Discover Community Create You

Loading publication...

Noodle always counts identifier-free feature events for service operation. With your permission, Google Analytics can also estimate audience and engagement. Search text, publication identifiers, cookies, IP addresses and browser fingerprints are never included in Noodle's first-party event counters.

Privacy details

Article

Function of BID -- a molecule of the bcl-2 family -- in ischemic cell death in the brain.

European surgical research. Europaische chirurgische Forschung. Recherches chirurgicales europeennes - 1 Jan 2000

Plesnila Nikolaus, Zinkel Sandra, Amin-Hanjani Sepideh, Qiu Jianhua, Korsmeyer Stanley J, Moskowitz Michael A

Abstract excerpt

Mitochondrial mechanisms, particularly the release of cytochrome c, play a role in the death of nerve and glial cells in cerebral ischemia. We have currently investigated whether BID, a proapoptotic molecule of the bcl-2 family and promoter of the release of cytochrome c is expressed in the brain, activated by cerebral ischemia in vivo, and contributes to ischemic cell death. We found BID in the cytosol of mouse...

Read the complete abstract on PubMed

Topics

Share this publication in a Topic to start or enrich a Post.

Share to Apoptosis
Share to BH3 Interacting Domain Death Agonist Protein

Methodology Data sources Editorial policy Privacy About Contact Helena Bioinformatics

Share to Brain Ischemia

Share to Carrier Proteins

Share to Cytochrome c Group

Share to Mice, Knockout

Share to Proto-Oncogene Proteins c-bcl-2

Source

Identifiers

PMID: 11867899
DOI: 10.1159/000048885

Genes

BID

Provenance

PubMed metadata and Literature Corpus relationships. Corpus snapshot updated 7 Sept 2026. Manifest publication-graph-cohort-2026-09-07.1.

Source receipt: pubmed, retrieved 7 Sept 2026.

Related research

Semantic proximity does not establish scientific evidence.

Research trail→

Click a neighbor to travelStep 1 · 12 closest

Function of BID -- a molecule of the bcl-2 family -- in ischemic cell death in the brain.PMID 11867899Read ↗

BID mediates neuronal cell death after oxygen/ glucose deprivation and focal cerebral ischemia.Semantic proximity Read ↗

BH3-only protein Bid is dispensable for seizure-induced neuronal death and the associated nuclear accumulation of apoptosis-inducing factor.Semantic proximity Read ↗

Signal transduction mediated by Bid, a pro-death Bcl-2 family proteins, connects the death receptor and mitochondria apoptosis pathwaysSemantic proximity Read ↗

Dynamics of expression of apoptosis-regulatory proteins Bid, Bcl-2, Bcl-X, Bax and Bak during development of murine nervous systemSemantic proximity Read ↗

Pro-apoptotic Bid induces membrane perturbation by inserting selected lysolipids into the bilayer.Semantic proximity Read ↗

Enhanced oxidative stress and altered antioxidants in brains of Bcl-2-deficient mice.Semantic proximity Read ↗

The role of Bcl-2 proteins in modulating neuronal Ca2+ signaling in health and in Alzheimer's diseaseSemantic proximity Read ↗

Mutations to bid cleavage sites protect hepatocytes from apoptosis after ischemia/reperfusion injury.Semantic proximity Read ↗

Caspase-2-induced apoptosis requires bid cleavage: a physiological role for bid in heat shock-induced death.Semantic proximity Read ↗

BID-D59A is a potent inducer of apoptosis in primary embryonic fibroblasts.Semantic proximity Read ↗

Fundamental role of the Rip2/caspase-1 pathway in hypoxia and ischemia-induced neuronal cell deathSemantic proximity Read ↗

BIM and other BCL-2 family proteins exhibit cross-species conservation of function between zebrafish and mammals.Semantic proximity Read ↗

⌁Select a neighboring publication to make it the new centre.