MNAT1 antibody - N-terminal region (P100992_P050)
- Known as:
- MNAT1 (anti-) - N-terminal region (P100992_P050)
- Catalog number:
- p100992_p050
- Product Quantity:
- USD
- Category:
- -
- Supplier:
- Aviva Systems Biology
- Gene target:
- MNAT1 antibody - N-terminal region (P100992_P050)
Related genes to: MNAT1 antibody - N-terminal region (P100992_P050)
- Gene:
- MNAT1 NIH gene
- Name:
- MNAT1 component of CDK activating kinase
- Previous symbol:
- -
- Synonyms:
- MAT1, RNF66
- Chromosome:
- 14q23.1
- Locus Type:
- gene with protein product
- Date approved:
- 1997-10-09
- Date modifiied:
- 2019-01-25
Related products to: MNAT1 antibody - N-terminal region (P100992_P050)
Related articles to: MNAT1 antibody - N-terminal region (P100992_P050)
- Decades of artificial selection have left distinct genomic signatures in Pekin duck. Here, we used whole-genome resequencing data from six Pekin duck populations, including two conservation populations and four breeding populations, to explore the genomic footprints left by decades of artificial selection in Pekin ducks. Through allele frequency analyses, we identified specific selective regions among the breeding populations. Compared with the conservation populations, the strongest selection signals in Maple Leaf ducks were found in genomic regions encompassing FAM184B and LAP3, with two missense mutations in FAM184B showing marked allele frequency differences between Maple Leaf and conservation populations, while in Cherry Valley ducks, the top signals were located within or near XRCC3, MNAT1, and SLC34A2. In comparisons between the Nankou Pekin duck breeding populations and the conservation population, NUDT6 and INPP4A were identified as the candidate genes under selection in PK4 and PK3, respectively. Analysis of the shared selective regions revealed 214 candidate genes, which were mainly enriched in pathways related to lipid metabolism and organ development. These results suggest that different breeding programs have imposed distinct selection pressures on the Pekin duck genome. Overall, this study provides valuable insights for the conservation and genetic improvement of Pekin ducks. - Source: PubMed
Publication date: 2026/01/18
Zhang XinyeZhao XiurongYang FangxiWang GangRen XufangChen AnqiJiang XiaoyuLi XianyaoQu Lujiang - Oral squamous cell carcinoma, with high global incidence and mortality, requires improved early intervention strategies. Ubiquitination - a critical post-translational modification - has been strongly implicated in tumorigenesis, with particularly significant roles in T-cell regulation. We developed a T Cell-Related ubiquitination risk model that enhances prognostic prediction and immunotherapy response assessment, offering a framework for personalized OSCC manageme. - Source: PubMed
Publication date: 2025/10/29
Gao HanLiu LehuaQian WeixiangWu YanfeiWang JiayaoYang WeipingShi Yinfang - Understanding the role of transcript isoforms is essential for elucidating disease mechanisms. TDP-43 regulates RNA splicing, and its dysfunction in neurons is a hallmark of some neurodegenerative diseases, including amyotrophic lateral sclerosis (ALS) and frontotemporal degeneration (FTD). While an association between TDP-43-dependent cryptic exons and disease pathogenesis has been suggested, an approach to investigate how cryptic exons disrupt transcript isoforms has yet to be established. In this study, we developed IsoRefiner, a novel method for identifying full-length transcript structures using long-read RNA-seq. Leveraging this method, we performed long-read RNA-seq, guided by prior short-read RNA-seq, to comprehensively determine the full-length structures of aberrant transcripts due to TDP-43 dysregulation in human iPSC-derived motor neurons. We identified a novel TDP-43-dependent cryptic exon in the MNAT1 gene, along with its full-length transcript structure. Furthermore, we confirmed the presence of the MNAT1 cryptic exon in patients with ALS and FTD. Our findings deepen understanding of TDP-43 proteinopathy and advance splicing research. - Source: PubMed
Publication date: 2025/07/16
Tanaka YoshihisaSunamura NaohiroKajitani ReiIkeguchi MarieKunimoto Ryo - Laryngeal squamous cell carcinoma (LSCC), the predominant histological subtype of laryngeal cancer with a poor diagnosis, requires further exploration of its molecular mechanisms and potential therapeutic targets. - Source: PubMed
Publication date: 2025/07/11
An RanYang FanTeng YujianGuo YanZhao RuiCao JingLiu YaohuiWang YueLiu PengyanLiu MingTian Linli - Cell cycle protein E2 (CCNE2) is a member of the Cyclin family, known for driving tumor cell proliferation and invasion. However, the mechanism of its action in head and neck squamous cell carcinoma (HNSCC) remains unclear. The aim of this study is to investigate the relationship between CCNE2 and cisplatin resistance and survival prognosis of head and neck squamous cell carcinoma. We performed transcriptomic sequencing of HNSCC and HNSCC/DDP. Kaplan-Meier analysis and COX regression analysis were used to evaluate the relationship between CCNE2 expression and survival prognosis of HNSCC patients. Multiple potential biological functions of CCNE2 in HNSCC were identified using Gene Ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG). Single-sample gene set enrichment analysis (ssGSEA) was used to explore tumor immune infiltration. The potential mechanism of CCNE2 was explored by molecular docking and immunoprecipitation. Cell migration, cell invasion and cell proliferation assays were used to investigate the mechanism of CCNE2 in HNSCC. CCNE2 is up-regulated in HNSCC tissues and cell lines and is associated with poor prognosis. The high expression of CCNE2 in HNSCC is associated with clinical significance. GO and KEGG analysis showed that ccne2 related genes may be involved in the regulation of DNA double-strand break repair and DNA metabolic process. CCNE2 expression was positively correlated with the infiltration levels of helper T cells, Tcm cells and Th2 cells, and negatively correlated with the infiltration levels of DC, neutrophils and pDC. CCNE2 regulates the invasion, migration and proliferation of HNSCC cells by targeting MNAT1. CCNE2 also altered cisplatin resistance in HNSCC/DDP. CCNE2 may be an independent prognostic biomarker of HNSCC through MNAT1, which provides new ideas for cisplatin resistance and therapeutic targets of HNSCC. - Source: PubMed
Publication date: 2025/04/23
An RanXu XiaolinWang YueDing JiayiLi BoyuYang FanLiu MingTian Linli