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L A O'Reilly
English
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Article
Open AccessImpact of the combined loss of BOK, BAX and BAK on the hematopoietic system is slightly more severe than compound loss of BAX and BAK
It is well established that BAX and BAK play crucial, overlap** roles in the intrinsic pathway of apoptosis. Gene targeted mice lacking both BAX and BAK have previously been generated, but the majority of th...
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Loss of c-REL but not NF-κB2 prevents autoimmune disease driven by FasL mutation
FASL/FAS signaling imposes a critical barrier against autoimmune disease and lymphadenopathy. Mutant mice unable to produce membrane-bound FASL (FasLΔm/Δm), a prerequisite for FAS-induced apoptosis, develop lymph...
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Open AccessCharacterisation of a novel A1-specific monoclonal antibody
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Loss of Prkar1a leads to Bcl-2 family protein induction and cachexia in mice
Loss of function mutations in the Prkar1a gene are the cause of most cases of Carney complex disorder. Defects in Prkar1a are thought to cause hyper-activation of PKA signalling, which drives neoplastic transform...
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Open AccessEvidence against upstream regulation of the unfolded protein response (UPR) by pro-apoptotic BIM and PUMA
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ER stress does not cause upregulation and activation of caspase-2 to initiate apoptosis
A recent report claimed that endoplasmic reticulum (ER) stress activates the ER trans-membrane receptor IRE1α, leading to increased caspase-2 levels via degradation of microRNAs, and consequently induction of apo...
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Erratum: BCL-2 family member BOK is widely expressed but its loss has only minimal impact in mice
Correction to: Cell Death and Differentiation (2012) 19, 915–925; doi: 10.1038/cdd.2011.210; published online 27 January 2012 Since the publication of this issue, the authors have noticed that the y-axis numbe...
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BCL-2 family member BOK is widely expressed but its loss has only minimal impact in mice
BOK/MTD was discovered as a protein that binds to the anti-apoptotic Bcl-2 family member MCL-1 and shares extensive amino-acid sequence similarity to BAX and BAK, which are essential for the effector phase of ...
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Puma indirectly activates Bax to cause apoptosis in the absence of Bid or Bim
Bcl-2 family members regulate apoptosis in response to cytokine withdrawal and a broad range of cytotoxic stimuli. Pro-apoptotic Bcl-2 family members Bax and Bak are essential for apoptosis triggered by interl...
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Apoptosis-based dual molecular targeting by INNO-406, a second-generation Bcr-Abl inhibitor, and ABT-737, an inhibitor of antiapoptotic Bcl-2 proteins, against Bcr-Abl-positive leukemia
Bcr-Abl is the cause of Philadelphia-positive (Ph+) leukemias and also constitutes their principal therapeutic target, as exemplified by dramatic effects of imatinib mesylate. However, mono-targeting of Bcr-Abl d...
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Bcl-2 transgene expression fails to prevent fatal hepatocyte apoptosis induced by endogenous TNFα in mice lacking RelA
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Modifications and intracellular trafficking of FADD/MORT1 and caspase-8 after stimulation of T lymphocytes
The adaptor protein FADD/MORT1 is essential for apoptosis induced by ‘death receptors’, such as Fas (APO-1/CD95), mediating aggregation and autocatalytic activation of caspase-8. Perhaps surprisingly, FADD and...
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Caspase-2 is not required for thymocyte or neuronal apoptosis even though cleavage of caspase-2 is dependent on both Apaf-1 and caspase-9
We have generated rat monoclonal antibodies that specifically recognise caspase-2 from many species, including mouse, rat and humans. Using these antibodies, we have investigated caspase-2 expression, subcellu...
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Tissue expression and subcellular localization of the pro-survival molecule Bcl-w
Anti-apoptotic members of the Bcl-2 family, such as Bcl-w, maintain cell viability by preventing the activation of the cell death effectors, the caspases. Gene targeting experiments in mice have demonstrated t...
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Apoptosis and autoimmune disease
The process of programmed cell death or apoptosis was already noted in 1842 by Vogt [1], but it was not until the more recent studies of Kerr et al. 1972 [2] that an explosion of interest in apoptosis researc...
