Bim and Noxa are candidates to mediate the deleterious effect of the NF-kappa B subunit RelA in cerebral ischemia. (Q48338905)

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23 December 2019

title

Bim and Noxa are candidates to mediate the deleterious effect of the NF-kappa B subunit RelA in cerebral ischemia (English)

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Marina Pizzi

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PierFranco Spano

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Ilenia Sarnico

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Hsiou-Chi Liou

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Ioana Inta

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author name string

Stephan Paxian

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Ira Maegele

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Wen Zhang

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Sajjad Muhammad

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Oliver Herrmann

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Dragos Inta

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Bernd Baumann

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Roland M Schmid

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language of work or name

English

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publication date

1 December 2006

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23 December 2019

published in

Journal of Neuroscience

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volume

26

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issue

50

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page(s)

12896-12903

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describes a project that uses

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ImageJ

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11 June 2022

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inferred from PubMed Central ID database lookup

cites work

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NF-kappaB is activated and promotes cell death in focal cerebral ischemia

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NF-kappaB-mediated up-regulation of Bcl-x and Bfl-1/A1 is required for CD40 survival signaling in B lymphocytes

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Noxa, a BH3-only member of the Bcl-2 family and candidate mediator of p53-induced apoptosis

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In Vivo Delivery of a Bcl-xL Fusion Protein Containing the TAT Protein Transduction Domain Protects against Ischemic Brain Injury and Neuronal Apoptosis

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Temporal profiles of the subcellular localization of Bim, a BH3-only protein, during middle cerebral artery occlusion in mice

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BMS-345541 is a highly selective inhibitor of I kappa B kinase that binds at an allosteric site of the enzyme and blocks NF-kappa B-dependent transcription in mice

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Recombinant adenoviral expression of dominant negative IkappaBalpha protects brain from cerebral ischemic injury

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Stimulus-dependent activation of NF-kappaB specifies apoptosis or neuroprotection in cerebellar granule cells

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Regulation of body temperature and neuroprotection by endogenous interleukin-6 in cerebral ischemia

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FOXO transcription factors directly activate bim gene expression and promote apoptosis in sympathetic neurons

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FoxO3a transcriptional regulation of Bim controls apoptosis in paclitaxel-treated breast cancer cell lines

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Genetic analysis of NF- B/Rel transcription factors defines functional specificities

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Forebrain-specific neuronal inhibition of nuclear factor-kappaB activity leads to loss of neuroprotection.

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No PUMA, no death: implications for p53-dependent apoptosis

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A critical role of neural-specific JNK3 for ischemic apoptosis

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Up-regulation of Bcl-2 homology 3 (BH3)-only proteins by E2F1 mediates apoptosis

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Nuclear factor-kappaB contributes to infarction after permanent focal ischemia

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Targeting of TAK1 by the NF-kappa B protein Relish regulates the JNK-mediated immune response in Drosophila

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Nuclear factor-(kappa)B modulates the p53 response in neurons exposed to DNA damage.

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IkappaB kinase promotes tumorigenesis through inhibition of forkhead FOXO3a

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12 December 2020

The role of NF-kappaB in 6-hydroxydopamine- and TNFalpha-induced apoptosis of PC12 cells

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12 December 2020

The c-Jun N-terminal protein kinase signaling pathway mediates Bax activation and subsequent neuronal apoptosis through interaction with Bim after transient focal cerebral ischemia

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Tumor Necrosis Factor-Like Weak Inducer of Apoptosis-Induced Neurodegeneration

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Neuronal activation of NF-kappaB contributes to cell death in cerebral ischemia.

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IKK mediates ischemia-induced neuronal death

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The characterization of the promoter of the gene encoding the p50 subunit of NF-kappa B indicates that it participates in its own regulation

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NF-kappa B as inducible transcriptional activator of the granulocyte-macrophage colony-stimulating factor gene

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Embryonic lethality and liver degeneration in mice lacking the RelA component of NF-κB

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Multiorgan inflammation and hematopoietic abnormalities in mice with a targeted disruption of RelB, a member of the NF-kappa B/Rel family

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Altered expression of Bcl-2, Bcl-X, Bax, and c-Fos colocalizes with DNA fragmentation and ischemic cell damage following middle cerebral artery occlusion in rats.

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Bypass of lethality with mosaic mice generated by Cre– loxP -mediated recombination

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Apoptosis repressor genes Bcl-2 and Bcl-x-long are expressed in the rat brain following global ischemia.

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10.1523/JNEUROSCI.3670-06.2006

Identifiers

DOI

1 reference

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23 December 2019

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23 December 2019

PubMed publication ID

17167080

1 reference