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2015 ; 75
(18
): 3692-5
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NF-?B: Regulation by Methylation
#MMPMID26337909
Lu T
; Stark GR
Cancer Res
2015[Sep]; 75
(18
): 3692-5
PMID26337909
show ga
In normal cells exposed to stress, the central transcription factor NF-?B is
activated only transiently, to modulate the activation of downstream immune
responses. However, in most cancers, NF-?B is abnormally activated
constitutively, contributing thus to oncogenesis and tumor progression.
Therefore, downregulating NF-?B activity is an important goal of cancer
treatment. In order to control NF-?B activity therapeutically, it is helpful to
understand the molecular mechanisms that normally govern its activation and how
dysregulated NF-?B activity may aid the development of disease. Recent evidence
from our laboratories and others indicates that, in addition to various
posttranslational modifications of NF-?B that have been observed previously,
including phosphorylation, ubiquitination, and acetylation, NF-?B can be
methylated reversibly on lysine or arginine residues by histone-modifying
enzymes, including lysine and arginine methyl transferases and demethylases.
Furthermore, these methylations are required to activate many downstream genes.
Interestingly, amplifications and mutations of several such enzymes have been
linked to cancer. We propose that some of these mutations may alter the
methylation not only of histones but also of NF-?B, making them attractive
therapeutic targets.
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