Ask about this productRelated genes to: TMCC3 Blocking Peptide
- Gene:
- TMCC3 NIH gene
- Name:
- transmembrane and coiled-coil domain family 3
- Previous symbol:
- -
- Synonyms:
- KIAA1145
- Chromosome:
- 12q22
- Locus Type:
- gene with protein product
- Date approved:
- 2005-01-21
- Date modifiied:
- 2016-11-10
Related products to: TMCC3 Blocking Peptide
Related articles to: TMCC3 Blocking Peptide
- The causal association between plasma proteomes and the risk of developing hepatocellular carcinoma (HCC) in human populations has not been fully elucidated. Mendelian randomization (MR) is an innovative epidemiological study design that enables the unbiased identification of causal relationships by utilizing genetic variants as instrumental variables. Consequently, we employed a two-sample MR approach to investigate the potential causal link between plasma protein levels and the incidence of HCC. A comprehensive bidirectional two-sample MR analysis was performed using genome-wide significant published genome-wide association studies of plasma proteomes (N: 35,559 healthy individuals) and HCC (168 cases and 372,016 controls). Sensitivity analyses were conducted for identified causal proteins. Furthermore, we pursued pathway exploration using Kyoto Encyclopedia of Genes and Genomes and gene ontology analyses. Protein-protein interaction network analysis provided insights into plasma protein-HCC interactions. We identified 17 plasma proteins causally associated with HCC risk (PIVW < .05). Sixteen proteins were positively associated, including TMCC3, METTL1, SNRPF, KRT19, MED4, RFNG, IL26, NRXN1, MSH2, CLCA2, AKT2, CRYZL1, RDH16, CSF3, CPA4 and COPS7B, while EPHA2 was inversely associated. Gene ontology and Kyoto Encyclopedia of Genes and Genomes enrichment analyses implicated key gene correlations with JAK-STAT, PI3K-AKT and chemokine pathways. The protein-protein interaction network highlighted potential plasma protein-HCC relationships. Our genetics-based approach provides evidence supporting a causal role for specific plasma proteomes in influencing HCC risk. Results support causal effects on HCC for TMCC3, METTL1, SNRPF, KRT19, MED4, RFNG, IL26, NRXN1, MSH2, CLCA2, AKT2, CRYZL1, RDH16, CSF3, CPA4, EPHA2, and COPS7B. Experimental validation and mechanistic study are warranted to confirm findings. - Source: PubMed
Chen XueZheng ZhenHu JingYe ShuangLiu Kaitai - Clear cell renal cell carcinoma (ccRCC) is the most common subtype of renal cell carcinoma (RCC). Although we have made many achievements in the therapy of RCC with the progress of medicine, the clinical management of metastatic RCC remains a daunting challenge. SWI/SNF chromatin remodeling complex-related genes (SCRGs) are significantly associated with tumor progression and cancer cell evolution in ccRCC. This study aimed to investigate the prognostic significance of SCRGs in ccRCC to elucidate its molecular subtype characteristics. Using 29 known SCRGs, 532 ccRCC patients from the TCGA-KIRC cohort were classified into two subtypes (SCRGcluster A and SCRGcluster B). Patients in SCRGcluster B exhibited a significantly poorer prognosis compared to those in SCRGcluster A. Functional enrichment and immune microenvironment profiles significantly differed between the subtypes, with SCRGcluster B showing higher levels of immune infiltration. Five core genes (TMCC3, TOP2A, EPS8, PIK3R3, KCNK5) were identified through the integration of multiple machine learning approaches and multivariate Cox regression analysis. A novel prognostic model based on these core genes was validated in an external cohort. Additionally, single-cell data analysis revealed the expression patterns of these core genes in ccRCC. In vitro experiments demonstrated that KCNK5 is underexpressed in ccRCC cell lines and tissues, and that its overexpression suppresses malignant phenotypes. Specifically, KCNK5 overexpression significantly inhibited the proliferation, migration, and invasion capabilities of ccRCC cell lines. Although the precise functional mechanisms of these core genes in ccRCC are not yet fully elucidated, this study provides new insights for the treatment of ccRCC. - Source: PubMed
Publication date: 2025/11/21
Xu KaiYan ZhiweiLiu YunxunQiu QiangminNi XinmiaoTang HaoWang LeiChen ZhiyuanLiu Xiuheng - The pathogenesis of rectal cancer (RC) involves a variety of biological mechanisms; however, the prognostic significance of temperature-sensitive receptor (TRP) channels in RC patients remains unclear. This study aimed to explore the role of TRP-related genes in RC prognosis and their potential clinical implications. - Source: PubMed
