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Tuning NF-κB activity: A touch of COMMD proteins
被引:96
|作者:
Bartuzi, Paulina
[1
]
Hofker, Marten H.
[1
]
van de Sluis, Bart
[1
]
机构:
[1] Univ Groningen, Univ Med Ctr Groningen, NL-9713 AV Groningen, Netherlands
来源:
BIOCHIMICA ET BIOPHYSICA ACTA-MOLECULAR BASIS OF DISEASE
|
2013年
/
1832卷
/
12期
关键词:
Inflammation;
NF-kappa B;
COMMD family;
Scaffold;
Termination;
COPPER TOXICOSIS;
GENE-EXPRESSION;
ACTIVATION;
MURR1;
PHOSPHORYLATION;
P65;
CYLINDROMATOSIS;
CYLD;
UBIQUITINATION;
IDENTIFICATION;
D O I:
10.1016/j.bbadis.2013.09.014
中图分类号:
Q5 [生物化学];
Q7 [分子生物学];
学科分类号:
071010 ;
081704 ;
摘要:
NF-kappa B is an important regulator of immunity and inflammation, and its activation pathway has been studied extensively. The mechanisms that downregulate the activity of NF-kappa B have also received a lot of attention, particularly since its activity needs to be terminated to prevent chronic inflammation and subsequent tissue damage. The COMMD family has been identified as a new group of proteins involved in NF-kappa B termination. All ten COMMD members share the structurally conserved carboxy-terminal motif, the COMM domain, and are ubiquitously expressed. They seem to play distinct and non-redundant roles in various physiological processes, including NF-kappa B signaling. In this review, we describe the mechanisms and proteins involved in the termination of canonical NF-kappa B signaling, with a specific focus on the role of the COMMD family in the down-modulation of NF-kappa B. (C) 2013 Elsevier B.V. All rights reserved.
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页码:2315 / 2321
页数:7
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