MNAT1 antibody
- Known as:
- MNAT1 (anti-)
- Catalog number:
- orb101218
- Product Quantity:
- EUR
- Category:
- -
- Supplier:
- Biorbyt biorb
- Gene target:
- MNAT1 antibody
Related genes to: MNAT1 antibody
- 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
Related articles to: MNAT1 antibody
- Excessive mechanical stress is a main cause of intervertebral disc degeneration (IDD). However, the specific mechanism remains unclear. We established in vivo and in vitro models to investigate the role of cytoskeletal proteins in excessive mechanical stress-induced NP cell pyroptosis and IDD. The expression level of Vimentin was decreased in degenerated NP cells induced by excessive mechanical stress. Knockdown of Vimentin promoted NP cell pyroptosis and IDD in rats, whereas Vimentin overexpression significantly alleviated excessive mechanical stress-induced NP cell pyroptosis and degeneration. Further mechanistic studies revealed that Vimentin ameliorated mitochondrial dysfunction triggered by excessive mechanical stress through PINK1-Parkin-dependent mitophagy, thereby attenuating NP cell pyroptosis and degeneration. Co-immunoprecipitation-mass spectrometry analysis suggested an interaction between Itgb1 and Vimentin, which was validated by Co-immunoprecipitation assays. Itgb1 enhanced Vimentin protein stability via the ubiquitin-proteasome pathway and inhibited mechanical stress-mediated Vimentin degradation. Subsequent experiments confirmed that Itgb1 reduced Vimentin ubiquitination and degradation by blocking the binding of MNAT1 to Vimentin. Itgb1 ameliorated excessive mechanical stress-induced NP cell pyroptosis and degeneration via Vimentin. Restoring Vimentin function through gene overexpression effectively inhibited NP cell pyroptosis and delayed the progression of IDD in rats. In summary, this study reveals a mechanotransduction pathway from mechanical stress sensing to cellular functional regulation in IDD, providing novel insights into the pathological mechanisms underlying IDD. Moreover, this study demonstrates that Vimentin exerts a significant protective effect against excessive mechanical stress-induced NP cell pyroptosis and IDD, offering a potential therapeutic target for the clinical management of IDD. - Source: PubMed
Publication date: 2026/07/14
Liu XueningYang FengguangDuan YanniXiao HefangCao ZhenyuWang ZhaohengZhang HaijunKang Xuewen - BACKGROUNDS: Neoadjuvant chemoradiation (nCRT) is a standard treatment for rectal carcinoma that reduces tumor size and local recurrence while improving the rate of sphincter preservation. However, many patients remain insensitive to nCRT, with some exhibiting tumor progression. To date, there is still a lack of clinically available prognostic models to differentiate the sensitivity of patients with rectal carcinoma to nCRT. This study aimed to develop a genetic predictive model that predicts the effectiveness of nCRT in patients with rectal carcinoma, offering guidance for future treatments and studies on the underlying mechanisms. METHODS: Based on the NCBI GEO database datasets, key hub genes affecting the efficacy of neoadjuvant chemoradiotherapy in rectal carcinoma were identified using WCGNA. Subsequently, a consistency analysis of 101 model combinations constructed using ten different machine learning algorithms was performed in two independent cohorts, and a prognostic model (chemoradiation resistance score, CRTR score) was developed and validated. Moreover, the clinical applicability of CRTR in immunotherapy and drug selection was investigated using multi-omics analysis and public databases. Finally, the effect of KIF14 on the radiosensitivity of rectal carcinoma cells was studied using in vitro experiments. RESULTS: The CRTR model was composed of 13 genes impacting nCRT sensitivity, whereas six genes (KIF4, DBF4, UBL4A, SLC10A3, PRRG4, and PAPSS2) acted as protective factors and seven (BMS1, DSC2, PROM2, MNAT1, PPID, SMPDL3B, and TNFRSF14) served as risk factors. The CRTR model showed a significant negative correlation with the prognosis of patients with rectal carcinoma undergoing nCRT. Furthermore, patients with higher CRTR values displayed an increased potential to benefit from immunotherapy. Drug sensitivity analysis indicated that aurora kinase inhibitors, telomerase inhibitors, JAK1 inhibitors, and others may enhance the efficacy of nCRT. Finally, we identified KIF14 as the gene that contributed the most to the model and performed preliminary validation. Radiation significantly upregulated the expression of KIF14, and overexpression of KIF14 increased the radiosensitivity of rectal carcinoma cells. CONCLUSION: The CRTR score, based on 13 genes, was able to predict the prognosis of patients with rectal carcinoma undergoing neoadjuvant chemoradiotherapy and demonstrated immense potential in providing personalized risk assessments and recommendations for targeted immunotherapy. The core gene, KIF14, in the CRTR model may serve as a potential predictive biomarker of radiosensitivity in rectal carcinioma. - Source: PubMed
Publication date: 2026/03/21
Gao ZhanhuaQiu MinghanYang ZhenFang XinyueYin GuoxingZhang QiaonanLiu JinpuLiu RuxueWang YayunLiu YuyaZhang MengZhang HaiyangZheng XiangqianWang HuiHao JieGao Ming - 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