Ask about this productRelated genes to: Slc22a3 antibody
- Gene:
- SLC22A3 NIH gene
- Name:
- solute carrier family 22 member 3
- Previous symbol:
- -
- Synonyms:
- OCT3, EMT
- Chromosome:
- 6q25.3
- Locus Type:
- gene with protein product
- Date approved:
- 1998-07-16
- Date modifiied:
- 2016-09-28
Related products to: Slc22a3 antibody
Related articles to: Slc22a3 antibody
- DNA methylation plays a key role in mediating the anti-aging effects of glucose-lowering drugs. This study aims to systematically explore the potential anti-aging effects of target genes of FDA-approved glucose-lowering drugs and the underlying epigenetic mediators. - Source: PubMed
Publication date: 2026/05/21
Sun YuqiZheng HaonanHuang LanhuiMa MinGu RongrongWang ManqingFang SiSun YangboYang QianBi YufangZheng Jie - BackgroundThe extent and biological relevance of shared genetic architecture between myocardial infarction (MI) and heart failure (HF) remain incompletely understood.MethodsWe analyzed large-scale European-ancestry genome-wide association studies summary statistics for MI and HF. Genome-wide genetic correlation was estimated using linkage disequilibrium score regression, and polygenic overlap was quantified using MiXeR. Shared loci were identified via conditional and conjunctional false discovery rate (condFDR/conjFDR) approaches. Functional prioritization incorporated Functional Mapping and Annotation-based annotation, Bayesian fine-mapping, transcriptome-wide association studies (TWAS), FOCUS gene fine-mapping, and summary-level Mendelian randomization (SMR) integrating UKB-PPP proteomic data.ResultsLinkage disequilibrium score regression revealed a robust positive genetic correlation between MI and HF (rg = 0.494, = 1.12 × 10). MiXeR demonstrated substantial polygenic overlap, with approximately 90% of MI-associated variants shared with HF and strong concordance in effect direction. The cond/conjFDR analyses identified multiple pleiotropic loci, including novel HF-associated regions. Fine-mapping prioritized rs544366796 within the SLC22A2/SLC22A3 locus as a high-confidence candidate variant for MI based on posterior probability. The TWAS and FOCUS highlighted canonical MI genes (CDKN2B, CELSR2, BRAP, NBEAL1) and identified MYOZ1 as an HF-specific candidate gene. Proteome-wide SMR analysis provided statistical evidence consistent with apolipoprotein E being a shared protein influenced by variants associated with both MI and HF.ConclusionThe MI and HF share substantial genetic liability characterized by strong polygenic overlap and pleiotropic loci. Our integrative analyses suggest a potential 2-stage genetic framework linking ischemic susceptibility to myocardial remodeling and HF progression, which should be interpreted as a hypothesis-generating conceptual model rather than direct evidence of temporal progression. - Source: PubMed
Publication date: 2026/05/16
Liu RuikangSun ChiyunJiang NanLiu YangLi JunZhang FuyuanChen CongLiu YiyingQi XiaodiGuo BingtingYang Kai - Maternal gut microbiota changes can profoundly shape on offspring health. The placenta may be vulnerable to maternal gut microbiota alterations. Placental disruptions can influence fetal brain development and underly risks for neurobehavioral disorders. Maternal gut microbiota disruptions might affect the placenta through alterations in bacterial short chain fatty acids (SCFA). The hypothesis tested is that depletion of maternal gut microbiota, as may occur in pregnant women treated with antibiotics and germ-free (GF) mice, impacts bacterial SCFA in her fecal samples and in placenta and fetal brain. We assessed whether transcriptomic changes would be evident in placenta and fetal brain from conceptuses derived from GF relative to multi-pathogen free (MPF) pregnant females. Maternal GF status reduced the concentrations of all measured SCFA within the stool. Surprisingly, two-methylbutanoic acid was significantly increased in male and female placenta and fetal brain samples in conceptuses from GF dams. In female and male placenta, several Prl form had altered expression in conceptuses from GF dams. In male placenta from GF dams, Hsd11b2 and Dio3 showed increased expression. Decreased expression of Sl6a2 and Slc22a3 in female fetal brain from GF dams might influence uptake of catecholamines. Results reveal depletion of maternal microbiota can lead to striking effects on the placenta-fetal brain axis. Findings raise concern as to whether maternal microbiota alterations due to other intrinsic or extrinsic factors, namely antibiotic treatment, might impact transcriptomic profiles in fetal placenta and brain. Underlying mechanisms remain uncertain but may relate to changes bacterial metabolites transferred from mother to conceptus. - Source: PubMed
