Ask about this productRelated genes to: TM7SF2 antibody
- Gene:
- TM7SF2 NIH gene
- Name:
- transmembrane 7 superfamily member 2
- Previous symbol:
- -
- Synonyms:
- ANG1, DHCR14A, NET47
- Chromosome:
- 11q13.1
- Locus Type:
- gene with protein product
- Date approved:
- 1997-11-05
- Date modifiied:
- 2014-11-18
Related products to: TM7SF2 antibody
Related articles to: TM7SF2 antibody
- The combined effects of thousands of genetic polymorphisms account for Alzheimer's disease (AD) genetic risk. Most AD polymorphisms affect gene expression. Thus, the transcriptome, the set of all gene expression levels for every gene in the genome, is a major mediator between the genotype to phenotype. This study uses genotypes, transcriptomes, and clinical phenotypes to identify the transcriptomic signature that mediates the causal effect of genotype on AD. By utilizing a causal inference method known as high dimensional mediation analysis (HDMA) on the Religious Orders Study/Memory and Aging Project (ROSMAP) longitudinal cohort, the genotype, transcriptome, and phenotype data were reduced to single scores encoding genotype, transcriptome, and phenotype correlations, and produce a ranked gene list based on putative causal importance of each gene for AD. Analysis of the up- and down-regulated genes prevalent in AD through Gene Ontology (GO) and KEGG databases reveals findings such as up-regulated functions which include angiogenesis and immune responses while down-regulated functions of genes include synaptic activity. Furthermore, utilizing Clue.io to identify candidate drugs to suppress AD-pathology reveals a plausible list of therapeutic candidates, including targeted genes and compounds such as , and , which counteract the transcriptomic signature identified and may block the devastating effects of AD related to inflammatory responses, Aβ-induced toxicity, and neuronal death. - Source: PubMed
Publication date: 2026/03/11
Kaur SimranTyler Anna LDurante Giovanna LCary Gregory ACarter Gregory WMahoney J Matthew - (1) Objective: This study aimed to systematically elucidate the molecular mechanisms by which gypenosides (GP), a major active component of , ameliorate hypercholesterolemia by modulating the hepatic steroidogenesis pathway, and to identify key therapeutic targets. (2) Methods: We established a high-fat diet (HFD)-induced hypercholesterolemia (HC) mouse model and performed GP intervention. An integrated multi-omics approach, combining transcriptomics and proteomics, was utilized to comprehensively analyze GP's effects on the expression of genes and proteins associated with hepatic cholesterol synthesis, transport, and steroid hormone metabolism. (3) Results: HFD induced significant dysregulation, with 48 steroidogenesis pathway-related genes and 35 corresponding proteins exhibiting altered expression in HC mouse livers. GP treatment remarkably reversed these HFD-induced abnormalities, significantly restoring the expression levels of 42 genes and 14 proteins. Multi-omics integration identified seven critical genes/proteins-, , , , , , and -that were consistently and significantly regulated by GP at both transcriptional and translational levels. Furthermore, correlation analyses demonstrated that was significantly negatively correlated with serum total cholesterol (TC) and low-density lipoprotein cholesterol (LDL-C), whereas , , , , , and showed significant positive correlations. (4) Conclusions: GP effectively ameliorates cholesterol dyshomeostasis through a multi-targeted mechanism in the liver. It inhibits endogenous cholesterol synthesis by downregulating key enzymes (, , , , , ), promotes cholesterol efflux and transport (upregulating , ), and accelerates steroid hormone metabolism (upregulating , ). These findings provide robust scientific evidence for the development of GP as a safe and effective novel therapeutic agent for hypercholesterolemia. - Source: PubMed
Publication date: 2025/08/21
Jiang QinYang TaoYang HaoChen YiXiong YuanQin LinZhang QianruTan DaopengWu XingdongZhao YongxiaXie JianHe Yuqi - Lipid reprogramming represents a pivotal stage in tumor progression. N6-methyladenosine (m6A), the most prevalent RNA modification in eukaryotic cells, plays a significant role in colorectal cancer (CRC) development, though its specific involvement in lipid reprogramming remains unclear. Bioinformatics analysis of The Cancer Genome Atlas (TCGA) and Gene Expression Omnibus (GEO) databases revealed differential expression of METTL16 (M16), which was further validated through qRT-PCR and Western blotting in CRC tissues and cell lines. The impact of M16 on CRC proliferation, metastasis, invasion, and lipid reprogramming was evaluated using both and approaches. Regulatory mechanisms underlying M16's role in CRC progression were explored using immunofluorescence (IF) staining, RNA immunoprecipitation (RIP), MERIP assay, RNA pull-down assay, total m6A measurement, RNA stability assay, protein stability analysis, and luciferase reporter assays. Analysis results demonstrated a significant upregulation of the m6A methyltransferase METTL16 in CRC, closely associated with poor prognosis and abnormal lipid droplet accumulation. Functional assays revealed that M16 overexpression markedly promotes CRC cell proliferation, migration, and invasion both and , primarily by enhancing lipid reprogramming. Mechanistically, M16 induces m6A modification of TM7SF2 mRNA, stabilizing it via an IGF2BP1- and IGF2BP2-dependent pathway, thereby upregulating TM7SF2 expression and driving lipid reprogramming in CRC. In conclusion, these findings highlight the critical role of the M16/m6A/TM7SF2 axis in lipid metabolic reprogramming in CRC, offering potential therapeutic targets for its treatment. - Source: PubMed
