Ask about this productRelated genes to: FAM3D Blocking Peptide
- 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 Blocking Peptide
Related articles to: FAM3D Blocking Peptide
- 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 - The location of nasopharyngeal carcinoma (NPC) is relatively hidden. Most patients are diagnosed at the middle or late stage of the disease, having missed the best time for treatment. - Source: PubMed
Publication date: 2025/08/26
Zhang BohanChen ZixiaoWu Zhinong - Kidney renal clear cell carcinoma (KIRC) is the most common subtype of kidney cancer, characterized by complex molecular alterations. The FAM3 gene family, comprising FAM3A, FAM3B, FAM3C, and FAM3D, has been implicated in various cancers, but their roles in KIRC are not well understood. This study investigated the expression, diagnostic potential, and functional significance of FAM3 family genes in KIRC. This study explores the expression and functional roles of FAM3 family genes in KIRC using in silico and in vitro experiments. We performed RT-qPCR analysis to assess the expression of FAM3A, FAM3B, FAM3C, and FAM3D in KIRC and normal cell lines, revealing significant upregulation of FAM3A and FAM3D and downregulation of FAM3B and FAM3C in cancerous cells. ROC analysis demonstrated that FAM3 genes possess high diagnostic potential. Further validation using TCGA, OncoDB, and Human Protein Atlas (HPA) databases confirmed these expression patterns and their association with cancer progression. Methylation analysis indicated hypomethylation of FAM3A and FAM3D and hypermethylation of FAM3B and FAM3C, correlating with differential gene expression. Survival analysis revealed that high FAM3A expression was linked to poor prognosis, while low FAM3C expression correlated with reduced survival. Functional assays demonstrated that knockdown of FAM3A in 786-O cells reduced proliferation, clonogenicity, and migration, underscoring its potential role in KIRC pathogenesis. Additionally, FAM3 genes exhibited significant correlations with immune cell infiltration, immune inhibitor genes, and drug resistance, suggesting their involvement in modulating the tumor microenvironment. The miRNA-mRNA network analysis identified hsa-mir-19b-3p as a key regulator of FAM3 genes, further implicating these genes in KIRC progression. This comprehensive analysis highlights the potential of FAM3 genes as biomarkers and therapeutic targets in KIRC. - Source: PubMed
Publication date: 2025/07/01
Muhammad ShoaibYan PengyuWang HuifangMahmood AhmadNaqvi Syed Shah Zaman HaiderZaeem MuhammadLiu Chun