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Bad functions as an essential sensitizer and Puma (Montrer BBC3 Kits ELISA) as an essential activator of IR-induced mitochondrial apoptosis specifically in embryonic neural tissue.
Stage-specific expression of TNFalpha (Montrer TNF Kits ELISA) regulates bad/bid (Montrer BID Kits ELISA)-mediated apoptosis and RIP1 (Montrer RALBP1 Kits ELISA)/ROS (Montrer ROS1 Kits ELISA)-mediated secondary necrosis in Birnavirus-infected fish cells.
Results indicate that zebrafish BH3-only (Montrer BBC3 Kits ELISA) 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 (Montrer PARK7 Kits ELISA) and Bcl-XL (Montrer BCL2L1 Kits ELISA), which will contribute to molecular understanding of the role of mitochondrial DJ-1 (Montrer PARK7 Kits ELISA) in Bcl-XL (Montrer BCL2L1 Kits ELISA) regulation in response to oxidative stress.
We will then review how the apoptotic and autophagic functions of Bcl-xL (Montrer BCL2L1 Kits ELISA) are modified by this post-translational modifications, and how this impacts on its oncogenic properties.
the membrane localization of BCL-xL (Montrer BCL2L1 Kits ELISA) enforces its control over cell survival and, importantly, limits the pro-apoptotic effects of BH3 mimetics by selectively influencing BCL-xL (Montrer BCL2L1 Kits ELISA) binding to key pro-apoptotic effectors.
The long unstructured region of Bcl-xl (Montrer BCL2L1 Kits ELISA) modulates its structural dynamics.
Short-term treatment of nascent melanoma tumors with PAK inhibitors that block RhoJ (Montrer RHOJ Kits ELISA) signaling halts the growth of BRAF (Montrer BRAF Kits ELISA) mutant melanoma tumors in vivo and induces apoptosis in melanoma cells in vitro via a BAD-dependent mechanism. As up to 50% of BRAF (Montrer BRAF Kits ELISA) mutant human melanomas express high levels of RhoJ (Montrer RHOJ Kits ELISA), these studies nominate the RhoJ (Montrer RHOJ Kits ELISA)-BAD signaling network as a therapeutic vulnerability for fledgling BRAF (Montrer BRAF Kits ELISA) 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 (Montrer BCL2L1 Kits ELISA) on the priming of Bax (Montrer BAX Kits ELISA). As demonstrated with the BH3-mimetic molecule ABT-737, this property of Bcl-xL (Montrer BCL2L1 Kits ELISA), and of Bcl-2 (Montrer BCL2 Kits ELISA), is crucial to elaborate about how apoptosis could be reactivated in tumoral cells.
the accumulation of reactive oxygen species (ROS (Montrer ROS1 Kits ELISA)) in cells expressing JAK2V617F compromises the NHE-1 (Montrer SLC9A1 Kits ELISA)/Bcl-xL (Montrer BCL2L1 Kits ELISA) deamidation pathway by repressing NHE-1 (Montrer SLC9A1 Kits ELISA) upregulation in response to DNA damage. hematopoietic stem cells (HSCs), FOXO3A (Montrer FOXO3 Kits ELISA) is largely localized within the nuclei despite the presence of JAK2V617F mutation, suggesting that JAK2 (Montrer JAK2 Kits ELISA)-FOXO (Montrer FOXO3 Kits ELISA) signaling has a different effect on progenitors compared with stem cells.
These results identify beta3 integrin (Montrer ITGB3 Kits ELISA) signaling via repression of BAD as an important survival pathway used by breast cancer cells to evade chemotherapy induced stress.
miR (Montrer MLXIP Kits ELISA)-377 was markedly downregulated in HCC (Montrer FAM126A Kits ELISA) cell lines and primary human HCC (Montrer FAM126A Kits ELISA) tissues. The decreased expression of miR (Montrer MLXIP Kits ELISA)-377 contributes to the upregulation of Bcl-xL (Montrer BCL2L1 Kits ELISA) expression by targeting its 3'-untranslated region (3'-UTR (Montrer UTS2R Kits ELISA)).
By the pharmacologic targeting of BCL2 (Montrer BCL2 Kits ELISA), MCL1 (Montrer MCL1 Kits ELISA), and BCL-XL (Montrer BCL2L1 Kits ELISA), we demonstrated that diffuse large B-cell lymphoma can be divided into BCL2 (Montrer BCL2 Kits ELISA)-dependent and MCL1 (Montrer MCL1 Kits ELISA)-dependent subgroups with a less pronounced role left for BCL-XL (Montrer BCL2L1 Kits ELISA).
Bad is dispensable for TNF (Montrer TNF Kits ELISA)-mediated cell death.
Results indicate the downstream targets of insulin (Montrer INS Kits ELISA), cyclin D1 (Montrer CCND1 Kits ELISA), BAD, alpha-MHC (Montrer MYH6 Kits ELISA), and GATA-4 (Montrer GATA4 Kits ELISA), elucidate a molecular mechanism of insulin (Montrer INS Kits ELISA) in promoting cell proliferation and differentiation.
our study suggests that Bad and Bmf (Montrer BMF Kits ELISA) 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 (Montrer CHUK Kits ELISA) inhibits TNFalpha (Montrer TNF Kits ELISA)-induced apoptosis through two distinct but cooperative mechanisms: activation of the survival factor NF-kappaB (Montrer NFKB1 Kits ELISA) and inactivation of the proapoptotic BH3-only (Montrer BBC3 Kits ELISA) BAD protein.
RNAi-mediated silencing of STAT1 (Montrer STAT1 Kits ELISA) in soft tissue sarcoma (STS (Montrer STS Kits ELISA)) cells was sufficient to increase expression of the apoptotic mediators Fas (Montrer FAS Kits ELISA) and Bad and to elevate the sensitivity of STS (Montrer STS Kits ELISA) cells to Fas (Montrer FAS Kits ELISA)-mediated apoptosis
Tonicity-induced COX-2 (Montrer COX2 Kits ELISA) 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 (Montrer CASP3 Kits ELISA) is activated by the BAD-BAX (Montrer BAX Kits ELISA) cascade resulting in long term depression induction in the hippocampus.
JNK1 (Montrer MAPK8 Kits ELISA) is required for erythropoietin (Montrer EPO Kits ELISA)-mediated cell survival through phosphorylation and inactivation of the pro-apoptotic, Bcl-2 (Montrer BCL2 Kits ELISA) homology domain 3 (BH3)-only (Montrer BBC3 Kits ELISA) Bcl-associated death protein (Bad).
Bad protein cooperate with bim (Montrer BCL2L11 Kits ELISA) protein in certain apoptotic responses and in the suppression of g-irradiation-induced thymic lymphoma.(Bad protein)
Data show that loss of Bmf (Montrer BMF Kits ELISA) reduced the pressure to inactivate p53 (Montrer TP53 Kits ELISA), whereas Bad deficiency did not, identifying Bmf (Montrer BMF Kits ELISA) as a novel component of the p53 (Montrer TP53 Kits ELISA)-independent tumor suppressor pathway triggered by c-Myc (Montrer MYC Kits ELISA).
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