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

Subtle Changes in the Levels of BCL-2 Proteins Cause Severe Craniofacial Abnormalities

1 Sept 2018

Abstract excerpt

Apoptotic cell death removes unwanted cells and is regulated by interactions between pro-survival and pro-apoptotic members of the BCL-2 protein family. The regulation of apoptosis is thought to be crucial for normal embryonic development. Accordingly, complete loss of pro-survival MCL-1 or BCL-XL (BCL2L1) causes embryonic lethality. However, it is not known whether minor reductions in pro-survival proteins could...

Read the complete abstract on PubMed

Topics

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

Share to Cell Adhesion Molecules Research
Share to Peptidase Inhibition and Analysis
Share to Ubiquitin and proteasome pathways

Methodology Data sources Editorial policy Privacy About Contact Helena Bioinformatics

Source

Identifiers

PMID: 30232009
DOI: 10.1016/j.celrep.2018.08.048

Provenance

PubMed metadata and Literature Corpus relationships. Corpus snapshot updated 8 Sept 2026.

Related research

Semantic proximity does not establish scientific evidence.

Research trail→

Click a neighbor to travelStep 1 · 12 closest

Subtle Changes in the Levels of BCL-2 Proteins Cause Severe Craniofacial AbnormalitiesPMID 30232009Read ↗

Bcl‐2 proteins in development, health, and disease of the hematopoietic systemSemantic proximity Read ↗

The combined functions of proapoptotic Bcl-2 family members bak and bax are essential for normal development of multiple tissues.Semantic proximity Read ↗

Role of Bcl-2 family members on apoptosis: what we have learned from knock-out miceSemantic proximity Read ↗

Mcl-1 is a key regulator of apoptosis during CNS development and after DNA damage.Semantic proximity Read ↗

Combined reduction in the expression of MCL-1 and BCL-2 reduces organismal size in mice.Semantic proximity Read ↗

Development and maintenance of B and T lymphocytes requires antiapoptotic MCL-1.Semantic proximity Read ↗

Oligodendrocytes depend on MCL-1 to prevent spontaneous apoptosis and white matter degenerationSemantic proximity Read ↗

Degenerative disorders caused by Bcl-2 deficiency prevented by loss of its BH3-only antagonist Bim.Semantic proximity Read ↗

Proapoptotic Bcl-2 Relative Bim Required for Certain Apoptotic Responses, Leukocyte Homeostasis, and to Preclude AutoimmunitySemantic proximity Read ↗

Apaf1 apoptotic function critically limits Sonic hedgehog signaling during craniofacial development.Semantic proximity Read ↗

Exon Skipping in Mcl-1 Results in a Bcl-2 Homology Domain 3 Only Gene Product That Promotes Cell DeathSemantic proximity Read ↗

Bax deficiency prevents the increased cell death of immature neurons in bcl-x-deficient mice.Semantic proximity Read ↗

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