Ask about this productRelated genes to: FAM3D antibody
- Gene:
- FAM3D NIH gene
- Name:
- family with sequence similarity 3 member D
- Previous symbol:
- -
- Synonyms:
- EF7, OIT1
- Chromosome:
- 3p14.2
- Locus Type:
- gene with protein product
- Date approved:
- 2002-06-18
- Date modifiied:
- 2017-01-18
Related products to: FAM3D antibody
Related articles to: FAM3D antibody
- Avian leukosis virus (ALV) causes immunosuppression and tumors, resulting in considerable economic losses in the poultry industry. However, the genetic basis of ALV susceptibility in indigenous breeds remains elusive. Herein, we conducted a genome-wide association study for ALV susceptibility in 259 Wuhua yellow chickens, an indigenous Chinese breed with known disease resistance. ALV infection status was determined by p27 antigen ELISA at 46 weeks of age, with 10 individuals (3.9%) classified as positive. We identified 58 significant SNPs, all located on chromosome 12 and concentrated within a 1.03-Mb region (12.19-13.22 Mb), using SAIGE to account for extreme case‑control imbalance. Gene annotation demonstrated 11 candidate genes, among which FHIT accounted for 44 of the 58 significant SNPs (76%). Additionally, PDHB, PTPRG, FAM3D, and FAM107A were identified as potential candidate genes associated with ALV susceptibility. Notably, conditional analysis confirmed that the lead SNP in FHIT (chr12:12,650,715) is the main driver of this cluster, given that its inclusion as a covariate eliminated all neighboring signals. Functional enrichment showed the citrate cycle as the most considerably enriched pathway, highlighted by PDHB, alongside pyruvate and carbon metabolism. The convergence of tumor suppression (FHIT, FAM107A), metabolic reprogramming (PDHB), and immune/signaling (PTPRG, FAM3D) genes within a single genomic region suggests a potential resistance-associated haplotype block. Our study provides promising candidate genetic markers for breeding ALV-resistant lines and offers novel insights into host-retrovirus interactions beyond traditional immune signaling. - Source: PubMed
Publication date: 2026/06/10
Huang XunheXie TingtingXu YongjieWeng ZhuoxianZhang LiDu Bingwang - This study comprehensively investigated the role of FAM3 family genes (, , , ) in Kidney Renal Clear Cell Carcinoma (KIRC) using an integrative multi-dimensional approach. Analyses included mRNA expression profiling, promoter methylation assessment, genetic alteration evaluation, prognostic modeling, immune and molecular subtype correlations, gene enrichment analysis, in vitro functional validation, and drug sensitivity evaluation based on TCGA datasets and experimental data. Expression analysis revealed significant upregulation of and and downregulation of and in KIRC tissues compared with normal kidney samples. ROC curve analysis demonstrated their diagnostic potential. Promoter methylation analysis indicated hypomethylation of and and hypermethylation of and , consistent with their expression profiles. Minimal genetic alterations were observed, suggesting that epigenetic regulation may primarily contribute to their dysregulation. Prognostic modeling associated gene expression with overall survival, indicating their potential as predictive biomarkers. Immune infiltration and subtype analyses suggested that genes are involved in the modulation of the tumor microenvironment. Functional validation demonstrated that knockdown of and suppressed cell proliferation and colony formation, while enhancing migratory and wound-healing abilities in KIRC cell lines. Drug sensitivity analysis identified correlations between expression and responsiveness to anticancer compounds. These findings highlight the diagnostic, prognostic, and therapeutic significance of family genes in KIRC, providing valuable insights for future clinical translation and potential targeted therapy development. - Source: PubMed
Publication date: 2026/05/06
Zhe WangAbbas MuhammadAbdel-Maksoud Mostafa AAlmanaa Taghreed NAlmutair SaeedahAlamri AbdulazizAufy MohammedAl-Qahtani Wahidah HHameed Yasir - In mice, the uterus undergoes dynamic changes regulated by estrogen and progesterone during the estrous cycle. Proper regulation of these changes is critical for successful pregnancy. The Family with sequence similarity 3 (Fam3) gene family, comprising , , , and , encodes cytokine-like proteins, but their uterine roles remain unclear. This study examined Fam3 expression in the mouse uterus across the estrous cycle and assessed estrogen-dependent regulation. RNA-seq analysis revealed increased , , and expression during proestrus and estrus. Notably, showed dynamic regulation, peaking in these stages. To test estrogen regulation, estradiol was administered to ovariectomized mice, showing maximal expression at 24 h post-injection. ERα antagonist treatment blocked this induction, indicating ERα-mediated regulation. Immunofluorescence localized FAM3D to the cytoplasm of luminal and glandular epithelia, especially in the apical region, with no stromal or nuclear expression. These findings suggest that estrogen and Erα (Estrogen receptor alpha) signaling control Fam3d expression, implicating FAM3D in uterine epithelial function. This study provides novel insights into 's role in uterine physiology and a foundation for exploring its function in reproduction. - Source: PubMed
