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Bad functions as an essential sensitizer and Puma (显示 BBC3 ELISA试剂盒) as an essential activator of IR-induced mitochondrial apoptosis specifically in embryonic neural tissue.
Stage-specific expression of TNFalpha (显示 TNF ELISA试剂盒) regulates bad/bid (显示 BID ELISA试剂盒)-mediated apoptosis and RIP1 (显示 RALBP1 ELISA试剂盒)/ROS (显示 ROS1 ELISA试剂盒)-mediated secondary necrosis in Birnavirus-infected fish cells.
Results indicate that zebrafish BH3-only (显示 BBC3 ELISA试剂盒) proapoptotic protein (BAD) could induce apoptosis in vitro and in vivo and may have biological implications in apoptosis during zebrafish development.
The long unstructured region of Bcl-xl (显示 BCL2L1 ELISA试剂盒) modulates its structural dynamics.
Short-term treatment of nascent melanoma tumors with PAK inhibitors that block RhoJ (显示 RHOJ ELISA试剂盒) signaling halts the growth of BRAF (显示 BRAF ELISA试剂盒) mutant melanoma tumors in vivo and induces apoptosis in melanoma cells in vitro via a BAD-dependent mechanism. As up to 50% of BRAF (显示 BRAF ELISA试剂盒) mutant human melanomas express high levels of RhoJ (显示 RHOJ ELISA试剂盒), these studies nominate the RhoJ (显示 RHOJ ELISA试剂盒)-BAD signaling network as a therapeutic vulnerability for fledgling BRAF (显示 BRAF ELISA试剂盒) mutant human tumor
Recent studies that combine experiments in yeast and in mammalian cells have shown the unexpected effect of the anti-apoptotic protein Bcl-xL (显示 BCL2L1 ELISA试剂盒) on the priming of Bax (显示 BAX ELISA试剂盒). As demonstrated with the BH3-mimetic molecule ABT-737, this property of Bcl-xL (显示 BCL2L1 ELISA试剂盒), and of Bcl-2 (显示 BCL2 ELISA试剂盒), is crucial to elaborate about how apoptosis could be reactivated in tumoral cells.
the accumulation of reactive oxygen species (ROS (显示 ROS1 ELISA试剂盒)) in cells expressing JAK2V617F compromises the NHE-1 (显示 SLC9A1 ELISA试剂盒)/Bcl-xL (显示 BCL2L1 ELISA试剂盒) deamidation pathway by repressing NHE-1 (显示 SLC9A1 ELISA试剂盒) upregulation in response to DNA damage. hematopoietic stem cells (HSCs), FOXO3A (显示 FOXO3 ELISA试剂盒) is largely localized within the nuclei despite the presence of JAK2V617F mutation, suggesting that JAK2 (显示 JAK2 ELISA试剂盒)-FOXO (显示 FOXO3 ELISA试剂盒) signaling has a different effect on progenitors compared with stem cells.
These results identify beta3 integrin (显示 ITGB3 ELISA试剂盒) signaling via repression of BAD as an important survival pathway used by breast cancer cells to evade chemotherapy induced stress.
miR (显示 MLXIP ELISA试剂盒)-377 was markedly downregulated in HCC (显示 FAM126A ELISA试剂盒) cell lines and primary human HCC (显示 FAM126A ELISA试剂盒) tissues. The decreased expression of miR (显示 MLXIP ELISA试剂盒)-377 contributes to the upregulation of Bcl-xL (显示 BCL2L1 ELISA试剂盒) expression by targeting its 3'-untranslated region (3'-UTR (显示 UTS2R ELISA试剂盒)).
By the pharmacologic targeting of BCL2 (显示 BCL2 ELISA试剂盒), MCL1 (显示 MCL1 ELISA试剂盒), and BCL-XL (显示 BCL2L1 ELISA试剂盒), we demonstrated that diffuse large B-cell lymphoma can be divided into BCL2 (显示 BCL2 ELISA试剂盒)-dependent and MCL1 (显示 MCL1 ELISA试剂盒)-dependent subgroups with a less pronounced role left for BCL-XL (显示 BCL2L1 ELISA试剂盒).
increased platelet apoptosis and activation as well as reduced expression of Bcl-xL (显示 BCL2L1 ELISA试剂盒), increased expression of Bax (显示 BAX ELISA试剂盒) and caspase-3 (显示 CASP3 ELISA试剂盒) activity were found in platelets after treated with ITP (显示 ITPA ELISA试剂盒) plasma in comparison with control plasma.
