BAX is required for neuronal death after trophic factor deprivation and during development (Q28592997)

31 January 2017

title

BAX is required for neuronal death after trophic factor deprivation and during development (English)

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BCL2-associated X protein

31 January 2017

main subject

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GOA release 2020-03-11

S. J. Korsmeyer

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31 January 2017

T. L. Deckwerth

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31 January 2017

J. L. Elliott

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31 January 2017

C. M. Knudson

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31 January 2017

E. M. Johnson

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31 January 2017

W. D. Snider

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31 January 2017

language of work or name

English

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publication date

1 September 1996

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31 January 2017

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31 January 2017

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31 January 2017

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31 January 2017

page(s)

401–411

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Axotomized neonatal motoneurons overexpressing the bcl2 proto-oncogene retain functional electrophysiological properties

31 January 2017

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bcl-x, a bcl-2-related gene that functions as a dominant regulator of apoptotic cell death

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The protein bcl-2 alpha does not require membrane attachment, but two conserved domains to suppress apoptosis

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Induction of apoptosis by the Bcl-2 homologue Bak

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Nucleotide sequence of a t(14;18) chromosomal breakpoint in follicular lymphoma and demonstration of a breakpoint-cluster region near a transcriptionally active locus on chromosome 18.

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Mice lacking nerve growth factor display perinatal loss of sensory and sympathetic neurons yet develop basal forebrain cholinergic neurons

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Temporal analysis of events associated with programmed cell death (apoptosis) of sympathetic neurons deprived of nerve growth factor

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Neurites can remain viable after destruction of the neuronal soma by programmed cell death (apoptosis).

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NT-3 stimulates sympathetic neuroblast proliferation by promoting precursor survival

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Neonatal motoneurons overexpressing the bcl-2 protooncogene in transgenic mice are protected from axotomy-induced cell death.

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Characterization of apoptosis in cultured rat sympathetic neurons after nerve growth factor withdrawal

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bcl-2 transgene expression can protect neurons against developmental and induced cell death

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Cloning of a bcl-2 homologue by interaction with adenovirus E1B 19K

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Analysis of cell cycle-related gene expression in postmitotic neurons: selective induction of Cyclin D1 during programmed cell death

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Experimental autoimmune model of nerve growth factor deprivation: Effects on developing peripheral sympathetic and sensory neurons

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Superoxide dismutase delays neuronal apoptosis: a role for reactive oxygen species in programmed neuronal death

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7 January 2021

Role of BCL-2 in the survival and function of developing and mature sympathetic neurons

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7 January 2021

C. elegans cell survival gene ced-9 encodes a functional homolog of the mammalian proto-oncogene bcl-2.

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7 January 2021

Naturally occurring and axotomy-induced motoneuron death and its prevention by neurotrophic agents: a comparison between chick and mouse

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7 January 2021

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MCL1, a gene expressed in programmed myeloid cell differentiation, has sequence similarity to BCL2

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Upregulation of bax protein levels in neurons following cerebral ischemia.

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Motoneuron cell death in the developing lumbar spinal cord of the mouse.

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DESTRUCTION OF THE SYMPATHETIC GANGLIA IN MAMMALS BY AN ANTISERUM TO A NERVE-GROWTH PROTEIN.

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7 January 2021

Bcl-2 is upregulated at the CD4+ CD8+ stage during positive selection and promotes thymocyte differentiation at several control points

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7 January 2021

Overexpression of BCL-2 in transgenic mice protects neurons from naturally occurring cell death and experimental ischemia

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7 January 2021

Viral proteins E1B19K and p35 protect sympathetic neurons from cell death induced by NGF deprivation

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7 January 2021

Massive cell death of immature hematopoietic cells and neurons in Bcl-x-deficient mice

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7 January 2021

Targeted disruption of Bcl-2 alpha beta in mice: occurrence of gray hair, polycystic kidney disease, and lymphocytopenia

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7 January 2021

Checkpoints of dueling dimers foil death wishes

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7 January 2021

Bcl-2 heterodimerizes in vivo with a conserved homolog, Bax, that accelerates programmed cell death

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7 January 2021

Cell death during development of the nervous system

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7 January 2021

Brain-derived neurotrophic factor rescues developing avian motoneurons from cell death

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7 January 2021

Developing motor neurons rescued from programmed and axotomy-induced cell death by GDNF

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7 January 2021

Bcl-2 overexpression prevents motoneuron cell body loss but not axonal degeneration in a mouse model of a neurodegenerative disease

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7 January 2021

Interactions among members of the Bcl-2 protein family analyzed with a yeast two-hybrid system.

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7 January 2021

Multiple Bcl-2 family members demonstrate selective dimerizations with Bax

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7 January 2021

Ciliary neurotrophic factor prevents the degeneration of motor neurons after axotomy.

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7 January 2021

Axotomy-induced neuronal death during development

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7 January 2021

The t(14;18) chromosome translocations involved in B-cell neoplasms result from mistakes in VDJ joining

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7 January 2021

Bcl-2-deficient mice demonstrate fulminant lymphoid apoptosis, polycystic kidneys, and hypopigmented hair

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7 January 2021

Localization of FGF receptor mRNA in the adult rat central nervous system by in situ hybridization

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7 January 2021

The guidance molecule semaphorin III is expressed in regions of spinal cord and periphery avoided by growing sensory axons

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7 January 2021

Brain-derived neurotrophic factor rescues spinal motor neurons from axotomy-induced cell death

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7 January 2021

In vivo neurotrophic effects of GDNF on neonatal and adult facial motor neurons

1 reference

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7 January 2021

Bad, a heterodimeric partner for Bcl-XL and Bcl-2, displaces Bax and promotes cell death

1 reference

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7 January 2021

BH1 and BH2 domains of Bcl-2 are required for inhibition of apoptosis and heterodimerization with Bax.

1 reference

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7 January 2021

10.1016/S0896-6273(00)80173-7

Identifiers

DOI

1 reference

Consolidated OpenCitations Corpus – April 2017

1 reference

Consolidated OpenCitations Corpus – April 2017

1 reference

Consolidated OpenCitations Corpus – April 2017