| pubmed-article:7590249 | rdf:type | pubmed:Citation | lld:pubmed |
| pubmed-article:7590249 | lifeskim:mentions | umls-concept:C0021289 | lld:lifeskim |
| pubmed-article:7590249 | lifeskim:mentions | umls-concept:C0026809 | lld:lifeskim |
| pubmed-article:7590249 | lifeskim:mentions | umls-concept:C0167954 | lld:lifeskim |
| pubmed-article:7590249 | lifeskim:mentions | umls-concept:C0302090 | lld:lifeskim |
| pubmed-article:7590249 | lifeskim:mentions | umls-concept:C0079904 | lld:lifeskim |
| pubmed-article:7590249 | lifeskim:mentions | umls-concept:C1879547 | lld:lifeskim |
| pubmed-article:7590249 | lifeskim:mentions | umls-concept:C2349975 | lld:lifeskim |
| pubmed-article:7590249 | pubmed:issue | 22 | lld:pubmed |
| pubmed-article:7590249 | pubmed:dateCreated | 1995-12-28 | lld:pubmed |
| pubmed-article:7590249 | pubmed:abstractText | Transcription factors belonging to the NF-kappa B family are controlled by inhibitory I kappa B proteins, mainly I kappa B alpha and I kappa B beta. Apparently normal at birth, I kappa B alpha-/- mice exhibit severe runting, skin defects, and extensive granulopoiesis postnatally, typically dying by 8 days. Hematopoietic tissues from these mice display elevated levels of both nuclear NF-kappa B and mRNAs of some, but not all, genes thought to be regulated by NF-kappa B. NF-kappa B elevation results in these phenotypic abnormalities because mice lacking both I kappa B alpha and the p50 subunit of NF-kappa B show a dramatically delayed onset of abnormalities. In contrast to hematopoietic cells, I kappa B alpha-/- embryonic fibroblasts show minimal constitutive NF-kappa B, as well as normal signal-dependent NF-kappa B activation that is concomitant with I kappa B beta degradation. Our results indicate that I kappa b beta, but not I kappa B alpha, is required for the signal-dependent activation of NF-kappa B in fibroblasts. However, I kappa B alpha is required for the postinduction repression of NF-kappa B in fibroblasts. These results define distinct roles for the two forms of I kappa B and demonstrate the necessity for stringent control of NF-kappa B. | lld:pubmed |
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| pubmed-article:7590249 | pubmed:language | eng | lld:pubmed |
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| pubmed-article:7590249 | pubmed:citationSubset | IM | lld:pubmed |
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| pubmed-article:7590249 | pubmed:status | MEDLINE | lld:pubmed |
| pubmed-article:7590249 | pubmed:month | Nov | lld:pubmed |
| pubmed-article:7590249 | pubmed:issn | 0890-9369 | lld:pubmed |
| pubmed-article:7590249 | pubmed:author | pubmed-author:BaltimoreDD | lld:pubmed |
| pubmed-article:7590249 | pubmed:author | pubmed-author:BronsonR TRT | lld:pubmed |
| pubmed-article:7590249 | pubmed:author | pubmed-author:BegA AAA | lld:pubmed |
| pubmed-article:7590249 | pubmed:author | pubmed-author:ShaW CWC | lld:pubmed |
| pubmed-article:7590249 | pubmed:issnType | Print | lld:pubmed |
| pubmed-article:7590249 | pubmed:day | 15 | lld:pubmed |
| pubmed-article:7590249 | pubmed:volume | 9 | lld:pubmed |
| pubmed-article:7590249 | pubmed:owner | NLM | lld:pubmed |
| pubmed-article:7590249 | pubmed:authorsComplete | Y | lld:pubmed |
| pubmed-article:7590249 | pubmed:pagination | 2736-46 | lld:pubmed |
| pubmed-article:7590249 | pubmed:dateRevised | 2007-11-14 | lld:pubmed |
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| pubmed-article:7590249 | pubmed:year | 1995 | lld:pubmed |
| pubmed-article:7590249 | pubmed:articleTitle | Constitutive NF-kappa B activation, enhanced granulopoiesis, and neonatal lethality in I kappa B alpha-deficient mice. | lld:pubmed |
| pubmed-article:7590249 | pubmed:affiliation | Department of Biology, Massachusetts Institute of Technology, Cambridge 02139, USA. | lld:pubmed |
| pubmed-article:7590249 | pubmed:publicationType | Journal Article | lld:pubmed |
| pubmed-article:7590249 | pubmed:publicationType | Research Support, U.S. Gov't, P.H.S. | lld:pubmed |
| pubmed-article:7590249 | pubmed:publicationType | Research Support, Non-U.S. Gov't | lld:pubmed |
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