TMCO3 Blocking Peptide, Blocking Peptides
- Known as:
- TMCO3 Blocking Peptide, Blocking Peptides
- Catalog number:
- 33R-4672
- Product Quantity:
- 100 ug
- Category:
- -
- Supplier:
- Fitzgerald
- Gene target:
- TMCO3 Blocking Peptide Peptides
Related genes to: TMCO3 Blocking Peptide, Blocking Peptides
- Gene:
- TMCO3 NIH gene
- Name:
- transmembrane and coiled-coil domains 3
- Previous symbol:
- C13orf11
- Synonyms:
- FLJ20623
- Chromosome:
- 13q34
- Locus Type:
- gene with protein product
- Date approved:
- 2003-01-29
- Date modifiied:
- 2015-11-12
Related products to: TMCO3 Blocking Peptide, Blocking Peptides
Related articles to: TMCO3 Blocking Peptide, Blocking Peptides
- Opioid dependence (OD) is epidemic in the United States and it is associated with a variety of adverse health effects. Its estimated heritability is ~50% in twin studies, and recent genome-wide association studies have identified more than a dozen common risk variants. However, there are no published studies of rare OD risk variants. In this study, we analyzed whole-exome sequencing data from the Yale-Penn cohort, comprising 2100 participants of European ancestry (EUR; 1321 OD cases) and 1790 of African ancestry (AFR; 864 cases). A novel low-frequency variant (rs746301110) in the RUVBL2 gene was identified in EUR (p = 6.59 × 10). Suggestive associations (p < 1 × 10; not passing the Bonferroni correction) were observed in TMCO3 in EUR, in NEIL2 and CFAP44 in AFR, and in FAM210B in the cross-ancestry meta-analysis. Gene-based collapsing tests identified SLC22A10, TMCO3, FAM90A1, DHX58, CHRND, GLDN, PLAT, H1-4, COL3A1, GPHB5 and QPCTL as top genes (p < 1 × 10) with most associations attributable to rare variants and driven by the burden of predicted loss-of-function and missense variants. This study begins to fill the gap in our understanding of the genetic architecture of OD, providing insights into the contribution of rare coding variants and potential targets for future functional studies and drug development. - Source: PubMed
Publication date: 2025/10/06
Wang LuNuñez Yaira ZMartínez-Magaña José JaimeRivera-Hernandez MelodyMao ZhongzhengBrennand Kristen JMontalvo-Ortiz Janitza LKranzler Henry RGelernter JoelZhou Hang - The growing demand for lithium-ion batteries (LIBs) has intensified the need for sustainable methods to recover critical metals. Current recycling strategies, including pyrometallurgy and hydrometallurgy, often involve high energy consumption, harsh reagents, and poor selectivity, limiting their environmental and economic viability. Here, we report a chemically autonomous and energy-neutral cathode recycling process driven by atmospheric corrosion. Under humid air and dissolved CO, aluminum current collectors undergo sustained oxidative dissolution, releasing electrons that selectively reduce transition metals (TM) in the layered oxide to TM(II). This redox reaction triggers H insertion, Li/H exchange, and lattice destabilization, forming LiHTMO intermediates that spontaneously coordinate with CO to yield TMCO or Ni(OH)CO, while Li precipitates as LiCO. CO acts both as a proton carrier and as a coordinating ligand, sustaining the redox-coordination loop. This chemistry-driven approach redefines corrosion as a tool for selective redox transformations and offers a reagent-free, scalable pathway for LIB recycling under ambient conditions. - Source: PubMed
Publication date: 2025/09/19
Tang WendiYan TianranDai WenbinShen KaidanZhang TingtingYu JialongZhang LiangZhang Wei - The transmembrane and coiled-coil domains 3 (TMCO3) are highly expressed in many tumors. However, the underlying mechanisms governing the way in which TMCO3 affects the progression of hepatocellular carcinoma (HCC) remain unclear. This study screens out the molecule TMCO3 with high N6-methyladenosine (mA) modification level in tumor samples compared to the adjacent non-cancerous tissues of three pairs of HCC patients through Methylated RNA Immunoprecipitation Sequencing (MeRIP-seq) and RNA sequencing (RNA-seq). Subsequently, the oncogenic effect of TMCO3 in HCC is verified through in vivo and in vitro experiments. AlkB Homolog 5 (ALKBH5), an mA demethylase of TMCO3 is then screened out. The following experiments demonstrate that TMCO3 can activate AKT directly through the Phosphatidylinositol-3-Kinase (PI3K) pathway, thus promoting the progression of HCC. Meanwhile, the phosphorylation site on TMCO3: the 85 amino acid-serine, and mutation of this site can directly impair the activity and membrane translocation of AKT is found. Finally, the carcinogenic effect of TMCO3 is further elucidated in HCC through the orthotopic treatment model and the hydrodynamic tail vein injection treatment model. The findings can provide a potential target for targeted AKT treatment in patients with HCC and verify a possible prognostic marker in HCC. - Source: PubMed
