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更新于：2025-01-23

CNOT7

更新于：2025-01-23

基本信息

别名

BTG1-binding factor 1、CAF-1、CAF1

+ [4]

简介

Has 3'-5' poly(A) exoribonuclease activity for synthetic poly(A) RNA substrate (PubMed:20634287, PubMed:31439799, PubMed:19276069). Its function seems to be partially redundant with that of CNOT8 (PubMed:19605561). Catalytic component of the CCR4-NOT complex which is one of the major cellular mRNA deadenylases and is linked to various cellular processes including bulk mRNA degradation, miRNA-mediated repression, translational repression during translational initiation and general transcription regulation (PubMed:20634287, PubMed:31439799, PubMed:19276069). During miRNA-mediated repression the complex seems also to act as translational repressor during translational initiation (PubMed:20065043). Additional complex functions may be a consequence of its influence on mRNA expression (PubMed:23236473, PubMed:19276069). Associates with members of the BTG family such as TOB1 and BTG2 and is required for their anti-proliferative activity (PubMed:23236473, PubMed:19276069).

关联

靶点

CNOT7

作用机制

CNOT7 inhibitors

在研机构

The University of Nottingham

原研机构

The University of Nottingham

在研适应症-

非在研适应症-

最高研发阶段药物发现

首次获批国家/地区-

首次获批日期1800-01-20

100 项与 CNOT7 相关的临床结果

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100 项与 CNOT7 相关的转化医学

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0 项与 CNOT7 相关的专利（医药）

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项与 CNOT7 相关的文献（医药）

2024-08-01·Biochemical and Biophysical Research Communications

CNOT7 regulates lipid deposition in nonalcoholic fatty liver disease

Article

作者: Chen, Hong ; Sun, Jia ; Li, Jitong ; Wen, Weiheng ; Liu, Tiancai ; Li, Jiahui

BACKGROUNDIn recent years, the incidence rate of nonalcoholic fatty liver disease (NAFLD) has ascended with the increasing number of metabolic diseases such as obesity and diabetes, which will bring great medical burden to society. At present, multiple scientific experiments have found that the CCR4-NOT complex can participate in regulating obesity and energy metabolism. This study is designed to explore the role and mechanism of CCR4-NOT transcription complex subunit 7 (CNOT7), a subunit of the CCR4-NOT complex in liver lipid deposition.METHODSTo establish the NAFLD cell model, palmitic acid (PA) was utilized to stimulate HepG2 cells and LO2 cells, promoting intracellular lipid deposition. CNOT7 was knockdown by siRNA and lentivirus to evaluate the effect of CNOT7 in NAFLD.RESULTSOur results demonstrated that the expression of CNOT7 was increased in the NAFLD cell model. After knocking down CNOT7, the lipid deposition declined in HepG2 or LO2 cells treated by PA reduced. We found the lipid synthesis genes and the lipid uptake and transport factors in the CNOT7 knockdown group were significantly downregulated compared to the non-knockdown group. Furthermore, knockdown of CNOT7 might promote fatty acid oxidation.CONCLUSIONKnocking down CNOT7 can improve lipid deposition and CNOT7 may be a potential therapeutic target for NAFLD.

2024-01-01·Methods in Molecular Biology

Engineered Protease-Responsive RNA-Binding Proteins (RBPs) to Expand the Toolbox of Synthetic Circuits in Mammalian Cells

Article

作者: Calandra, Fabiana ; Siciliano, Velia

Genetically encoded sensor-actuator circuits aim at reprogramming cellular functions and are inspired by intracellular networks: from the input signal (sensor) to the desired output response (actuator). In the last years, circuits with posttranscriptional regulation of gene expression have aroused great interest for their potential in the biomedical space. Posttranscriptional modulation can be achieved with ribozymes, riboswitches (simple regulatory elements based on RNA secondary structures), noncoding RNAs, and RNA-binding proteins (RBPs). RBPs are proteins that recognize specific motifs on the mRNA target inducing mRNA decay or translation inhibition. The use of RBPs deriving from different species in mammalian cells has allowed to create sophisticated and multilayered regulatory networks, addressing the previous limitation of regulatory orthogonal parts that can be assembled in synthetic devices. In this chapter, we describe the engineering and tests of protease-responsive RNA-binding proteins (L7Ae and MS2-cNOT7) to expand the toolbox of synthetic circuits in mammalian cells.

2024-01-01·Methods in molecular biology (Clifton, N.J.)

