Ask about this productRelated genes to: TRIM71 Blocking Peptide
- Gene:
- TRIM71 NIH gene
- Name:
- tripartite motif containing 71
- Previous symbol:
- -
- Synonyms:
- LIN41, LIN-41
- Chromosome:
- 3p22.3
- Locus Type:
- gene with protein product
- Date approved:
- 2006-03-30
- Date modifiied:
- 2016-06-30
Related products to: TRIM71 Blocking Peptide
Related articles to: TRIM71 Blocking Peptide
- Chorangiomas, benign capillary lesions of the placenta, occur in ~1% of births, typically as solitary nodules. Multiple chorangioma syndrome is rare and increases risk of fetal heart failure, hydrops fetalis, and intrauterine death due to placental hemodynamic disruption. While genetic and hypoxic factors have been suggested in chorangioma development, direct molecular evidence is lacking. Here, we present a unique case of multiple chorangiomas confined to half of a shared placenta in monozygotic monochorionic diamniotic twins, providing a rare opportunity to dissect molecular drivers of chorangioma formation. - Source: PubMed
Publication date: 2026/02/03
Wilk Brandon MGajapathy ManavalanBrown Donna MDuncan Virginia EWorthey Elizabeth A - Temperature has always been an important environmental factor, and changes in water temperature are closely related to the entire life process of fish. Investigating the impact of thermal stress on fish physiology is critical for optimizing aquaculture. This study employed transcriptomic and metabolomic approaches to investigate temperature-induced variations in the gene expression and metabolic profiles of turbot. The results showed that thermal stress could induce abnormal genes transcription, and functional annotation demonstrated predominant associations of these genes with key pathways including PI3K-Akt signaling, PPAR regulation, steroid biosynthesis, fatty acid metabolism, and FoxO signaling cascade. Metabolomic analysis revealed that amino acid metabolism was dysregulated, such as valine, leucine, and isoleucine. Joint analysis revealed significant positive associations between , , and genes and leucine/isoleucine metabolism. The expression levels of and genes exhibited significant regulatory effects on valine metabolism. Moreover, the gene cluster comprising , and was significantly involved in the metabolic regulation of galactonic acid. Collectively, these findings demonstrate that thermal stress induces significant alterations in gene expression, metabolic profiles, and signaling pathways in turbot, offering new perspectives for thermal stress mitigation strategies. - Source: PubMed
Publication date: 2025/10/14
Chen XiatianGao TaoWang ZiwenChen ShuaiyuZhang NanZhang XiaomingJia Yudong - Photoperiod is a critical environmental cue that orchestrates reproductive physiology and circadian biology in crustaceans, yet the neural gene networks linking photoperiod to ovarian maturation and clock regulation remain largely unknown. To elucidate the molecular mechanisms underlying photoperiod regulation of ovarian development and associated circadian rhythmicity, the eyestalk (SG) and brain ganglion (BG) of female Chinese mitten crab (Eriocheir sinensis) from two photoperiod groups (Light (L): Dark (D) = 0 h: 24 h (L0) and L: D = 18 h: 6 h (L18)) were used for transcriptome analysis. The analysis identified 298 differentially expressed genes (DEGs) in the brain and 109 DEGs in the eyestalk. KEGG enrichment analysis indicated these DEGs were primarily associated with ovarian development and circadian rhythm-related signaling pathways. Key ovarian development-related genes, including E3 ubiquitin-protein ligase lubel-like isoform X6, 5-hydroxytryptamine receptor-like, serine/threonine-protein phosphatase alpha-2, estrogen sulfotransferase, cytochrome P450 2 L1-like, follicle-stimulating hormone receptor-like isoform X1 and E3 ubiquitin-protein ligase CHIP (EULCHIP), exhibited significant upregulation or downregulation in the L18-BG group. Meanwhile, genes such as EULCHIP, E3 ubiquitin-protein ligase TRIM71-like, CREB-binding protein-like isoform X2, serine/threonine-protein phosphatase 6 regulatory ankyrin repeat subunit C, collagen alpha-5(IV) chain, integrin beta 1, ecdysone-induced protein 74EF-like, and insulin-like growth factor-binding protein complex acid labile subunit showed significant upregulation or downregulation in the L18-SG group. These findings suggest that prolonged photoperiods enhance ovarian development