Publication date: 2025/04/26
Li XinxinHan MengzhenZhu HePan YonglongSu ChenLiu YachongLiao ZhibinZhang BixiangChen Xiaoping - The present study utilized large-scale genome-wide association studies (GWAS) summary data (731 immune cell subtypes and three primary sclerosing cholangitis (PSC) GWAS datasets), meta-analysis, and two PSC transcriptome data to elucidate the pivotal role of Tregs proportion imbalance in the occurrence of PSC. Then, we employed weighted gene co-expression network analysis (WGCNA), differential analysis, and 107 combinations of 12 machine-learning algorithms to construct and validate an artificial intelligence-derived diagnostic model (Tregs classifier) according to the average area under curve (AUC) (0.959) in two cohorts. Quantitative real-time polymerase chain reaction (qRT-PCR) verified that compared to control, Akap10, Basp1, Dennd3, Plxnc1, and Tmco3 were significantly up-regulated in the PSC mice model yet the expression level of Klf13, and Scap was significantly lower. Furthermore, immune cell infiltration and functional enrichment analysis revealed significant associations of the hub Tregs-related gene with M2 macrophage, neutrophils, megakaryocyte-erythroid progenitor (MEP), natural killer T cell (NKT), and enrichment scores of the autophagic cell death, complement and coagulation cascades, metabolic disturbance, Fc gamma R-mediated phagocytosis, mitochondrial dysfunction, potentially mediating PSC onset. XGBoost algorithm and SHapley Additive exPlanations (SHAP) identified AKAP10 and KLF13 as optimal genes, which may be an important target for PSC. - Source: PubMed
Publication date: 2024/11/05
Hu JianlanWu YouxingZhang DanxiaWang XiaoyangSheng YaohuiLiao HuiOu YangpengChen ZhenShu BaolianGui Ruohu - Hepatocellular carcinoma (HCC) stands as the most prevalent and treatment-resistant malignant tumour, characterized by a dismal prognosis. Croton acylation (CA) has recently gained attention as a critical factor in cancer pathogenesis. This study sought to rapidly identify prognostic features of HCC linked to CA. Differential analysis was conducted between tumour tissues and adjacent non-tumour tissues in the TCGA-LIHC and GSE76427 datasets to uncover differentially expressed genes (DEG1 and DEG2). The intersection of DEG1 and DEG2 highlighted DEGs with consistent expression patterns. Single-sample gene set enrichment analysis scores were calculated for 18 lysine crotonylation-related genes (LCRGs) identified in prior research, showing significant differences between tumour and normal groups. Subsequently, weighted gene co-expression network analysis was employed to identify key module genes correlated with the LCRG score. Candidate genes were identified by overlapping consistently expressed DEGs with key module genes. Prognostic features were identified, and risk scores were determined via regression analysis. Patients were categorized into risk groups based on the optimal cutoff value. Gene set enrichment analysis (GSEA) and immunoassays were also performed. The prognostic features were further validated using reverse transcription-quantitative polymerase chain reaction (RT-qPCR). A total of 88 candidate genes were identified from 1179 consistently expressed DEGs and 4200 key module genes. Seven prognostic features were subsequently identified: TMCO3, RAP2A, ITGAV, ZFYVE26, CHST9, HMGN4, and KLHL21. GSEA revealed that DEGs between risk groups were primarily associated with chylomicron metabolism, among other pathways. Additionally, activated CD4+ T cells demonstrated the strongest positive correlation with risk scores, and most immune checkpoints showed significant differences between risk groups, with ASXL1 exhibiting the strongest correlation with risk scores. The Tumour Immune Dysfunction and Exclusion score was notably higher in the high-risk group. Moreover, in both the TCGA-LIHC and ICGC-LIRI-JP datasets, the expression of other prognostic features was elevated in tumour tissues, with the exception of CHST9. RT-qPCR confirmed the increased expression of TMCO3, RAP2A, ITGAV, ZFYVE26, and HMGN4. This study establishes a risk model for HCC based on seven crotonylation-associated prognostic features, offering a theoretical framework for the diagnosis and treatment of HCC. - Source: PubMed
Yang BailuWen FukaiCui Yifeng