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The p65 subunit of NF-kappa B regulates I kappa B by two distinct mechanisms.
Open accessAbstract
Transcription factor NF-kappa B (p50/p65) is generally localized to the cytoplasm by its inhibitor I kappa B. Overproduced I kappa B, free from NF-kappa B, is rapidly degraded. Overexpression of p65 increases endogenous I kappa B protein in both carcinoma and lymphoid cells by two mechanisms: protein stabilization and increased transcription of I kappa B mRNA. In contrast, p65 delta, a naturally occurring splice variant, fails to markedly augment I kappa B protein levels. Both overexpressed p65 and coexpressed p50 are cytoplasmic, whereas p65 delta is partly nuclear, indicating that the I kappa B induced by p65 can maintain NF-kappa B in the cytoplasm. Thus, p65 and I kappa B are linked in an autoregulatory loop, ensuring that NF-kappa B is held in the cytoplasm until cells are specifically induced to translocate it to the nucleus.
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Metadata
- Authors
- Scott, M. L., Fujita, T., Liou, H. C., Nolan, G. P., & Baltimore, D.
- Venue
- Genes & Development
- Publisher
- Cold Spring Harbor Laboratory
- Published
- 1993-07-01
- Volume
- 7
- Issue
- 7a
- Pages
- 1266-1276
- ISSN
- 0890-9369 (ISSN-L)
- OpenAlex
- W1981884734
- Cited by
- 354
- References
- 0
- Type
- posted content
- Language
- en
- Open access
- diamond
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