and modulate reproductive endocrine activity during ovarian maturation. Furthermore, circadian rhythm-related genes such as period circadian protein-like isoform X1, prostaglandin D synthase, and acetylcholine receptor subunit alpha-type acr-16 displayed marked differential expression between photoperiod groups, indicating disrupted molecular oscillations and gradual desynchronization of circadian rhythmicity under extended light exposure. This study provides critical, systems-level insights into the photoperiod-driven regulatory networks of ovarian development and endocrine dynamics in crustaceans, offering a molecular basis for optimizing aquaculture practices and advancing our understanding of crustacean reproductive physiology. - Source: PubMed
Publication date: 2025/09/09
Yuan GaoyuanHuo MeihuiZheng BoyiWang ZhichaoWu XuganLiu MeimeiDong Zhiguo - The RNA-binding protein TRIM71 is essential for brain development, and recent genetic studies in humans have identified as a risk gene for congenital hydrocephal-us (CH). Here, we show that monoallelic missense mutations in are associated with hearing loss (HL) and inner ear aplasia in humans. Utilizing conditional knockout mice carrying a CH and HL-associated mutation, we demonstrate that loss of TRIM71 function during early otic development (embryonic day 9 to 10) causes severe HL. While inner ear morphogenesis occurs normally in knockout mice, we find that early otic loss of TRIM71 function disrupts the highly stereotyped timing of cell cycle exit and differentiation within the inner ear auditory sensory organ (cochlea), resulting in the premature formation and innervation of mechanosensory hair cells. Transcriptomic profiling of -deficient cochlear progenitor cells identifies and as targets of TRIM71 repression, and our analysis of double knockout mice indicates that TRIM71 maintains hair cell progenitors in a proliferative and undifferentiated state by restricting TGFβ-type signaling. Characterization of hair cells and their associated neurons in adult knockout mice revealed reduced presynaptic terminals and neuronal degeneration in the outer hair cell region, providing a basis for the observed hearing deficits in knockout mice. - Source: PubMed
Publication date: 2025/09/02
Li Xiao-JunMorgan CharlesDuy Phan QEvsen LaleHao Le TMachavoine RoxaneBelhous KahinaErnest SylvainDenoyelle FrançoiseMignot CyrilBrioude FredericParodi MarineLi LinHuang HeNadar Ponniah Prathamesh TKolanus WaldemarKahle Kristopher TMarlin SandrineDoetzlhofer Angelika - To investigate the genetic etiology of ventriculomegaly (VM) in fetuses by analyzing chromosomal aberrations and genetic variations through high-throughput sequencing. Clinical data and samples (amniotic fluid or miscarriage tissue) were collected from fetuses with ventricular width >10 mm, diagnosed at Shanxi Children's Hospital between 2020 and 2023. All samples underwent copy number variation sequencing (CNV-seq), and those with negative CNV-seq result were further analyzed by whole exome sequencing (WES) to identify single-gene variants. Chromosomal abnormalities and monogenic variants were classified according to the American College of Medical Genetics and Genomics guidelines. Statistical analysis was performed using SPSS 26.0, and pregnancy outcomes were tracked. Among 73 VM fetuses, 23 (31.5%) cases exhibited chromosomal aberrations via CNV-seq, including 4 aneuploidies, 12 pathogenic CNVs, 2 likely pathogenic CNVs, and 8 variants of unknown significance. The incidence of chromosomal abnormalities was significantly higher in non-isolated VM fetuses compared to isolated VM (p < 0.05). WES analysis of 33 CNV-negative cases identified single-gene defects in 16 (48.5%) fetuses, including SPATA5, PDHA1, TRIM71, PIK3R2, TUBB, CRB2, PIDD1, RTTN, FGFR3, AIMP1, POGZ, MYH7, CNOT3, MACF1, and PURA gene, with 10 novel variants reported. Fetal VM is associated with heterogeneous neurodevelopmental outcomes, and genetic etiology plays an important role in its pathogenesis. WES enhances the efficiency of diagnosis, particularly for VM fetuses without detectable aneuploidy or CNVs. Identifying the genetic etiology of fetal VM is is crucial for informing birth defect prevention strategies and improving the overall health of the newborn population. - Source: PubMed
Publication date: 2025/07/02
Chenyue ZhaoHuiqin XueJingbo GaoMin GuoHao YueRong GuoGuizhi CaoXiayu SunJianrui Wu