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  • Your Good Partner in Biology Research

    Bad (Ab-155) Antibody

    • 货号:
    • 规格:
    • 图片:
      • Western blot analysis of extracts from 293 cells using BAD(Ab-155) Antibody and the same antibody preincubated with blocking peptide.
      • Immunohistochemical analysis of paraffin-embedded human breast carcinoma tissue using BAD(Ab-155) Antibody(left) or the same antibody preincubated with blocking peptide(right).
    • 其他:


    • Uniprot No.:
    • 宿主:
    • 反应种属:
    • 免疫原:
      Peptide sequence around aa.153~157 (R-M-S-D-E) derived from Mouse BAD.
    • 免疫原种属:
      Mus musculus (Mouse)
    • 克隆类型:
    • 纯化方式:
      Antibodies were produced by immunizing rabbits with synthetic peptide and KLH conjugates. Antibodies were purified by affinity-chromatography using epitope-specific peptide.
    • 浓度:
      It differs from different batches. Please contact us to confirm it.
    • 产品提供形式:
    • 应用范围:
    • 推荐稀释比:
      Application Recommended Dilution
      WB 1:500-1:1000
      IHC 1:50-1:200
    • Protocols:
    • 储存条件:
      Upon receipt, store at -20°C or -80°C. Avoid repeated freeze.
    • 货期:
      Basically, we can dispatch the products out in 1-3 working days after receiving your orders. Delivery time maybe differs from different purchasing way or location, please kindly consult your local distributors for specific delivery time.



