CNOT3 antibody - N-terminal region (ARP34318_T100)
- Known as:
- CNOT3 (anti-) - N-terminal region (ARP34318_T100)
- Catalog number:
- arp34318_t100
- Product Quantity:
- USD
- Category:
- -
- Supplier:
- Aviva Systems Biology
- Gene target:
- CNOT3 antibody - N-terminal region (ARP34318_T100)
Related genes to: CNOT3 antibody - N-terminal region (ARP34318_T100)
- Gene:
- CNOT3 NIH gene
- Name:
- CCR4-NOT transcription complex subunit 3
- Previous symbol:
- NOT3
- Synonyms:
- NOT3H, KIAA0691, LENG2
- Chromosome:
- 19q13.42
- Locus Type:
- gene with protein product
- Date approved:
- 1996-07-19
- Date modifiied:
- 2016-10-05
Related products to: CNOT3 antibody - N-terminal region (ARP34318_T100)
Related articles to: CNOT3 antibody - N-terminal region (ARP34318_T100)
- Synonymous codon usage significantly influences mRNA stability in yeast by guiding mRNA decay during translation. The CCR4-NOT complex is central to this process, interacting with ribosomes when the A and E sites are unoccupied, a state that arises when a nonoptimal codon with low tRNA availability is at the A site. This triggers recruitment of decay factors, reducing the stability of transcripts enriched in such codons. In humans, codon-mediated mRNA decay is less well-understood. Recent research has identified a related but distinct mechanism called P-site tRNA-mediated decay (PTMD). Unlike yeast, human CCR4-NOT recruitment depends on specific arginine codons (CGG, CGA, or AGG) at the P site and slow decoding at the A site, allowing E-site vacancy and CNOT3-dependent binding. Through analysis of public datasets, we explored the characteristics of human transcripts enriched in PTMD codons. Interestingly, these codons are mostly found in transcripts with longer half-lives. This suggests that, rather than targeting already unstable mRNAs as in yeast, PTMD in humans selectively reduces the stability of otherwise long-lived transcripts, indicating a regulatory role distinct from the decay associated with codon usage. - Source: PubMed
Publication date: 2026/06/12
Carneiro Rodolfo LopesPalhano Fernando Lucas - Innate lymphoid cells (ILCs) include T-bet-dependent NK and ILC1 cells, GATA-3-dependent ILC2 cells, and RORγt-dependent ILC3 cells. Their functional and developmental regulation at the posttranscriptional level remains elusive. The CCR4-NOT complex plays a central role in mRNA decay by mediating deadenylation. To explore the overall impact of mRNA decay on ILCs, we conditionally deleted Cnot3, an essential subunit of the CCR4-NOT complex. Loss of CNOT3 in ILC2 cells led to aberrant expression of T-bet and RORγt, accompanied by upregulation of type 1 and type 3 signature genes. Mechanistically, CNOT3 targeted the 3' untranslated regions of Tbx21 and Rorc mRNAs through interactions with Roquin and ZFP36L1, respectively. Elevated T-bet expression in CNOT3-deficient ILC2 cells suppressed GATA-3 levels, thereby impairing type 2 immune responses in models of airway allergy and helminth infection. Thus, our findings reveal that CNOT3 maintains ILC2 differentiation and function by restricting type 1 and type 3 transcriptional programs. - Source: PubMed
Publication date: 2026/05/12
Tatematsu MegumiTakasuga ShunsukeFuchimukai AkaneKimura YuumiIshii SatoshiTaniuchi IchiroIshiwata KenjiIkuta KoichiSexl VeronikaEberl GérardSawa ShinichiroKuba KeijiEbihara Takashi - Intellectual Developmental Disorder with Speech Delay, Autism, and Dysmorphic Faces (IDDSADF) is a rare neurodevelopmental disorder caused by heterozygous variants in CNOT3. Although several cohorts have been documented worldwide, no Japanese patients have been reported to date. Here, we present the first two Japanese cases of IDDSADF, an 8-year-old girl and a 19-year-old boy, both presenting with developmental delay, characteristic facial features, and short stature. Both individuals exhibited a thin, tented upper lip, a morphology that has been rarely reported in other cohorts and may represent an ethnicity-associated trait. Growth impairment was observed either from early childhood or emerging after puberty and may represent an underrecognized aspect of the phenotype. Trio-exome sequencing identified pathogenic CNOT3 variants in both patients, including a recurrent frameshift (c.732dup, p.Ser245fs) and a novel splice-site substitution (c.837+1G>A). Our findings expand the phenotypic and mutational spectrum of IDDSADF, highlighting the importance of longitudinal auxological assessment and recognition of potential ethnicity-associated facial traits in its clinical diagnosis and management. - Source: PubMed
