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Bad functions as an essential sensitizer and Puma (show BBC3 ELISA Kits) as an essential activator of IR-induced mitochondrial apoptosis specifically in embryonic neural tissue.
Stage-specific expression of TNFalpha (show TNF ELISA Kits) regulates bad/bid (show BID ELISA Kits)-mediated apoptosis and RIP1 (show RALBP1 ELISA Kits)/ROS (show ROS1 ELISA Kits)-mediated secondary necrosis in Birnavirus-infected fish cells.
Results indicate that zebrafish BH3-only (show BBC3 ELISA Kits) 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 (show BCL2L1 ELISA Kits) modulates its structural dynamics.
Short-term treatment of nascent melanoma tumors with PAK inhibitors that block RhoJ (show RHOJ ELISA Kits) signaling halts the growth of BRAF (show BRAF ELISA Kits) 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 ELISA Kits) mutant human melanomas express high levels of RhoJ (show RHOJ ELISA Kits), these studies nominate the RhoJ (show RHOJ ELISA Kits)-BAD signaling network as a therapeutic vulnerability for fledgling BRAF (show BRAF ELISA Kits) 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 ELISA Kits) on the priming of Bax (show BAX ELISA Kits). As demonstrated with the BH3-mimetic molecule ABT-737, this property of Bcl-xL (show BCL2L1 ELISA Kits), and of Bcl-2 (show BCL2 ELISA Kits), is crucial to elaborate about how apoptosis could be reactivated in tumoral cells.
the accumulation of reactive oxygen species (ROS (show ROS1 ELISA Kits)) in cells expressing JAK2V617F compromises the NHE-1 (show SLC9A1 ELISA Kits)/Bcl-xL (show BCL2L1 ELISA Kits) deamidation pathway by repressing NHE-1 (show SLC9A1 ELISA Kits) upregulation in response to DNA damage. hematopoietic stem cells (HSCs), FOXO3A (show FOXO3 ELISA Kits) is largely localized within the nuclei despite the presence of JAK2V617F mutation, suggesting that JAK2 (show JAK2 ELISA Kits)-FOXO (show FOXO3 ELISA Kits) signaling has a different effect on progenitors compared with stem cells.
These results identify beta3 integrin (show ITGB3 ELISA Kits) signaling via repression of BAD as an important survival pathway used by breast cancer cells to evade chemotherapy induced stress.
miR (show MLXIP ELISA Kits)-377 was markedly downregulated in HCC (show FAM126A ELISA Kits) cell lines and primary human HCC (show FAM126A ELISA Kits) tissues. The decreased expression of miR (show MLXIP ELISA Kits)-377 contributes to the upregulation of Bcl-xL (show BCL2L1 ELISA Kits) expression by targeting its 3'-untranslated region (3'-UTR (show UTS2R ELISA Kits)).
By the pharmacologic targeting of BCL2 (show BCL2 ELISA Kits), MCL1 (show MCL1 ELISA Kits), and BCL-XL (show BCL2L1 ELISA Kits), we demonstrated that diffuse large B-cell lymphoma can be divided into BCL2 (show BCL2 ELISA Kits)-dependent and MCL1 (show MCL1 ELISA Kits)-dependent subgroups with a less pronounced role left for BCL-XL (show BCL2L1 ELISA Kits).
increased platelet apoptosis and activation as well as reduced expression of Bcl-xL (show BCL2L1 ELISA Kits), increased expression of Bax (show BAX ELISA Kits) and caspase-3 (show CASP3 ELISA Kits) activity were found in platelets after treated with ITP (show ITPA ELISA Kits) plasma in comparison with control plasma.
These findings demonstrated that Akt (show AKT1 ELISA Kits) is related to NF-kappaB (show NFKB1 ELISA Kits) and Bad signaling pathway possibly playing a direct role in the progression of liver cancer. Thus, Akt (show AKT1 ELISA Kits) 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 (show BCL2L1 ELISA Kits) revealed by crystal structure and comparative analysis.
Bad is dispensable for TNF (show TNF ELISA Kits)-mediated cell death.
Results indicate the downstream targets of insulin (show INS ELISA Kits), cyclin D1 (show CCND1 ELISA Kits), BAD, alpha-MHC (show MYH6 ELISA Kits), and GATA-4 (show GATA4 ELISA Kits), elucidate a molecular mechanism of insulin (show INS ELISA Kits) in promoting cell proliferation and differentiation.
our study suggests that Bad and Bmf (show BMF ELISA Kits) 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 ELISA Kits) inhibits TNFalpha (show TNF ELISA Kits)-induced apoptosis through two distinct but cooperative mechanisms: activation of the survival factor NF-kappaB (show NFKB1 ELISA Kits) and inactivation of the proapoptotic BH3-only (show BBC3 ELISA Kits) BAD protein.
RNAi-mediated silencing of STAT1 (show STAT1 ELISA Kits) in soft tissue sarcoma (STS (show STS ELISA Kits)) cells was sufficient to increase expression of the apoptotic mediators Fas (show FAS ELISA Kits) and Bad and to elevate the sensitivity of STS (show STS ELISA Kits) cells to Fas (show FAS ELISA Kits)-mediated apoptosis
Tonicity-induced COX-2 (show COX2 ELISA Kits) 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 ELISA Kits) is activated by the BAD-BAX (show BAX ELISA Kits) cascade resulting in long term depression induction in the hippocampus.
JNK1 (show MAPK8 ELISA Kits) is required for erythropoietin (show EPO ELISA Kits)-mediated cell survival through phosphorylation and inactivation of the pro-apoptotic, Bcl-2 (show BCL2 ELISA Kits) homology domain 3 (BH3)-only (show BBC3 ELISA Kits) Bcl-associated death protein (Bad).
Bad protein cooperate with bim (show BCL2L11 ELISA Kits) 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 ELISA Kits) reduced the pressure to inactivate p53 (show TP53 ELISA Kits), whereas Bad deficiency did not, identifying Bmf (show BMF ELISA Kits) as a novel component of the p53 (show TP53 ELISA Kits)-independent tumor suppressor pathway triggered by c-Myc (show MYC ELISA Kits).
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