Publication date: 2025/12/08
Kim HyukjungKim ByeongseokKim JooheeSuh YeonjuLee JiminPark SangokLee Man RyulLee Hoi ChangChoi Youngsok - Proteomics serves as a primary source of therapeutic targets. In this study, we performed a Mendelian randomization (MR) analysis within the proteomic scope to identify candidate protein markers and potential therapeutic targets for duodenal ulcer (DU). This study utilized MR and co-localization analysis within the proteomic framework. Data on 2088 plasma proteins were carefully collected from a study that detected 4907 protein quantitative trait loci. The genetic association data for DU were sourced from the UK Biobank, which encompassed 1908 cases and 461,025 controls. MR used single nucleotide polymorphisms as a genetic tool to estimate the causal effects of exposure on outcomes, in order to screen candidate proteins associated with DU. Meanwhile, Bayesian co-localization analysis is used to determine the probability of shared causal genetic variation between features. Additionally, 2-step MR was employed to quantify the proportion of protein-mediated risk factors for DU. Finally, protein-protein interaction analysis was conducted to elucidate the potential link between proteins and drugs currently used for treating DU. Using the Drug Signature Database, potential targeted drugs for druggable proteins were explored. We identified 11 plasma proteins that were significantly associated with DU. Elevated levels of FLT4, IGSF3, IL6ST, EPHB4, DPEP2, SEMA6A, and IL1R1 were found to have a risk-conferring effect. Conversely, increased levels of REG1B, GOLM1, FAM3D, and QSOX2 exhibited a protective effect. Notably, none of these 11 proteins demonstrated evidence of reverse causality. Bayesian co-localization analysis indicated that REG1B, FLT4, GOLM1, EPHB4, and FAM3D shared the same genetic variations as those associated with DUs. Additionally, the protein target IL1R1, which is related to DU drugs, and 6 pharmaceutically relevant proteins, namely REG1B, IL6ST, FLT4, DPEP2, QSOX2, and EPHB4, were identified. Our research found that REG1B, FLT4, IGSF3, IL6ST, GOLM1, EPHB4, DPEP2, FAM3D, QSOX2, SEMA6A, and IL1R are associated with DU. Among them, IL1R1, REG1B, IL6ST, FLT4, DPEP2, QSOX2, and EPHB4 may become drug targets for further clinical research on DU. Targeting these proteins during drug development may provide a preferred and cost-effective approach for treating DU. - Source: PubMed
Luo XuLuo DanLiu ChenhaoZhang HuizeLong MingyueCao SiminLiu Yi - Non-small cell lung cancer (NSCLC), as one of the most commonly diagnosed cancers globally, requires expedited identification of new drug targets. We conducted proteome-wide MR using genetic data for 4,853 plasma proteins. Summary-level data on lung adenocarcinoma (LUAD) and squamous cell carcinoma (LUSC) were extracted from GWAS meta-analyses (11,273 and 7,426 cases, respectively) and FinnGen cohort (1,590 and 1,510 cases, respectively). We genetically identified eight proteins with a causal role in the etiology of NSCLC. Lower levels of five proteins (CDH17, CXADR, FAM3D, POGLUT3, SFTPB) and higher levels of two proteins (CEACAM5, KLK1) were linked to increased LUAD risk, while higher CD14 levels were associated with elevated LUSC risk. Two proteins, POGLUT3 and SFTPB were validated through Bayesian colocalization. One protein SFTPB was identified using SMR and HEIDI tests. Bidirectional MR found no reverse causality. The primary findings were validated through scRNA-seq, GeneMANIA, GO analysis, druggability assessments and PheWAS analysis. These protein-coding genes are primarily expressed in epithelial cells, macrophages, monocytes, and endothelial cells. Furthermore, CEACAM5, KLK1, and CD14 correspond to existing drugs. These proteins may deepen our comprehension of the etiology and could serve as appealing novel biomarkers and drug targets for NSCLC management. - Source: PubMed
Publication date: 2025/09/12
Zhao MinghuiDi XiaokeZhao Yucui