FTSJD1 Blocking Peptide
- Known as:
- FTSJD1 Blocking Peptide
- Catalog number:
- 33r-5216
- Product Quantity:
- USD
- Category:
- -
- Supplier:
- Fitzgerald industries international
- Gene target:
- FTSJD1 Blocking Peptide
Related genes to: FTSJD1 Blocking Peptide
- Gene:
- CMTR2 NIH gene
- Name:
- cap methyltransferase 2
- Previous symbol:
- FTSJD1
- Synonyms:
- FLJ11171, AFT, MTr2
- Chromosome:
- 16q22.2
- Locus Type:
- gene with protein product
- Date approved:
- 2008-07-25
- Date modifiied:
- 2014-11-19
Related products to: FTSJD1 Blocking Peptide
Related articles to: FTSJD1 Blocking Peptide
- Cap-adjacent 2'-O-ribose methylation (cOMe) of the first two transcribed nucleotides of RNA polymerase II transcripts is a conserved feature in many eukaryotes. In mammals, these modifications are key to a transcript surveillance system that regulates the interferon response, but the broader functions of cOMe remain poorly understood. To understand the role of cOMe in Caenorhabditis elegans, we functionally characterized the methyltransferases (CMTR-1 and CMTR-2) responsible for installing these modifications. These enzymes have distinct expression patterns, protein interaction partners, and loss-of-function phenotypes. Loss of CMTR-1 causes dramatic reductions in cOMe, impaired growth, and sterility. In contrast, animals lacking CMTR-2 are superficially wild-type, though CMTR-2 loss enhances the severity of the cmtr-1 mutant phenotype. Depletion of CMTR-1 causes downregulation of transcripts associated with germline sex determination and upregulation of those involved in the intracellular pathogen response (IPR). We show that the absence of the decapping exonuclease, EOL-1, an IPR component, completely suppresses the sterility and growth defects caused by CMTR-1 loss, and reverses the associated steady-state transcript changes. Our work shows the physiological relevance of cOMe in protecting transcripts from decapping exonucleases, raising the possibility that cOMe plays a role in RNA-mediated immune surveillance beyond the vertebrates. - Source: PubMed
Clemens EileenBrivio SarahAl-Khafaji MohammedEijlers PeterKurukulasuriya MaheshikaHaussmann Irmgard UMacLeod DavidWenzel MariusMüller BerndtSoller MatthiasPettitt Jonathan - In modern swine breeding, there has been a shift from maximizing productivity to improving quality to enhance overall efficiency. A key goal is achieving a balance between litter size and piglet birth weight. This study focused on Danish Large White pigs and aimed to evaluate a novel placental efficiency (PEA) index based on placental area (PA) as a biologically relevant and measurable trait for breeding programs. - Source: PubMed
Publication date: 2026/04/02
Yu ShiXinCui ShengDiChen DongZhao ZhenJianTecku Patrick Kofi MakafuiChen JiaMiaoHuang RunJieZhou YaoXiTang GuoQing - Human RNA capping is critical for mRNA splicing, protection of RNA from 5' exonucleases in the cytoplasm, and targeting to the ribosome. Human RNMT, CMTR1, and CMTR2 are RNA methyltransferases involved in the RNA capping process. They play a significant role in the proliferation and differentiation of embryonic stem cells and have been implicated in cancer. Substrate specificities of human RNA capping methyltransferases have been somewhat explored in a few studies. Here, we report on a comprehensive, systematic, and quantitative assessment of their substrate specificities along with SARS-CoV-2 counterparts, nsp14 and nsp16. We discovered novel cooperative activities of human enzymes. We designed and synthesized various RNA substrates with defined patterns of methylation to systematically assess the dependency or cooperativity of their activities using radiometric assays followed by mass spectrometry to verify RNA methylation status. We have tested all five enzymes in parallel against these substrates and determined kinetic parameters. Our data not only indicate that the catalytic activities of human RNMT, CMTR1, and CMTR2 are distinct and nonoverlapping, but also provide a novel quantitative assessment of their activities, indicating how and to what extent these proteins affect each other's function. Unlike nsp14 and nsp16, their functions are not necessarily sequential, but show significant cooperativity. Altogether, our data provide a comprehensive understanding of substrate specificities of human RNA capping methyltransferases, enabling the development of potential future anticancer therapeutics and assessment of antiviral therapeutics' selectivity. - Source: PubMed
