorylation of Bad in mesangial cells. PMID: 12761242
  15. Bad may be engaged in survival pathways in the immature retina PMID: 12838582
  16. Glioma cells treated with cannabinoids undergo apoptosis and down regulation of bad protein. PMID: 15451022
  17. Results report the expression levels of pro-apoptotic factors Bad and Bax, and anti-apoptotic Bcl(2) mRNA following ethanol administration in newborn rats. PMID: 15469889
  18. We conclude that oxidative stress may play a role in modulating Akt/Bad signaling and subsequent motor neuron survival after SCI. PMID: 15896972
  19. Results demonstrate that wild-type alpha-synuclein interacts with the pro-apoptotic molecules BAD and protein kinase C delta to protect dopaminergic neuronal cells against neurotoxic insults. PMID: 15978696
  20. Our findings suggest that estradiol prevents cell death due to brain injury and that Akt activation and Bad phosphorylation by estradiol mediated these protective effects. PMID: 16087293
  21. Maintenance of Bad phosphorylation is important in the prevention of SEC apoptosis and that the anti-apoptotic property of OV might have therapeutic utility. PMID: 16565486
  22. the interaction of BAD with membranes is tied to binding of 14-3-3 protein and activation and membrane translocation of Bcl-XL PMID: 16603546
  23. the diabetic condition increased the interaction of Bad and Bcl-X(L), and decreased the binding of pBad and 14-3-3. 14-3-3 acts as an anti-apoptotic factor through interaction with Bad PMID: 17870134
  24. arachidonic acid, at physiological concentrations, reduced the binding of 14-3-3zeta to phosphorylated BAD, an interaction that is important in regulating apoptosis PMID: 17940884
  25. BNIP3 and Bad levels were significantly increased in obese rat hearts. PMID: 18070754
  26. Preconditioning acts via PI3K/Akt signaling to block ischemia-induced cascade involving mitochondrial translocation of Bad, assembly of Bad with Bcl-x(L), cleavage of Bcl-x(L) activation of large-conductance channels in the mitochondrial outer membrane. PMID: 18347331
  27. two different pathways mediated by downstream products of arachidonic acid metabolism converge in Bad phosphorylation emphasizes the relevance of this strategy for the regulation of macrophage survival to peroxynitrite at the inflammatory sites. PMID: 18832722

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Subcellular Location Mitochondrion outer membrane, Cytoplasm
Protein Families Bcl-2 family
Tissue Specificity Expressed in all tissues tested, including brain, liver, spleen and heart. In the brain, restricted to epithelial cells of the choroid plexus. Isoform alpha is the more abundant form.
Database Links

KEGG: rno:64639

STRING: 10116.ENSRNOP00000061855

UniGene: Rn.36696

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