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Bad functions as an essential sensitizer and Puma (show BBC3 Proteins) as an essential activator of IR-induced mitochondrial apoptosis specifically in embryonic neural tissue.
Stage-specific expression of TNFalpha (show TNF Proteins) regulates bad/bid (show BID Proteins)-mediated apoptosis and RIP1 (show RALBP1 Proteins)/ROS (show ROS1 Proteins)-mediated secondary necrosis in Birnavirus-infected fish cells.
Results indicate that zebrafish BH3-only (show BBC3 Proteins) proapoptotic protein (BAD) could induce apoptosis in vitro and in vivo and may have biological implications in apoptosis during zebrafish development.
Taken together, our results provide a structural basis for the binding mechanism between DJ-1 (show PARK7 Proteins) and Bcl-XL (show BCL2L1 Proteins), which will contribute to molecular understanding of the role of mitochondrial DJ-1 (show PARK7 Proteins) in Bcl-XL (show BCL2L1 Proteins) regulation in response to oxidative stress.
We will then review how the apoptotic and autophagic functions of Bcl-xL (show BCL2L1 Proteins) are modified by this post-translational modifications, and how this impacts on its oncogenic properties.
the membrane localization of BCL-xL (show BCL2L1 Proteins) enforces its control over cell survival and, importantly, limits the pro-apoptotic effects of BH3 mimetics by selectively influencing BCL-xL (show BCL2L1 Proteins) binding to key pro-apoptotic effectors.
The long unstructured region of Bcl-xl (show BCL2L1 Proteins) modulates its structural dynamics.
Short-term treatment of nascent melanoma tumors with PAK inhibitors that block RhoJ (show RHOJ Proteins) signaling halts the growth of BRAF (show BRAF Proteins) mutant melanoma tumors in vivo and induces apoptosis in melanoma cells in vitro via a BAD-dependent mechanism. As up to 50% of BRAF (show BRAF Proteins) mutant human melanomas express high levels of RhoJ (show RHOJ Proteins), these studies nominate the RhoJ (show RHOJ Proteins)-BAD signaling network as a therapeutic vulnerability for fledgling BRAF (show BRAF Proteins) 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 (show BCL2L1 Proteins) on the priming of Bax (show BAX Proteins). As demonstrated with the BH3-mimetic molecule ABT-737, this property of Bcl-xL (show BCL2L1 Proteins), and of Bcl-2 (show BCL2 Proteins), is crucial to elaborate about how apoptosis could be reactivated in tumoral cells.
the accumulation of reactive oxygen species (ROS (show ROS1 Proteins)) in cells expressing JAK2V617F compromises the NHE-1 (show SLC9A1 Proteins)/Bcl-xL (show BCL2L1 Proteins) deamidation pathway by repressing NHE-1 (show SLC9A1 Proteins) upregulation in response to DNA damage. hematopoietic stem cells (HSCs), FOXO3A (show FOXO3 Proteins) is largely localized within the nuclei despite the presence of JAK2V617F mutation, suggesting that JAK2 (show JAK2 Proteins)-FOXO (show FOXO3 Proteins) signaling has a different effect on progenitors compared with stem cells.
These results identify beta3 integrin (show ITGB3 Proteins) signaling via repression of BAD as an important survival pathway used by breast cancer cells to evade chemotherapy induced stress.
miR-377 was markedly downregulated in HCC cell lines and primary human HCC tissues. The decreased expression of miR-377 contributes to the upregulation of Bcl-xL expression by targeting its 3'-untranslated region (3'-UTR).
By the pharmacologic targeting of BCL2 (show BCL2 Proteins), MCL1 (show MCL1 Proteins), and BCL-XL (show BCL2L1 Proteins), we demonstrated that diffuse large B-cell lymphoma can be divided into BCL2 (show BCL2 Proteins)-dependent and MCL1 (show MCL1 Proteins)-dependent subgroups with a less pronounced role left for BCL-XL (show BCL2L1 Proteins).
Bad is dispensable for TNF (show TNF Proteins)-mediated cell death.
Results indicate the downstream targets of insulin (show INS Proteins), cyclin D1 (show CCND1 Proteins), BAD, alpha-MHC (show MYH6 Proteins), and GATA-4 (show GATA4 Proteins), elucidate a molecular mechanism of insulin (show INS Proteins) in promoting cell proliferation and differentiation.
our study suggests that Bad and Bmf (show BMF Proteins) 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 (show CHUK Proteins) inhibits TNFalpha (show TNF Proteins)-induced apoptosis through two distinct but cooperative mechanisms: activation of the survival factor NF-kappaB (show NFKB1 Proteins) and inactivation of the proapoptotic BH3-only (show BBC3 Proteins) BAD protein.
RNAi-mediated silencing of STAT1 (show STAT1 Proteins) in soft tissue sarcoma (STS (show STS Proteins)) cells was sufficient to increase expression of the apoptotic mediators Fas (show FAS Proteins) and Bad and to elevate the sensitivity of STS (show STS Proteins) cells to Fas (show FAS Proteins)-mediated apoptosis
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.
Caspase-3 (show CASP3 Proteins) is activated by the BAD-BAX (show BAX Proteins) cascade resulting in long term depression induction in the hippocampus.
JNK1 (show MAPK8 Proteins) is required for erythropoietin (show EPO Proteins)-mediated cell survival through phosphorylation and inactivation of the pro-apoptotic, Bcl-2 (show BCL2 Proteins) homology domain 3 (BH3)-only (show BBC3 Proteins) Bcl-associated death protein (Bad).
Bad protein cooperate with bim (show BCL2L11 Proteins) protein in certain apoptotic responses and in the suppression of g-irradiation-induced thymic lymphoma.(Bad protein)
Data show that loss of Bmf (show BMF Proteins) reduced the pressure to inactivate p53 (show TP53 Proteins), whereas Bad deficiency did not, identifying Bmf (show BMF Proteins) as a novel component of the p53 (show TP53 Proteins)-independent tumor suppressor pathway triggered by c-Myc (show MYC Proteins).
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