Constitutive NF-kappa B activation, enhanced granulopoiesis, and neonatal lethality in I kappa B alpha-deficient mice. Export

@article{citeulike:6076319, abstract = {10.1101/gad.9.22.2736 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.}, author = {Beg, A. A. and Sha, W. C. and Bronson, R. T. and Baltimore, D.}, citeulike-article-id = {6076319}, citeulike-linkout-0 = {http://dx.doi.org/10.1101/gad.9.22.2736}, citeulike-linkout-1 = {http://genesdev.cshlp.org/content/9/22/2736.abstract}, citeulike-linkout-2 = {http://genesdev.cshlp.org/content/9/22/2736.full.pdf}, citeulike-linkout-3 = {http://view.ncbi.nlm.nih.gov/pubmed/7590249}, citeulike-linkout-4 = {http://www.hubmed.org/display.cgi?uids=7590249}, comment = {generation of the ikb-alpha reporter (lacz) mice}, day = {15}, doi = {10.1101/gad.9.22.2736}, journal = {Genes \& Development}, keywords = {ikb-alpha}, month = {November}, number = {22}, pages = {2736--2746}, posted-at = {2009-11-05 19:45:14}, priority = {2}, title = {Constitutive NF-kappa B activation, enhanced granulopoiesis, and neonatal lethality in I kappa B alpha-deficient mice.}, url = {http://dx.doi.org/10.1101/gad.9.22.2736}, volume = {9}, year = {1995} }

TY - JOUR ID - citeulike:6076319 L3 - citeulike-article-id:6076319 N2 - 10.1101/gad.9.22.2736 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. IS - 22 JF - Genes & Development EP - 2746 TI - Constitutive NF-kappa B activation, enhanced granulopoiesis, and neonatal lethality in I kappa B alpha-deficient mice. VL - 9 SP - 2736 KW - ikb-alpha N1 - generation of the ikb-alpha reporter (lacz) mice AU - Beg, AA AU - Sha, WC AU - Bronson, RT AU - Baltimore, D PY - 1995/11/15/ UR - http://dx.doi.org/10.1101/gad.9.22.2736 ER -