Medizinische Universität Graz - Research portal

Go directly to the nagivation.
Go directly to the content.

Navigation/Search

Selected Publication:

SHR Neuro Cancer Cardio Lipid Metab Microb

Grabow, S; Kueh, AJ; Ke, F; Vanyai, HK; Sheikh, BN; Dengler, MA; Chiang, W; Eccles, S; Smyth, IM; Jones, LK; de Sauvage, FJ; Scott, M; Whitehead, L; Voss, AK; Strasser, A.
Subtle Changes in the Levels of BCL-2 Proteins Cause Severe Craniofacial Abnormalities.
Cell Rep. 2018; 24(12):3285-3295 Doi: 10.1016/j.celrep.2018.08.048
Web of Science PubMed FullText FullText_MUG

Co-authors Med Uni Graz: Dengler Michael
Altmetrics:
Dimensions Citations:
Plum Analytics:
Scite (citation analytics):
Abstract:: 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 cause developmental abnormalities. We explored the rate-limiting roles of MCL-1 and BCL-XL in development and show that combined loss of single alleles of Mcl-1 and Bcl-x causes neonatal lethality. Mcl-1^+/-;Bcl-x^+/- mice display craniofacial anomalies, but additional loss of a single allele of pro-apoptotic Bim (Bcl2l11) restores normal development. These findings demonstrate that the control of cell survival during embryogenesis is finely balanced and suggest that some human craniofacial defects, for which causes are currently unknown, may be due to subtle imbalances between pro-survival and pro-apoptotic BCL-2 family members. Copyright © 2018 The Authors. Published by Elsevier Inc. All rights reserved.
Find related publications in this database (using NLM MeSH Indexing): Animals -; Apoptosis -; Bcl-2-Like Protein 11 - genetics; Bcl-2-Like Protein 11 - metabolism; Cells, Cultured -; Craniofacial Abnormalities - genetics; Female -; Heterozygote -; Male -; Mice -; Mice, Inbred C57BL -; Myeloid Cell Leukemia Sequence 1 Protein - genetics; Myeloid Cell Leukemia Sequence 1 Protein - metabolism; bcl-X Protein - genetics; bcl-X Protein - metabolism