Publication date: 2026/05/14
Herrington Rosalind T BLyu ZhenRaman RagaviSeda Sarah ESnyder ClaireBivens Nathan JLei ZhentianIslam TanhaulSumner Lloyd WJoshi TruptiRosenfeld Cheryl S - Androgen receptor splice variant 7 (AR-V7) is a principal driver of resistance to androgen receptor signaling inhibitors in castration-resistant prostate cancer. By virtue of its truncated ligand-binding domain, AR-V7 functions as a constitutively active transcription factor, sustaining oncogenic signaling independently of androgenic ligands. Its biogenesis is orchestrated by epigenetic regulators and splicing factors, including jumonji domain-containing 6 and eukaryotic translation initiation factor 4A3, which facilitate the production of stabilizing peptides such as that encoded by circSRCAP. AR-V7 establishes a distinct transcriptional programme, frequently cooperating with full-length AR and co-activators like YAP1/TAZ to activate proliferative genes (e.g., UBE2C) and repress tumor suppressors (e.g., SLC22A3). Protein stability is tightly controlled by deubiquitinases USP22 and USP14, while targeted degradation is mediated by the HSP70-STUB1 complex. Clinically, detection of AR-V7 in circulating tumor cells serves as an actionable biomarker, enabling selection of taxane chemotherapy over ineffective androgen receptor signaling inhibitors. Emerging therapeutic strategies include proteolysis-targeting chimaeras, N-terminal domain inhibitors, and agents targeting CDK9 or PRMT1. Overcoming AR-V7-mediated resistance will require deeper biological dissection using single-cell multi-omics and the development of rational combination therapies, representing a pivotal challenge in precision oncology for castration-resistant prostate cancer. - Source: PubMed
Publication date: 2026/05/11
Li JunWang XiongTang Xiaoshuang - Genetic correlation is a key characteristic of the global genetic similarity of human traits. Its primary underlying mechanism is pleiotropy, which operates at various biological levels. Gene-level pleiotropy is of particular interest, as genes are the fundamental functional units of the genome. Using publicly available results from genome-wide association studies for 324 diseases, we selected a set of 45 diseases in which every pair exhibited a significant genetic correlation. These diseases belonged to 10 nosological categories. The search for genes with pleiotropic effects was carried out using three approaches: (1) gene-based association analysis, (2) selection of single nucleotide polymorphisms (SNP) within gene coding regions significantly associated with at least two diseases, and (3) a cross-trait meta-analysis of SNP association signals followed by the identification of independent loci and gene prioritization within those loci. A comprehensive bioinformatic analysis was performed on all genes identified through these methods. We identified 167 pleiotropic genes implicated in 39 diseases. The most pleiotropic genes in our study were LPA, TCF7L2, SLC22A3, FES, CDKN2B, and APOE, which were associated with 7 to 9 diseases each. Bioinformatic analysis revealed that the pleiotropic genes identified for these 39 diseases are also involved in the genetic architecture of 501 other diseases and traits. This indicates a high degree of pleiotropy, facilitated by the involvement of these genes in diverse biological processes - including homeostasis, cell-cell signaling, regulation of cell proliferation, transport, and catalytic activity - and various molecular functions, such as signaling receptor binding. Thus, we demonstrated that 87% of diseases within a fully connected correlation network share associated genes with at least one other disease. This finding strongly suggests that genetic correlations between human diseases are largely driven by the pleiotropic effects of shared genes. - Source: PubMed
Zorkoltseva I VBelonogova N MKirichenko A VTsepilov Y AAxenovich T I