Publication date: 2025/07/24
Li JieLuo QianLu MinjieLu ChenXu CaihongDing JieZhan TianZhu JingQian MengsenLin ShuhuiChang LishaLi JuanWang Keming - : Protein is essential for basic physiological functions of the body, but the relationship between excessive protein intake and health is controversial. The association between dietary protein and mortality may depend on protein intake and source. This study examined the links between the total/animal/plant protein-energy ratios and mortality from all causes, cardiovascular disease (CVD) and cancer. : The population study included 13 490 participants with a median follow-up of 26.5 years from NHANES III. The study examined the relationship between total, animal, and plant protein-energy ratios, and their combinations, with mortality through Cox proportional hazards models, restricted cubic splines (RCS), and isocaloric (2.5%, 5%, and 10%) substitution analysis. In an animal experiment, 60 male Wistar rats were randomly assigned to normal protein diets (NC = 30) or isocaloric high-protein (HP) diets (HP = 30) for 101 weeks. Subsequently, renal histologic staining was performed using hematoxylin and eosin, and serum amino acid levels were measured through targeted metabolomics. Changes in hepatic gene expression profiles were assessed principal component analysis (PCA), analyzed using protein interaction networks and modules with the STRING online database, and validated through quantitative real-time PCR (q-PCR). : Total protein-energy ratio was positively associated with all-cause mortality (-trend = 0.003), and animal-protein-energy ratio was also positively associated with mortality (all-cause: -trend = 0.007, cancer: -trend = 0.020). RCS showed increased risks of all-cause and cancer mortality when total protein-energy ratio exceeded 14.8%. The risk of all-cause and cancer mortality showed a downward trend when isocaloric plant-protein-energy ratios replaced animal-protein-energy ratios. Rats fed high-animal-protein diets showed higher risk for tumorigenesis. HP diet may alter the transcriptome profiles of rat liver, with upregulated ACSM5, AMACR and TM7SF2, and downregulated HAO2. : Keeping the total protein-energy ratio below 14.8% may be beneficial to reducing all-cause and cancer mortality. Substitution of animal protein with plant protein (by 2.5%, 5%, and 10% of energy) was associated with a decreasing trend in all-cause and cancer mortality. Animal experiments confirmed that the risk of tumorigenesis was associated with a high animal-protein-energy ratio, highlighting the effects of different sources of protein on health and the mechanisms of cancer development. - Source: PubMed
Publication date: 2025/08/11
Li ZicanHuang LianjieZhu QiushuangWang FanyunLi DefangQu BoZhang RunanGuan YueOkekunl Akinkunmi PaulYu JiayingWu YuqingTang XuanfengLi XiaoqingLv XinyiShu XiangKong XiangjuFeng Rennan - Dairy goats represent a crucial species within global dairy livestock. In temperate regions with distinct seasons, dairy goats exhibit reduced reproductive activity under long photoperiod conditions-a phase termed the non-breeding season. This poses a significant challenge to sustaining year-round goat milk production. As the pivotal organ for reproduction, the molecular regulatory mechanisms of the ovary in seasonal breeding remain incompletely characterized. This study investigated the variations in gonadotropin levels in dairy goats across breeding and non-breeding seasons, alongside an evaluation of follicle size and quantity. Furthermore, ovarian differences were explored at the molecular level using transcriptomic and proteomic methodologies. The findings indicate that follicle-stimulating hormone (FSH) and luteinizing hormone (LH) levels in dairy goats are significantly reduced during the non-breeding season compared to the breeding season ( < 0.05). Furthermore, follicle sizes in dairy goats are notably larger during the breeding season relative to the non-breeding season ( < 0.05). A total of 1,115 differentially expressed genes (DEGs) were identified, comprising 749 upregulated and 366 downregulated genes. Additionally, 520 differentially expressed proteins (DEPs) were identified, with 162 upregulated and 358 downregulated. The identified common DEGs and DEPs exhibiting consistent expression patterns include , , , , and . These DEGs and DEPs suppress follicular development during the non-breeding season by regulating steroid hormone biosynthesis. In conclusion, this study reveals the molecular basis underlying seasonal reproductive differences at the ovarian level in dairy goats, offering new insights into the mechanisms of their seasonal reproduction. - Source: PubMed
Publication date: 2025/07/03
Shi ChenboLiu QingqingWang WeiHe QiuyaZhao JianqingZhang FuhongZhu LuLuo Jun