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CCR4-NOT transcription complex subunit 7 (CNOT7)

Target
CNOT7
Molecular classification
Deadenylase enzyme, Component of transcriptional regulatory complex, Other (CCR4-NOT complex subunit)
01

Overview

CCR4-NOT transcription complex subunit 7 (CNOT7) is a highly conserved enzyme that forms part of the multi-subunit CCR4-NOT deadenylase complex, which is the major cytoplasmic machinery responsible for deadenylation—removal of the poly(A) tail from mRNA transcripts, leading to mRNA decay and regulation of gene expression[1][2][4]. CNOT7 possesses 3'-5' poly(A) exoribonuclease activity and works in concert with related subunits such as CNOT8, showing partial functional redundancy[6]. The protein also participates in transcriptional regulatory events: it suppresses or potentiates transcription of specific genes, in part by interacting with nuclear hormone receptors (e.g., estrogen and retinoic acid receptors) and members of the BTG/Tob family of cell cycle regulatory proteins[2][3][4][5]. CNOT7 is essential for cell proliferation and viability in mammalian cells, with roles in mRNA turnover, cell cycle progression, and possibly in immune and metabolic function. Loss of CNOT7 in mice results in male infertility and altered bone formation but is otherwise compatible with life, highlighting tissue-specific dependencies[3][4]. No drugs are currently approved to directly target CNOT7, and its central function in mRNA biology and gene regulation suggests that indiscriminate inhibition could result in broad and severe phenotypic effects.

Other names
CAF1CAF-1BTG1-binding factor 1CCR4-associated factor 1Caf1aBTG1 binding factor 1hCAF-1carbon catabolite repressor protein (CCR4)-associative factor 1
02

Mechanism of action

Not targeted by approved drugs; as an endogenous enzyme, functions by enzymatic removal of poly(A) tails from mRNA substrates, regulating transcript stability and gene expression

03

Biological functions

mRNA deadenylation (3'-5' poly(A) exoribonuclease activity)Regulation of mRNA degradationRegulation of gene transcription (transcriptional activation and repression)Regulation of cell proliferationInvolvement in cell cycle progressionNuclear-cytoplasmic mRNA transport
04

Disease associations

Cancer (e.g., involvement in cell cycle and proliferation; associated signaling in tumorigenesis and antiproliferative pathways)Male infertility (defective spermatogenesis in null mice)Increased bone mass (from knockout data)Potential roles in other diseases via regulation of mRNA stability and gene expression
05

Safety considerations

Knockout in mice is generally viable but leads to male infertility and increased bone massTherapeutic inhibition or modulation risks broadly affecting gene expression and mRNA stability, with potential widespread cellular consequences

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