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The p65 subunit of NF-kappa B regulates I kappa B by two distinct mechanisms.

The p65 subunit of NF-kappa B regulates I kappa B by two distinct mechanisms. Downloaded from genesdev.cshlp.org on October 23, 2021 - Published by Cold Spring Harbor Laboratory Press The p65 subunit of NF-KB regulates IKB by two distinct mechanisms Martin L. Scott, Takashi Fujita, Hsiou-Chi Liou, Garry P. Nolan, 1 and David Baltimore The Rockefeller University, New York, New York 10021 USA; ~Department of Pharmacology, Stanford University School of Medicine, Stanford, California 94305 USA Transcription factor NF-KB (p50/p65) is generally localized to the cytoplasm by its inhibitor IKB. Overproduced IKB, free from NF-KB, is rapidly degraded. Overexpression of p65 increases endogenous IKB protein in both carcinoma and lymphoid cells by two mechanisms: protein stabilization and increased transcription of IKB mRNA. In contrast, p65zX, a naturally occurring splice variant, fails to markedly augment IKB protein levels. Both overexpressed p65 and coexpressed p50 are cytoplasmic, whereas p65~X is partly nuclear, indicating that the IKB induced by p65 can maintain NF-KB in the cytoplasm. Thus, p65 and IKB are linked in an autoregulatory loop, ensuring that NF-KB is held in the cytoplasm until cells are specifically induced to translocate it to the nucleus. [Key Words: NF-KB; autoregulation; B-cell development] Received March 22, 1993; revised version accepted April 20, 1993. NF-KB is a widely expressed factor http://www.deepdyve.com/assets/images/DeepDyve-Logo-lg.png Genes & Development Unpaywall

The p65 subunit of NF-kappa B regulates I kappa B by two distinct mechanisms.

Scott, M L; Fujita, T; Liou, H C; Nolan, G P; Baltimore, D
Genes & Development – Jul 1, 1993
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Unpaywall
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0890-9369
DOI
10.1101/gad.7.7a.1266
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Abstract

Downloaded from genesdev.cshlp.org on October 23, 2021 - Published by Cold Spring Harbor Laboratory Press The p65 subunit of NF-KB regulates IKB by two distinct mechanisms Martin L. Scott, Takashi Fujita, Hsiou-Chi Liou, Garry P. Nolan, 1 and David Baltimore The Rockefeller University, New York, New York 10021 USA; ~Department of Pharmacology, Stanford University School of Medicine, Stanford, California 94305 USA Transcription factor NF-KB (p50/p65) is generally localized to the cytoplasm by its inhibitor IKB. Overproduced IKB, free from NF-KB, is rapidly degraded. Overexpression of p65 increases endogenous IKB protein in both carcinoma and lymphoid cells by two mechanisms: protein stabilization and increased transcription of IKB mRNA. In contrast, p65zX, a naturally occurring splice variant, fails to markedly augment IKB protein levels. Both overexpressed p65 and coexpressed p50 are cytoplasmic, whereas p65~X is partly nuclear, indicating that the IKB induced by p65 can maintain NF-KB in the cytoplasm. Thus, p65 and IKB are linked in an autoregulatory loop, ensuring that NF-KB is held in the cytoplasm until cells are specifically induced to translocate it to the nucleus. [Key Words: NF-KB; autoregulation; B-cell development] Received March 22, 1993; revised version accepted April 20, 1993. NF-KB is a widely expressed factor

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Genes & Development – Unpaywall

Published: Jul 1, 1993

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