Monoclonal Mouse CNOT4 Antibody
- Known as:
- Monoclonal Mouse CNOT4 Antibody
- Catalog number:
- abx000077
- Product Quantity:
- EUR
- Category:
- -
- Supplier:
- Abbexa
- Gene target:
- Monoclonal Mouse CNOT4 Antibody
Related genes to: Monoclonal Mouse CNOT4 Antibody
- Gene:
- CNOT4 NIH gene
- Name:
- CCR4-NOT transcription complex subunit 4
- Previous symbol:
- NOT4
- Synonyms:
- CLONE243, NOT4H
- Chromosome:
- 7q33
- Locus Type:
- gene with protein product
- Date approved:
- 1996-07-19
- Date modifiied:
- 2017-12-01
Related products to: Monoclonal Mouse CNOT4 Antibody
Related articles to: Monoclonal Mouse CNOT4 Antibody
- Tripartite motif-containing protein 21 (TRIM21), an E3 ubiquitin ligase of the TRIM superfamily, modulates critical cellular processes including ubiquitination, autophagy, and oxidative stress response. Accumulating evidence highlights its context-dependent regulatory roles in hepatocellular carcinoma (HCC)-the most prevalent primary liver malignancy with high mortality and limited therapeutic efficacy. This review systematically summarizes the core mechanisms by which TRIM21 orchestrates HCC progression: ① Autophagy regulation: TRIM21 modulates HCC autophagy via multiple axes, including CCR4-NOT complex (TNKS1BP1/CNOT4)-mediated substrate ubiquitination, ATG14-dependent autophagosome initiation, and RETREG1-driven reticulophagy, with context-dependent effects on tumor proliferation. ② Drug resistance: TRIM21 enhances oxaliplatin sensitivity by ubiquitinating and degrading G6PD (the rate-limiting enzyme of the pentose phosphate pathway), while its role in sorafenib resistance involves dual pathways-the MST1/YAP axis and the ApoE/cholesterol/PI3K-AKT cascade. ③ Metastasis suppression: TRIM21 restricts HCC invasion and metastasis by ubiquitinating key oncoproteins, preserving epithelial integrity and inhibiting mesenchymal transition. ④ Reactive oxygen species (ROS) balance: TRIM21 regulates oxidative stress in HCC via the SQSTM1/p62-Keap1-NRF2 axis, coordinating with HIF1α to modulate antioxidant responses and tumor cell survival. Additionally, we discuss the regulatory significance of TRIM21 in HCC associated with hepatitis B virus (HBV) infection (via HBx/DNA polymerase ubiquitination) and nonalcoholic steatohepatitis (NASH) (via suppressing lipogenic enzymes to reduce steatosis-driven carcinogenesis). This review provides a theoretical basis for TRIM21 as a potential diagnostic marker and therapeutic target for HCC. - Source: PubMed
Publication date: 2026/01/13
Sun JiatongGao ZixuanLi YuanhaoGao JiajunWang PeiyinQin YiboChen YanruZhang Ruihong - Non-small cell lung cancer (NSCLC) is a leading cause of cancer mortality. This study examines whether the deubiquitinase USP4 promotes NSCLC progression by stabilizing PAF1 and opposing the E3 ligase CNOT4. - Source: PubMed
Publication date: 2026/03/19
Chen ShaomuWang YuxuanHan SongZhang Biao - CCR4-NOT regulates multiple steps in gene regulation and has been well studied in budding yeast. Although primarily cytoplasmic, where it plays an essential role in mRNA degradation, the human complex has poorly characterized nuclear functions. Here, we used auxin-induced degradation to rapidly deplete the scaffold subunit CNOT1 and the E3 ligase CNOT4, and characterized the transcriptional functions of the human CCR4-NOT complex. Using transient transcriptome profiling (TT-Seq) to measure ongoing transcription, we found widespread activation of RNA synthesis in depleted cells across genic and intergenic regions. Interestingly, fewer genes were repressed, including KRAB-Zinc-Finger-protein (KZNF) genes, especially those on chromosome 19. KZNFs repress genes and retrotransposable elements (rTEs), and consistent with decreased KZNF expression, rTEs, mainly Long Interspersed Nuclear Elements (LINEs), were activated. Full-length active LINEs and rTEs lying outside of genes were activated, suggesting that the increased transcription is not the direct result of transcription of the genes the rTEs are embedded in. We found that most activated transcription events were in proximity to KZNF binding sites, suggesting that KZNF regulation contributes to the suppression of genic and rTE transcription. Finally, we demonstrate that CCR4-NOT regulates the stability of rTE RNAs, indicating that the complex tightly controls transposon expression by repressing transcription and targeting their RNAs for decay. - Source: PubMed
Publication date: 2026/01/17
Kulkarni ShardulMorrissey AlexisSebastian AswathyAkinniyi Oluwasegun TKeller Cheryl AAlbert IstvanMahony ShaunReese Joseph C - This study evaluated the long-term metabolic effects of prenatal nutrition in Nellore bulls. Pregnant cows (n = 126) received mineral supplementation only (NP), protein-energy supplementation during the last trimester (PP), or supplementation throughout pregnancy (FP). At slaughter, longissimus (muscle and meat) and subcutaneous fat samples from the offspring were collected for transcriptomics and metabolomics analyses. Data were reduced using Weighted Gene Co-expression Network Analysis, followed by functional enrichment, and then integrated via Spearman's correlations and holistic pathway analysis. Distinct molecular patterns emerged across prenatal nutrition treatments, although all groups influenced energy metabolism and cellular processes. The NP group was strongly associated with protein and lipid metabolism, highlighted by PPAR and sphingolipid signaling pathways, and key hub components including CNOT4 and tryptophan. In contrast, PP and FP groups were more closely linked to immune function, stress resilience, with enrichment of NF-kB signaling, cortisol synthesis, and hub components including TIE1, YWHAZ, carnitine, and glutaconylcarnitine. Shared transcriptome-metabolome modules between groups displayed inverse correlations, suggesting potential antagonistic effects driven by maternal diet. Overall, these results indicate that prenatal nutrition shapes key metabolic processes in muscle, meat, and fat, offering insights to enhance meat quality and production through maternal feeding strategies. - Source: PubMed
Publication date: 2025/12/13
Polizel Guilherme Henrique GebimCánovas ÁngelaDiniz Wellison J SRamírez-Zamudio German Dda Luz E Silva SauloDahlen Carl RFernandes Arícia ChristofaroPrati Barbara Carolina TeixeiraFurlan Édisondo Vale Pombo Gabrielade Almeida Santana Miguel Henrique - Codon usage biases play a significant role in determining gene expression levels. Codon usage was thought to primarily influence translation-dependent processes. Using an unbiased genome-wide screening to search for factors involved in codon usage effects on gene expression, we identified the CCR4-NOT complex subunit CNOT4 and many nuclear factors, including nuclear RNA exosome, PAXT complex components, and transcription factors. The CCR4-NOT complex has been shown to affect codon usage-dependent co-translational mRNA decay in yeast. Surprisingly, human CNOT4 was found to influence codon usage-dependent gene expression largely by its impact on nuclear RNA levels due to transcriptional effect. On the other hand, nuclear exosome and PAXT complex, regulate nuclear mRNA stability through the RNA quality control pathway, leading to preferential cytoplasmic accumulation of mRNAs with optimal codon usage. Overall, our results show that different nuclear mechanisms play a key role in determining nucleotide composition-dependent gene expression levels in human cells. - Source: PubMed
Publication date: 2025/12/03
Garg RenuXie PanchengDuan JiabinLiu HuanLiu Yi