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Bad functions as an essential sensitizer and Puma (zeige BBC3 Proteine) as an essential activator of IR-induced mitochondrial apoptosis specifically in embryonic neural tissue.
Stage-specific expression of TNFalpha (zeige TNF Proteine) regulates bad/bid (zeige BID Proteine)-mediated apoptosis and RIP1 (zeige RALBP1 Proteine)/ROS (zeige ROS1 Proteine)-mediated secondary necrosis in Birnavirus-infected fish cells.
Results indicate that zebrafish BH3-only (zeige BBC3 Proteine) proapoptotic protein (BAD) could induce apoptosis in vitro and in vivo and may have biological implications in apoptosis during zebrafish development.
BAD phosphorylation is essential in the cytoprotective effect of vasoactive intestinal peptide (zeige Vip Proteine) on cancer stem cells.
NDRG2 (zeige NDRG2 Proteine) could inhibit Bad degradation by increasing its protein stability in breast cancer cells.
Taken together, our results provide a structural basis for the binding mechanism between DJ-1 (zeige PARK7 Proteine) and Bcl-XL (zeige BCL2L1 Proteine), which will contribute to molecular understanding of the role of mitochondrial DJ-1 (zeige PARK7 Proteine) in Bcl-XL (zeige BCL2L1 Proteine) regulation in response to oxidative stress.
We will then review how the apoptotic and autophagic functions of Bcl-xL (zeige BCL2L1 Proteine) are modified by this post-translational modifications, and how this impacts on its oncogenic properties.
the membrane localization of BCL-xL (zeige BCL2L1 Proteine) enforces its control over cell survival and, importantly, limits the pro-apoptotic effects of BH3 mimetics by selectively influencing BCL-xL (zeige BCL2L1 Proteine) binding to key pro-apoptotic effectors.
The long unstructured region of Bcl-xl (zeige BCL2L1 Proteine) modulates its structural dynamics.
Short-term treatment of nascent melanoma tumors with PAK inhibitors that block RhoJ (zeige RHOJ Proteine) signaling halts the growth of BRAF (zeige BRAF Proteine) 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 Proteine) mutant human melanomas express high levels of RhoJ (zeige RHOJ Proteine), these studies nominate the RhoJ (zeige RHOJ Proteine)-BAD signaling network as a therapeutic vulnerability for fledgling BRAF (zeige BRAF Proteine) 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 Proteine) on the priming of Bax (zeige BAX Proteine). As demonstrated with the BH3-mimetic molecule ABT-737, this property of Bcl-xL (zeige BCL2L1 Proteine), and of Bcl-2 (zeige BCL2 Proteine), is crucial to elaborate about how apoptosis could be reactivated in tumoral cells.
the accumulation of reactive oxygen species (ROS (zeige ROS1 Proteine)) in cells expressing JAK2V617F compromises the NHE-1 (zeige SLC9A1 Proteine)/Bcl-xL (zeige BCL2L1 Proteine) deamidation pathway by repressing NHE-1 (zeige SLC9A1 Proteine) upregulation in response to DNA damage. hematopoietic stem cells (HSCs), FOXO3A (zeige FOXO3 Proteine) is largely localized within the nuclei despite the presence of JAK2V617F mutation, suggesting that JAK2 (zeige JAK2 Proteine)-FOXO (zeige FOXO3 Proteine) signaling has a different effect on progenitors compared with stem cells.
These results identify beta3 integrin (zeige ITGB3 Proteine) signaling via repression of BAD as an important survival pathway used by breast cancer cells to evade chemotherapy induced stress.
Bad is dispensable for TNF (zeige TNF Proteine)-mediated cell death.
Results indicate the downstream targets of insulin (zeige INS Proteine), cyclin D1 (zeige CCND1 Proteine), BAD, alpha-MHC (zeige MYH6 Proteine), and GATA-4 (zeige GATA4 Proteine), elucidate a molecular mechanism of insulin (zeige INS Proteine) in promoting cell proliferation and differentiation.
our study suggests that Bad and Bmf (zeige BMF Proteine) 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 Proteine) inhibits TNFalpha (zeige TNF Proteine)-induced apoptosis through two distinct but cooperative mechanisms: activation of the survival factor NF-kappaB (zeige NFKB1 Proteine) and inactivation of the proapoptotic BH3-only (zeige BBC3 Proteine) BAD protein.
RNAi-mediated silencing of STAT1 (zeige STAT1 Proteine) in soft tissue sarcoma (STS (zeige STS Proteine)) cells was sufficient to increase expression of the apoptotic mediators Fas (zeige FAS Proteine) and Bad and to elevate the sensitivity of STS (zeige STS Proteine) cells to Fas (zeige FAS Proteine)-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 (zeige CASP3 Proteine) is activated by the BAD-BAX (zeige BAX Proteine) cascade resulting in long term depression induction in the hippocampus.
JNK1 (zeige MAPK8 Proteine) is required for erythropoietin (zeige EPO Proteine)-mediated cell survival through phosphorylation and inactivation of the pro-apoptotic, Bcl-2 (zeige BCL2 Proteine) homology domain 3 (BH3)-only (zeige BBC3 Proteine) Bcl-associated death protein (Bad).
Bad protein cooperate with bim (zeige BCL2L11 Proteine) 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 Proteine) reduced the pressure to inactivate p53 (zeige TP53 Proteine), whereas Bad deficiency did not, identifying Bmf (zeige BMF Proteine) as a novel component of the p53 (zeige TP53 Proteine)-independent tumor suppressor pathway triggered by c-Myc (zeige MYC Proteine).
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