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BAX Is Required for Neuronal Death after Trophic Factor Deprivation and during Development
Members of the BCL2-related family of proteins either promote or repress programmed cell death. BAX, a death-promoting member, heterodimerizes with multiple death-repressing molecules, suggestingExpand
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Bax-Deficient Mice with Lymphoid Hyperplasia and Male Germ Cell Death
BAX, a heterodimeric partner of BCL2, counters BCL2 and promotes apoptosis in gain-of-function experiments. A Bax knockout mouse was generated that proved viable but displayed lineage-specificExpand
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Widespread Elimination of Naturally Occurring Neuronal Death inBax-Deficient Mice
The proapoptotic molecule BAX is required for death of sympathetic and motor neurons in the setting of trophic factor deprivation. Furthermore, adult Bax−/− mice have more motor neurons than do theirExpand
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Complete Dissociation of Motor Neuron Death from Motor Dysfunction by Bax Deletion in a Mouse Model of ALS
The death of cranial and spinal motoneurons (MNs) is believed to be an essential component of the pathogenesis of amyotrophic lateral sclerosis (ALS). We tested this hypothesis by crossingExpand
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Bax Involvement in p53-Mediated Neuronal Cell Death
The tumor suppressor gene p53 has been implicated in the loss of neuronal viability, but the signaling events associated with p53-mediated cell death in cortical and hippocampal neurons are notExpand
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bax-deficiency promotes drug resistance and oncogenic transformation by attenuating p53-dependent apoptosis.
Inactivation of p53-dependent apoptosis promotes oncogenic transformation, tumor development, and resistance to many cytotoxic anticancer agents. p53 can transcriptionally activate bax, a bcl-2Expand
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Prolongation of ovarian lifespan into advanced chronological age by Bax-deficiency
Female mammals are endowed with a finite number of oocytes at birth, each enclosed by a single layer of somatic (granulosa) cells in a primordial follicle. The fate of most follicles is atreticExpand
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Bax suppresses tumorigenesis and stimulates apoptosis in vivo
The protein p53 is a key tumour-suppressor, as evidenced by its frequent inactivation in human cancers. Animal models have indicated that attenuation of p53-dependent cell death (apoptosis) canExpand
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The brain ryanodine receptor: A caffeine-sensitive calcium release channel
The release of stored Ca2+ from intracellular pools triggers a variety of important neuronal processes. Physiological and pharmacological evidence has indicated the presence of caffeine-sensitiveExpand
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Bax Deletion Further Orders the Cell Death Pathway in Cerebellar Granule Cells and Suggests a Caspase-independent Pathway to Cell Death
Dissociated cerebellar granule cells maintained in medium containing 25 mM potassium undergo an apoptotic death when switched to medium with 5 mM potassium. Granule cells from mice in which Bax, aExpand
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