Publication date: 2026/05/12
Ariyasu DaisukeKosaki RikaCho HideoNakashima MoekoTsuchihashi TakatoshiKosaki KenjiroYamazawa Kazuki - - Source: PubMed
Publication date: 2026/04/02
Engel CamilleRendek MichaelaAssoumani JessicaArgilli EmanuelaAriani FrancescaAvice-Denizet Anne-LaudeBijlsma Emilia KBlanc PierreBruno Lucia PiaCallewaert BertCapra ValeriaCarullo MicheleChesneau BertrandCoppens SandraCurry CynthiaDale BreanneDahlen EricDelahaye-Duriez AndréeDenommé-Pichon Anne-SophieDemeer BénédicteDvořáková LenkaFischer JanGeneviève DavidGiacomini TheaHandrup Mette MHeron DelphineHüning IrinaIacomino MichelleIsidor BertrandKeren BorisKmoch StanislavKoolen David AKübler AndreaLaštůvková JanaLe CarolynLevy JonathanRizzo Caterina LoMaitz SilviaMarlin SandrineMignot CyrilMirzaa GhaydaNagel IngaNeuens SebastianNosková LenkaPao EmilyPecková AnnaPlaisancie JuliePorrmann JosephPrivitera FlaviaReis AndréRenieri AlessandraRio MarlèneRippert AlyssaRyba LukášScala MarcelloSchieving Jolanda HSherr Elliott HShuen AndrewSidlow RichardSmol ThomasSoblet JulieStriano PasqualeSuri MohnishSyryn HannesTran Mau-Them FrédéricTravessa Andre MVan Gils JulienVasileiou GeorgiaVerseput Jolijn J AVilain CathelineVincent-Delorme CatherineVyhnálková EmílieWakeling Emma LZacher PiaZara FedericoKuentz PaulPiard Juliette - Lung cancer remains a major global health burden. RNA-binding proteins (RBPs) play crucial roles in post-transcriptional gene regulation, and their dysregulation is frequently implicated in tumorigenesis. The present study aimed to elucidate the molecular network governed by the highly expressed RBP TIMELESS in lung adenocarcinoma (LUAD) and determine its mechanistic role in LUAD progression. The Cancer Genome Atlas-LUAD, Gene Expression Omnibus, and single-cell RNA sequencing datasets were analyzed to identify aberrantly expressed RBP genes. The RBP gene exhibited the most significant effect on LUAD cell death and was selected for further study. Photoactivatable ribonucleoside-enhanced crosslinking and immunoprecipitation sequencing and RNA sequencing were employed to identify ferroptosis-related targets directly bound by TIMELESS. Molecular mechanisms underlying the TIMELESS-mediated regulation of ferroptosis in LUAD were investigated via immunoprecipitation-mass spectrometry, glutathione -transferase pull-down, immunofluorescence-fluorescence in situ hybridization, RNA immunoprecipitation, poly(A)-tail, and RNA stability assays. In an orthotopic lung cancer mouse model treated with erastin (a ferroptosis inducer) and programmed cell death protein 1 (PD-1) blockade, the role of TIMELESS in therapeutic response was assessed via flow cytometry and multiplex immunofluorescence (mIF). Infiltrating immune cells in LUAD were analyzed by tissue microarrays (TMAs) via mIF. TIMELESS significantly affected LUAD cell proliferation and death, and knockdown significantly enriched RNA-binding and ferroptosis pathways. Transferrin (TF) was identified as a direct TIMELESS target governing ferroptosis. TIMELESS was revealed to bind Ccr4-Not transcription complex subunit 3 (CNOT3) to promote TF mRNA degradation. TIMELESS depletion combined with erastin and PD-1 blockade enhances efficacy, prolongs survival, increases T cell and M1 macrophage infiltration, and reduces M2 macrophage infiltration. Further, high TIMELESS expression was inversely correlated with ferroptosis marker 4-hydroxynonenal but positively correlated with programmed cell death ligand 1 (PD-L1), reduced T cell and M1 macrophage infiltration, and increased M2 macrophage infiltration. TIMELESS recruits CNOT3 to accelerate TF mRNA degradation, thereby suppressing ferroptosis and promoting LUAD growth. These findings suggest that the TIMELESS/TF regulatory axis may be a promising therapeutic target for LUAD. - Source: PubMed
Publication date: 2026/02/03
Hu ChenchenHu FeimingShao ChangjianHe YuanliSu LipingShi DaimeiYu LingyingSun YuanjieWang JingZhang XiyangDuan HongtaoZhang JunqiSun YuboJiang DongboYan XiaolongYang ShuyaYang Kun