A FRET-Based Assay and Computational Tools to Quantify Enzymatic Rates and Explore the Mechanisms of RNA Deadenylases in Heterogeneous Environments.

Article

作者: Harkness, Robert W ; Forman-Kay, Julie D ; Irwin, Rose

We developed a medium-throughput assay that can measure the time-dependent distribution of RNA products generated as a deadenylase degrades a polyadenosine (poly(A)) RNA tract, thereby providing insight into the mechanism of deadenylation. Importantly, this assay can be performed in both homogeneous and heterogeneous environments without relying on gel electrophoresis of RNA products or coupled enzymatic reactions that indirectly report on the RNA distribution through the detection of freed adenosine monophosphate. In parallel, we have established an open-source, Python-based command-line software package, deadenylationkinetics, that can be used to numerically simulate and/or fit the datasets afforded by our assay with different deadenylation mechanisms to determine the most likely case and estimate the associated rate constants. In this chapter, we detail the implementation of our method and the quantification of poly(A) RNA binding and degradation kinetics in application to a truncated version of CNOT7 from the CCR4-NOT deadenylation complex, which serves as a model deadenylase with enhanced activity.

项与 CNOT7 相关的新闻（医药）

2024-07-08

·生物探索

Nat Commun | 吴克良/陆发隆/王加强/刘玉胜等揭示体外成熟的人和小鼠卵母细胞的关键缺陷

引言不孕不育是世界范围内日益突出的重大问题。卵母细胞体外成熟是辅助生殖的重要技术之一。然而，体外成熟卵母细胞来源的胚胎在发育质量和妊娠结局等方面均比体内成熟卵母细胞来源的胚胎差，其分子机制所知甚少。 2024年7月2日，山东大学陈子江院士团队吴克良、中国科学院遗传与发育生物学研究所陆发隆、东北农业大学王加强及东北林业大学刘玉胜通过紧密合作在Nature Communications发表题为Maternal mRNA deadenylation is defective in in vitro matured mouse and human oocytes的研究论文，发现人和小鼠体外成熟卵母细胞中母源mRNA去腺苷酸化（也称poly(A)尾去尾）受损导致数千个基因poly(A)+转录本丰度增加；机制上是去腺苷酸化复合物关键因子Btg4和Cnot7的mRNA在体外成熟过程中不能正常通过多聚腺苷酸化翻译激活从而蛋白水平下降，进而影响卵母细胞中母源mRNA的去腺苷酸化过程。这一重要工作揭示了体外成熟卵母细胞的关键分子缺陷，对将来辅助生殖技术中提升体外成熟卵母细胞的质量具有指导意义。卵母细胞在生长过程中积累大量母源mRNA，并在发育至完全生长阶段后关闭转录，在随后的卵母细胞成熟过程中母源mRNA需要经过严格转录后调控为受精和早期胚胎发育做好准备。本研究使用团队先前开发的PAIso-seq技术对人和小鼠体外和体内成熟的卵母细胞进行了包含完整poly(A)尾巴的全长转录组测序，发现与先前报道一致的数千个基因在体外成熟卵母细胞中poly(A)+转录本水平异常上调。因为在卵子成熟过程中无新的转录本合成，并且已知在此过程中母源mRNA发生大量的mRNA去腺苷酸化。因此研究人员提出新的假设：在体外成熟卵母细胞中观察到的poly(A)+转录本水平异常上调是由去腺苷酸化受损导致的。对全转录组poly(A)尾进行深入分析很好地支持了上述假设。进一步对分子机制进行探索表明编码去腺苷酸化复合物重要组分的Btg4和Cnot7的mRNA在卵子成熟过程中通过poly(A)尾加尾驱动的翻译激活受损；导致去腺苷酸化复合物重要组分的蛋白水平降低；从而导致体外成熟卵母细胞中发生全局性的母源mRNA去腺苷酸化重大缺陷。研究示意图（Credit: Nature Communications）参考文献 https://www-nature-com.libproxy1.nus.edu.sg/articles/s41467-024-49695-y 责编|探索君排版|探索君文章来源|“BioArt” End 往期精选围观一文读透细胞死亡(Cell Death) | 24年Cell重磅综述（长文收藏版）热文 Cell | 是什么决定了细胞的大小？热文 Nature | 2024年值得关注的七项技术热文 Nature | 自身免疫性疾病能被治愈吗？科学家们终于看到了希望热文 CRISPR技术进化史 | 24年Cell综述

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