    • 功能:
      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. Appears to act as a link between growth factor receptor signaling and the apoptotic pathways.
    • 基因功能参考文献:
      1. This study shows for the first time that genetic knockout of Bad provides epileptic seizure protection in Kcna1-/- mice, a genetic model of epilepsy with sudden unexplained death. PMID: 29171006
      2. BAD knockout reduced epileptiform activity, and this effect was lost upon knockout or pharmacological inhibition of KATP channels. PMID: 29368690
      3. Bad is dispensable for TNF-mediated cell death. PMID: 25611386
      4. Results suggest that regulation of the proapoptotic activity of BAD plays a key role in the pathogenic mechanisms resulting in primary pigmented nodular adrenocortical disease tumor formation. PMID: 24865460
      5. fasting may increase the uptake beta-hydroxybutyrate by decreasing BAD in the brain during hypoglycemia PMID: 25043191
      6. Results indicate the downstream targets of insulin, cyclin D1, BAD, alpha-MHC, and GATA-4, elucidate a molecular mechanism of insulin in promoting cell proliferation and differentiation. PMID: 24020834
      7. our study suggests that Bad and Bmf co-regulate lymphocyte homeostasis and limit spontaneous transformation by mechanisms that may not exclusively be linked to the induction of lymphocyte apoptosis. PMID: 22430207
      8. Results reveal that IKK inhibits TNFalpha-induced apoptosis through two distinct but cooperative mechanisms: activation of the survival factor NF-kappaB and inactivation of the proapoptotic BH3-only BAD protein. PMID: 23332762
      9. RNAi-mediated silencing of STAT1 in soft tissue sarcoma (STS) cells was sufficient to increase expression of the apoptotic mediators Fas and Bad and to elevate the sensitivity of STS cells to Fas-mediated apoptosis PMID: 22805310
      10. BAD modulates counterregulatory responses to hypoglycemia and protective glucoprivic feeding PMID: 22162752
      11. the regulation of BAD by uremic toxins and report the sensitization of vascular smooth muscle cells to apoptosis upon BAD induction was explored. PMID: 22172950
      12. Tonicity-induced COX-2 expression and PGE2 synthesis in the renal medulla entails phosphorylation and inactivation of the pro-apoptotic protein Bad, thereby counteracting apoptosis in renal medullary epithelial cells. PMID: 21716255
      13. Caspase-3 is activated by the BAD-BAX cascade resulting in long term depression induction in the hippocampus. PMID: 21609830
      14. JNK1 is required for erythropoietin-mediated cell survival through phosphorylation and inactivation of the pro-apoptotic, Bcl-2 homology domain 3 (BH3)-only Bcl-associated death protein (Bad). PMID: 21095239
      15. Bad protein cooperate with bim protein in certain apoptotic responses and in the suppression of g-irradiation-induced thymic lymphoma.(Bad protein) PMID: 20431598
      16. Data show that loss of Bmf reduced the pressure to inactivate p53, whereas Bad deficiency did not, identifying Bmf as a novel component of the p53-independent tumor suppressor pathway triggered by c-Myc. PMID: 19965635
      17. The beta-arrestin 1-dependent ERK1/2 activation engaged by GLP-1 mediates the Ser-112 phosphorylation of Bad. PMID: 19915011
      18. The interaction of Bad with lipid rafts is a dynamic process regulated by IL-4 and involved in the control of apoptosis. PMID: 11907096
      19. activation by therapeutic inhibition of epidermal growth factor receptor and transactivation by insulin-like growth factor receptor PMID: 12011069
      20. Bcl-x(L) and Bcl-w target protein phosphatase 1alpha to Bad PMID: 12115603
      21. phosphorylation at serine 128 by activation of the JNK signaling pathway PMID: 12189144
      22. BAD phosphorylation protects cells from the deleterious effects of apoptotic stimuli and attenuates death pathway signaling by raising the threshold at which mitochondria release cytochrome c to induce cell death PMID: 12431371
      23. Bad apoptotic protein alone or in combination with bax apoptotic protein and the prostatic-specific promoter ARR(2)PB was an effective therapy for experimental prostatic neoplasms. PMID: 12490000
      24. Candida albicans phospholipomannan promotes survival of phagocytosed yeasts through modulation of of this protein's phosphorylation and macrophage apoptosis. PMID: 12551950
      25. HSV-1 US3 protein kinase blocks the caspases that cleave BAD at either residue 56 or 61 predicted to render the protein more proapoptotic or at residue 156, which would inactivate the protein. PMID: 12743316
      26. proapoptotic BAD suppresses tumorigenesis in the lymphocyte lineage PMID: 12876200
      27. combination of proteomics, genetics and physiology indicates an unanticipated role for BAD in integrating pathways of glucose metabolism and apoptosis PMID: 12931191
      28. PP2A dephosphorylation of pSer112 is the key initiating event regulating the activation of BAD during interleukin-3 withdrawal-induced apoptosis PMID: 12944463
      29. BAD is a substrate for pim-2 oncogene proto-oncogene PMID: 12954615
      30. regulation of Bad phosphorylation plays an active role in mediating anti-IgM-induced apoptosis of immature B cells PMID: 14585539
      31. JNK is required for IL-3-mediated cell survival through phosphorylation and inactivation of the proapoptotic Bcl-2 family protein BAD. PMID: 14967141
      32. Data show that the Bcl-2 homology 3 domain-only protein, Bad, is involved in cell death following IL-7 withdrawal from D1 cells, an IL-7-dependent murine thymocyte cell line. PMID: 15123689
      33. mechanisms that regulate the conversion of BAD from an anti-death to a pro-death factor include alternative splicing that produces N-terminally truncated BAD(S)and conversion by caspases into a pro-death fragment that resembles the short splice variant PMID: 15231831
      34. alteration of lipid rafts is an early event in the apoptotic cascade indirectly induced by interleukin-4 deprivation via PP1alpha activation, dephosphorylation of cytoplasmic Bad, and caspase activation PMID: 15634756
      35. Bad phosphorylation is not essential for PKB-mediated survival signaling in hemopoietic cells PMID: 15843895
      36. Pak1-dependent Raf-1 phosphorylation regulates its mitochondrial localization, phosphorylation of BAD, and Bcl-2 association PMID: 15849194
      37. BAD induces apoptosis upon detecting the coincidence of G2/M phase and growth factor deprivation PMID: 15901741
      38. phosphorylation of BAD Serine 128 exerts cell-specific effects on apoptosis PMID: 15907327
      39. All three Pim kinase family members predominantly phosphorylate Bad on Ser112 and in addition are capable of phosphorylating Bad on multiple sites associated with the inhibition of the pro-apoptotic function of Bad in HEK-293 cells PMID: 16403219
      40. cellular cholesterol biosynthesis is critical for the activation and maintenance of the Akt-Bad cell survival cascade in response to growth factors such as insulin. PMID: 16513830
      41. These data establish a connection between calcium overload and mitochondria-mediated death pathways in outer hair cells and also suggest a dual role for BAD. PMID: 16521126
      42. 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
      43. Study shows, using spectroscopic methods, that the BH3-only proteins Bim, Bad and Bmf are unstructured in the absence of binding partners. PMID: 16645638
      44. Bad was not required for cell death following IL-3 withdrawal, suggesting changes to phosphorylation of Bad play only a minor role in apoptosis. PMID: 16705087
      45. Both gonadotropin releasing hormone andepidermal growth factor (EGF) caused rapid phosphorylation of BAD. PMID: 16741954
      46. The proapoptotic protein Bad is a key player in cell survival decisions, and is regulated post-translationally by several signaling networks. PMID: 17535812
      47. Raf-1 in beta-cells led to a striking loss of Bad phosphorylation at serine 112 and an increase in the protein levels of both Bad and Bax PMID: 18006502
      48. These findings provide genetic proof of the bifunctional activities of BAD in both beta cell survival and insulin secretion. PMID: 18223655
      49. Thr-201 phosphorylation of Bad by JNK1 is required for PFK-1 activation PMID: 18469002
      50. BAD is the only BCL-2 family protein expressed in parietal cells PMID: 18779780



    • 亚细胞定位:
      Mitochondrion outer membrane. Cytoplasm.
    • 蛋白家族:
      Bcl-2 family
    • 数据库链接:

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