Absence of tumor necrosis factor rescues RelA-deficient mice from embryonic lethality Journal Article

   

Authors:	Doi, T. S.; Marino, M. W.; Takahashi, T.; Yoshida, T.; Sakakura, T.; Old, L. J.; Obata, Y.
Article Title:	Absence of tumor necrosis factor rescues RelA-deficient mice from embryonic lethality
Abstract:	Mice lacking the RelA (p65) subunit of NF-κB die between days 14 and 15 of embryogenesis because of massive liver destruction. Fibroblasts and macrophages isolated from relA-/- embryos were found to be highly sensitive to tumor necrosis factor (TNF) cytotoxicity, raising the possibility that endogenous TNF is the cause of liver cell apoptosis. To test this idea, we generated mice lacking both TNF and RelA. Embryogenesis proceeds normally in such mice, and TNF/RelA double-deficient mice are viable and have normal livers. Thus, the RelA-mediated-antiapoptotic signal that protects normal cells from TNF injury in vitro can be shown to be operative in vivo.
Keywords:	immunohistochemistry; histopathology; nonhuman; conference paper; mouse; phenotype; animals; mice; mice, knockout; reverse transcription polymerase chain reaction; apoptosis; animal model; genotype; embryo development; immunoglobulin enhancer binding protein; transcription factor rela; gene expression regulation, developmental; tumor necrosis factor-alpha; nf-kappa b; liver injury; knockout mouse; tumor necrosis factor; embryo death; priority journal; embryonic and fetal development; fetal death; tissue degeneration
Journal Title:	Proceedings of the National Academy of Sciences of the United States of America
Volume:	96
Issue:	6
ISSN:	0027-8424
Publisher:	National Academy of Sciences
Date Published:	1999-03-01
Start Page:	2994
End Page:	2999
Language:	English
DOI:	10.1073/pnas.96.6.2994
PUBMED:	10077625
PROVIDER:	scopus
PMCID:	PMC15883
DOI/URL:	https://www.scopus.com/inward/record.uri?eid=2-s2.0-0032980504&partnerID=40&md5=0b05244ade36426ec897fd476d150af3
Notes:	Conference Paper -- Export Date: 16 August 2016 -- Source: Scopus

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