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Bad functions as an essential sensitizer and Puma (zeige BBC3 ELISA Kits) as an essential activator of IR-induced mitochondrial apoptosis specifically in embryonic neural tissue.
Stage-specific expression of TNFalpha (zeige TNF ELISA Kits) regulates bad/bid (zeige BID ELISA Kits)-mediated apoptosis and RIP1 (zeige RALBP1 ELISA Kits)/ROS (zeige ROS1 ELISA Kits)-mediated secondary necrosis in Birnavirus-infected fish cells.
Results indicate that zebrafish BH3-only (zeige BBC3 ELISA Kits) 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 (zeige PARK7 ELISA Kits) and Bcl-XL (zeige BCL2L1 ELISA Kits), which will contribute to molecular understanding of the role of mitochondrial DJ-1 (zeige PARK7 ELISA Kits) in Bcl-XL (zeige BCL2L1 ELISA Kits) regulation in response to oxidative stress.
We will then review how the apoptotic and autophagic functions of Bcl-xL (zeige BCL2L1 ELISA Kits) are modified by this post-translational modifications, and how this impacts on its oncogenic properties.
the membrane localization of BCL-xL (zeige BCL2L1 ELISA Kits) enforces its control over cell survival and, importantly, limits the pro-apoptotic effects of BH3 mimetics by selectively influencing BCL-xL (zeige BCL2L1 ELISA Kits) binding to key pro-apoptotic effectors.
The long unstructured region of Bcl-xl (zeige BCL2L1 ELISA Kits) modulates its structural dynamics.
Short-term treatment of nascent melanoma tumors with PAK inhibitors that block RhoJ (zeige RHOJ ELISA Kits) signaling halts the growth of BRAF (zeige 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 (zeige BRAF ELISA Kits) mutant human melanomas express high levels of RhoJ (zeige RHOJ ELISA Kits), these studies nominate the RhoJ (zeige RHOJ ELISA Kits)-BAD signaling network as a therapeutic vulnerability for fledgling BRAF (zeige 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 (zeige BCL2L1 ELISA Kits) on the priming of Bax (zeige BAX ELISA Kits). As demonstrated with the BH3-mimetic molecule ABT-737, this property of Bcl-xL (zeige BCL2L1 ELISA Kits), and of Bcl-2 (zeige BCL2 ELISA Kits), is crucial to elaborate about how apoptosis could be reactivated in tumoral cells.
the accumulation of reactive oxygen species (ROS (zeige ROS1 ELISA Kits)) in cells expressing JAK2V617F compromises the NHE-1 (zeige SLC9A1 ELISA Kits)/Bcl-xL (zeige BCL2L1 ELISA Kits) deamidation pathway by repressing NHE-1 (zeige SLC9A1 ELISA Kits) upregulation in response to DNA damage. hematopoietic stem cells (HSCs), FOXO3A (zeige FOXO3 ELISA Kits) is largely localized within the nuclei despite the presence of JAK2V617F mutation, suggesting that JAK2 (zeige JAK2 ELISA Kits)-FOXO (zeige FOXO3 ELISA Kits) signaling has a different effect on progenitors compared with stem cells.
These results identify beta3 integrin (zeige ITGB3 ELISA Kits) signaling via repression of BAD as an important survival pathway used by breast cancer cells to evade chemotherapy induced stress.
miR (zeige MLXIP ELISA Kits)-377 was markedly downregulated in HCC (zeige FAM126A ELISA Kits) cell lines and primary human HCC (zeige FAM126A ELISA Kits) tissues. The decreased expression of miR (zeige MLXIP ELISA Kits)-377 contributes to the upregulation of Bcl-xL (zeige BCL2L1 ELISA Kits) expression by targeting its 3'-untranslated region (3'-UTR (zeige UTS2R ELISA Kits)).
By the pharmacologic targeting of BCL2 (zeige BCL2 ELISA Kits), MCL1 (zeige MCL1 ELISA Kits), and BCL-XL (zeige BCL2L1 ELISA Kits), we demonstrated that diffuse large B-cell lymphoma can be divided into BCL2 (zeige BCL2 ELISA Kits)-dependent and MCL1 (zeige MCL1 ELISA Kits)-dependent subgroups with a less pronounced role left for BCL-XL (zeige BCL2L1 ELISA Kits).
Bad is dispensable for TNF (zeige TNF ELISA Kits)-mediated cell death.
Results indicate the downstream targets of insulin (zeige INS ELISA Kits), cyclin D1 (zeige CCND1 ELISA Kits), BAD, alpha-MHC (zeige MYH6 ELISA Kits), and GATA-4 (zeige GATA4 ELISA Kits), elucidate a molecular mechanism of insulin (zeige INS ELISA Kits) in promoting cell proliferation and differentiation.
our study suggests that Bad and Bmf (zeige 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 (zeige CHUK ELISA Kits) inhibits TNFalpha (zeige TNF ELISA Kits)-induced apoptosis through two distinct but cooperative mechanisms: activation of the survival factor NF-kappaB (zeige NFKB1 ELISA Kits) and inactivation of the proapoptotic BH3-only (zeige BBC3 ELISA Kits) BAD protein.
RNAi-mediated silencing of STAT1 (zeige STAT1 ELISA Kits) in soft tissue sarcoma (STS (zeige STS ELISA Kits)) cells was sufficient to increase expression of the apoptotic mediators Fas (zeige FAS ELISA Kits) and Bad and to elevate the sensitivity of STS (zeige STS ELISA Kits) cells to Fas (zeige FAS ELISA Kits)-mediated apoptosis
Tonicity-induced COX-2 (zeige 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 (zeige CASP3 ELISA Kits) is activated by the BAD-BAX (zeige BAX ELISA Kits) cascade resulting in long term depression induction in the hippocampus.
JNK1 (zeige MAPK8 ELISA Kits) is required for erythropoietin (zeige EPO ELISA Kits)-mediated cell survival through phosphorylation and inactivation of the pro-apoptotic, Bcl-2 (zeige BCL2 ELISA Kits) homology domain 3 (BH3)-only (zeige BBC3 ELISA Kits) Bcl-associated death protein (Bad).
Bad protein cooperate with bim (zeige 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 (zeige BMF ELISA Kits) reduced the pressure to inactivate p53 (zeige TP53 ELISA Kits), whereas Bad deficiency did not, identifying Bmf (zeige BMF ELISA Kits) as a novel component of the p53 (zeige TP53 ELISA Kits)-independent tumor suppressor pathway triggered by c-Myc (zeige 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