These findings demonstrated that Akt (显示 AKT1 ELISA试剂盒) is related to NF-kappaB (显示 NFKB1 ELISA试剂盒) and Bad signaling pathway possibly playing a direct role in the progression of liver cancer. Thus, Akt (显示 AKT1 ELISA试剂盒) might be an important and potential treatment choice for the clinical diagnosis and treatment in the future.
Bh3 domain induced conformational changes in Bcl-Xl (显示 BCL2L1 ELISA试剂盒) revealed by crystal structure and comparative analysis.
Bad is dispensable for TNF (显示 TNF ELISA试剂盒)-mediated cell death.
Results indicate the downstream targets of insulin (显示 INS ELISA试剂盒), cyclin D1 (显示 CCND1 ELISA试剂盒), BAD, alpha-MHC (显示 MYH6 ELISA试剂盒), and GATA-4 (显示 GATA4 ELISA试剂盒), elucidate a molecular mechanism of insulin (显示 INS ELISA试剂盒) in promoting cell proliferation and differentiation.
our study suggests that Bad and Bmf (显示 BMF ELISA试剂盒) co-regulate lymphocyte homeostasis and limit spontaneous transformation by mechanisms that may not exclusively be linked to the induction of lymphocyte apoptosis.
Results reveal that IKK (显示 CHUK ELISA试剂盒) inhibits TNFalpha (显示 TNF ELISA试剂盒)-induced apoptosis through two distinct but cooperative mechanisms: activation of the survival factor NF-kappaB (显示 NFKB1 ELISA试剂盒) and inactivation of the proapoptotic BH3-only (显示 BBC3 ELISA试剂盒) BAD protein.
RNAi-mediated silencing of STAT1 (显示 STAT1 ELISA试剂盒) in soft tissue sarcoma (STS (显示 STS ELISA试剂盒)) cells was sufficient to increase expression of the apoptotic mediators Fas (显示 FAS ELISA试剂盒) and Bad and to elevate the sensitivity of STS (显示 STS ELISA试剂盒) cells to Fas (显示 FAS ELISA试剂盒)-mediated apoptosis
Tonicity-induced COX-2 (显示 COX2 ELISA试剂盒) 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.
Caspase-3 (显示 CASP3 ELISA试剂盒) is activated by the BAD-BAX (显示 BAX ELISA试剂盒) cascade resulting in long term depression induction in the hippocampus.
JNK1 (显示 MAPK8 ELISA试剂盒) is required for erythropoietin (显示 EPO ELISA试剂盒)-mediated cell survival through phosphorylation and inactivation of the pro-apoptotic, Bcl-2 (显示 BCL2 ELISA试剂盒) homology domain 3 (BH3)-only (显示 BBC3 ELISA试剂盒) Bcl-associated death protein (Bad).
Bad protein cooperate with bim (显示 BCL2L11 ELISA试剂盒) protein in certain apoptotic responses and in the suppression of g-irradiation-induced thymic lymphoma.(Bad protein)
Data show that loss of Bmf (显示 BMF ELISA试剂盒) reduced the pressure to inactivate p53 (显示 TP53 ELISA试剂盒), whereas Bad deficiency did not, identifying Bmf (显示 BMF ELISA试剂盒) as a novel component of the p53 (显示 TP53 ELISA试剂盒)-independent tumor suppressor pathway triggered by c-Myc (显示 MYC ELISA试剂盒).
The protein encoded by this gene is a member of the BCL-2 family. BCL-2 family members are known to be regulators of programmed cell death. This protein positively regulates cell apoptosis by forming heterodimers with BCL-xL and BCL-2, and reversing their death repressor activity. Proapoptotic activity of this protein is regulated through its phosphorylation. Protein kinases AKT and MAP kinase, as well as protein phosphatase calcineurin were found to be involved in the regulation of this protein. Alternative splicing of this gene results in two transcript variants which encode the same isoform.
proapoptotic BH3-only protein
, BCL2-antagonist of cell death
, BCL2-associated agonist of cell death
, BCL-X/BCL-2 binding protein
, BCL2-antagonist of cell death protein
, BCL2-binding component 6
, BCL2-binding protein
, bcl-2-binding component 6
, bcl-2-like protein 8
, bcl-XL/Bcl-2-associated death promoter
, bcl2 antagonist of cell death
, Bcl-associated death promoter
, bcl-xL/Bcl-2-associated death promoter
, Bcl2-antagonist of cell death
, bcl-2 associated death agonist
, bcl2-associated death promoter