Ask about this productRelated genes to: VZV ORF9 protein
- Gene:
- FAM3B NIH gene
- Name:
- family with sequence similarity 3 member B
- Previous symbol:
- C21orf11
- Synonyms:
- D21M16SJHU19e, PRED44, 2-21, ORF9, C21orf76, PANDER
- Chromosome:
- 21q22.3
- Locus Type:
- gene with protein product
- Date approved:
- 2000-05-23
- Date modifiied:
- 2016-09-30
Related products to: VZV ORF9 protein
Related articles to: VZV ORF9 protein
- BackgroundIndividuals with Down syndrome (DS), caused by triplication of chromosome 21 (Hsa21), face a significantly increased risk of early-onset Alzheimer's disease (AD) and epilepsy. However, the specific impact of Hsa21 genes on these risks is not yet fully understood.ObjectiveTo investigate how triplication of mouse chromosome 16 (Mmu16), homologous to Hsa21, affects amyloid-β (Aβ) accumulation in the brain and epileptic seizures in AD-DS model mice.MethodsTo generate AD-DS model mice, we crossed a mouse model of aspects of AD-an APPswe/PS1 mouse exhibiting brain Aβ accumulation and sudden death associated with epileptic seizures with DS mouse models carrying an extra copy of partial segments of mouse chromosome 16. We used three DS model lines: Ts1Cje, harboring a triplicated region encoding ∼70 Hsa21-homologous genes (-); Ts1Rhr with triplication of the - region; and a newly developed Ts1Kei mouse carrying an extra copy of the - region. Aβ accumulation was assessed by immunohistochemistry and enzyme-linked immunosorbent assay.ResultsCompared with APPswe/PS1 mice, Aβ deposition and insoluble Aβ levels in the brain decreased in APPswe/PS1-Ts1Cje mice but not in APPswe/PS1-Ts1Rhr mice. The high mortality in APPswe/PS1 mice was suppressed by either Ts1Cje- or Ts1Rhr-triplicated region. Despite a tendency for decreased Aβ accumulation in APPswe/PS1-Ts1Kei mice, the study could not be finished due to the extremely high mortality.ConclusionsThe trisomic region in Ts1Kei mice is suggested to harbor genes associated with decreased Aβ accumulation. Alternatively, the trisomic region in Ts1Rhr mice contains genes suppressing sudden death in APPswe/PS1 mice. - Source: PubMed
Publication date: 2026/07/23
Ishihara KeiichiYasui HarukaHarada KokiAmano KenjiSaito MichikoKaneda KinoKatsuda MizukiKawashita EriHata TomokaAnnoura ReinaNishimura KaneyasuTerasaki RyoSago HaruhikoShimohama ShunAkiba SatoshiYamakawa KazuhiroTakata Kazuyuki - 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 - This study systematically analyzed the expression profiles of exosome-associated genes in Major Depressive Disorder (MDD), constructed diagnostic models, and explored their association with immune regulation, pharmacological targeting, and molecular regulatory networks. - Source: PubMed
Publication date: 2026/04/22
Li YingHuang JinsongMiao PeidongLi FangFan LijunZhang Yunan - Recent studies suggest a link among the gut microbiota, its metabolites, and postpartum depression (PPD); however, the specific effects on host metabolism remain unclear. - Source: PubMed
Publication date: 2026/01/09
Zhang ZhiyuanHu XiaobingTao WeiminMa RuijingZheng YuhanFang XinGao JiamengXu Zhendong - 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