Publication date: 2025/09/02
Wang XiaojunPeng JieqiongSong DongHou LijunWang QingshanZhou YanMa YananQiu ChenGuo QinpingWang Ganggang - Vascular dementia (VaD) is a prevalent form of dementia caused by cerebrovascular disease, leading to cognitive impairment. While various risk factors have been identified, the role of plasma proteins in VaD etiology remains poorly understood. This study employs Mendelian randomization (MR) to investigate the causal relationship between plasma proteins and VaD risk, complemented by experimental validation. We conducted a two-sample MR analysis using summary statistics from genome-wide association studies (GWAS) on plasma proteins and VaD. Plasma protein data were derived from the deCODE Health study, encompassing 35,559 Icelandic participants and genetic associations for 4907 circulating proteins. VaD GWAS data were obtained from the FinnGen biobank, comprising 2717 VaD patients and 393,024 controls. Instrumental variables (IVs) were selected based on genome-wide significance thresholds (P < 5 × 10 for plasma proteins, P < 5 × 10 for VaD). The primary analysis used inverse variance weighting (IVW), supplemented by weighted median, MR-Egger, simple mode, and weighted mode methods. The Sensitivity analyses included heterogeneity tests, horizontal pleiotropy assessments, and leave-one-out analyses. Additionally, a 2-vessel occlusion (2-VO) animal model was used to validate key genes, with gene expression measured by quantitative real-time PCR (qPCR). Our initial MR analysis identified 123 plasma proteins significantly associated with VaD (P < 0.05), of which 12 maintained significance after FDR correction (FDR < 0.05). Importantly, the comprehensive pleiotropy analysis ultimately confirmed robust causal relationships for nine of these proteins with VaD. Among these, MED4 (OR = 1.819, 95% CI: 1.493-2.217, FDR < 0.001), COPS7B (OR = 1.136, 95% CI: 1.076-1.199, FDR < 0.001), CSF3 (OR = 1.262, 95% CI: 1.139-1.398, FDR < 0.001), IL26 (OR = 1.125, 95% CI: 1.066-1.186, FDR < 0.001), NRXN1 (OR = 1.125, 95% CI: 1.066-1.187, FDR < 0.001), LRRTM4 (OR = 1.418, 95% CI: 1.225-1.614, FDR < 0.001), and MAGEA3 (OR = 1.883, 95% CI: 1.403-2.529, FDR < 0.001) were identified as risk factors for VaD, with MED4 showing the strongest association. Conversely, CRYZL1 (OR = 0.387, 95% CI: 0.246-0.609, FDR < 0.001) and TMCC3 (OR = 0.327, 95% CI: 0.191-0.558, FDR < 0.001) were identified as protective factors. The Reverse MR analysis indicated no significant association between VaD and the 9 plasma proteins. In the 2-VO model, MED4 expression was significantly reduced, while NRXN1 expression was elevated compared to the sham group (P < 0.05). This study identifies several plasma proteins with a significant causal relationship with VaD, highlighting MED4 and NRXN1 as potential biomarkers and therapeutic targets. The findings were further validated in an experimental model, providing robust evidence for their roles in VaD pathogenesis. Further research is needed to elucidate the underlying mechanisms and confirm their clinical relevance. - Source: PubMed
Publication date: 2025/07/07
Chen YunmengGuo ChunyanLiang XiaoChi XiansuZhang ZixuanChang ZeZhang Yunling - The peroxisome proliferator-activated receptor gamma (PPARγ) is a nuclear receptor abundantly expressed in the nonalcoholic fatty liver disease (NAFLD). In this study, we investigated the mechanism by which PPARγ regulates the transmembrane and coiled-coil domain family 3 (Tmcc3) gene in the liver. We found that TMCC3 is highly expressed in the fatty liver of humans and mice with NAFLD and alcoholic fatty liver disease. Three exon 1 variants (Tmcc3-1a, -1b, and -1c) of mouse Tmcc3 were identified. TMCC3-1B was highly expressed in the fatty liver of type 2 diabetic ob/ob mice; however, this increase in expression was ameliorated by liver-specific knockout of PPARγ. Reporter assays and electrophoretic mobility shift assays showed that PPARγ positively regulates Tmcc3-1b and -1c transcription through the same PPARγ-responsive element present in the 5'-region of each Tmcc3. Altogether, our results indicate that Tmcc3 is a novel PPARγ target in the fatty liver disease. - Source: PubMed
Publication date: 2024/09/24
Aibara DaisukeSakaguchi AiMatsusue Kimihiko