Taherian FatemehMabanglo Mark FHajian TaranehTucker SarahKalinic EmilijaPerveen SumeraAman AhmedVedadi Masoud - RNA splicing dysregulation has emerged as a hallmark of cancer and a promising therapeutic target; however, its full landscape in human solid cancer remains poorly characterized. To address this, we perform alternative splicing analyses using RNA-sequencing data from 751 lung adenocarcinoma samples from our cohort integrated with 519 samples from The Cancer Genome Atlas. Visualization of splicing patterns using t-distributed stochastic neighbor embedding reveals substantial inter-tumor heterogeneity driven by distinct molecular subtypes and histological differentiation. We identify a unique molecular subtype associated with inactivating mutations in CMTR2, which encodes Cap-specific mRNA (nucleoside-2'-O-)-methyltransferase 2. CMTR2 mutations are observed in 3.8% of cases and are predominantly truncating mutations, which form an isolated cluster within the splicing landscape. Intrinsic and CRISPR-Cas9-engineered CMTR2 mutations disrupt alternative splicing and sensitize cancer cells to sulfonamide-based RNA splicing modulators and immune checkpoint blockade therapy. Retrospective patient data confirm the increased sensitivity of CMTR2-deficient tumors to immune checkpoint blockade therapy. These findings uncover a previously unrecognized RNA splicing deficiency in human cancers and define a molecular subtype of lung adenocarcinoma driven by RNA splicing dysregulation, suggesting targets for therapeutic intervention in lung cancer. - Source: PubMed
Publication date: 2025/11/06
Nukaga ShigenariShiraishi KouyaHamabe KentaMochizuki AkifumiHamaguchi YuOgawa EmiLe Nguyen ThaiShimada YokoOno HanakoNishinakamura HitomiKobayashi YoshihisaHamamoto JunkoUi AyakoAraki MitsuguSagae YukariOhgino KeikoSugihara KaiEndo SatoshiMiyakoshi JunShiraishi YuichiYasuda HiroyukiOkuno YasushiYoshida TatsuyaGoto YasushiOhe YuichiroWatanabe Shun-IchiYatabe YasushiNishikawa HiroyoshiHamamoto RyujiKohno TakashiNakaoku Takashi - Cap-adjacent 2`--ribose methylation (cOMe) of the first two transcribed nucleotides of RNA polymerase II transcripts is a conserved feature in many eukaryotes. In mammals, these modifications are key to a transcript surveillance system that regulates the interferon response, but the broader functions of cOMe remain poorly understood. To understand the role of cOMe in , we functionally characterised the methyltransferases (CMTR-1 and CMTR-2) responsible for installing these modifications. These enzymes have distinct expression patterns, protein interaction partners, and loss of function phenotypes. Loss of CMTR-1 causes dramatic reductions in cOMe, impaired growth and sterility. In contrast, animals lacking CMTR-2 are superficially wild-type, though CMTR-2 loss enhances the severity of the mutant phenotype. Depletion of CMTR-1 causes downregulation of transcripts associated with germline sex determination and upregulation of those involved in the intracellular pathogen response (IPR). We show that absence of the decapping exonuclease, EOL-1, an IPR component, completely suppresses the sterility and growth defects caused of loss of CMTR-1, suggesting that EOL-1 degrades cellular transcripts lacking cOMe. Our work shows the physiological relevance of cOMe in protecting transcripts from decapping exonucleases, raising the possibility that cOMe plays a role in RNA-mediated immune surveillance beyond the vertebrates. - Source: PubMed
Publication date: 2025/05/12
Clemens EileenBrivo SarahAl-Khafaji MohammedEijlers PeterKurukulasuriya MaheshikaHaussmann Irmgard UMacLeod DavidWenzel MariusMüller BerndtSoller MatthiasPettitt Jonathan