Ask about this productRelated genes to: DENND1A antibody
- Gene:
- DENND1A NIH gene
- Name:
- DENN domain containing 1A
- Previous symbol:
- KIAA1608
- Synonyms:
- FLJ21129, FAM31A
- Chromosome:
- 9q33.3
- Locus Type:
- gene with protein product
- Date approved:
- 2004-01-29
- Date modifiied:
- 2016-10-05
Related products to: DENND1A antibody
Related articles to: DENND1A antibody
- Major depressive disorder (MDD) is a complex disorder with numerous risk genes identified through genome-wide association studies, but their in vivo functions remain unclear. Here we built an in vivo adeno-associated virus (AAV)-Perturb-seq system to perform parallel loss-of-function screening of MDD risk genes in the mouse brain and to define their transcriptional effects and functional relationships. By comparing perturbation profiles with transcriptomic data from patients with MDD, we identified a cluster of risk genes whose loss led to neuronal downregulation of oxytocin signaling, a feature shared with patients with MDD. Mechanistic studies using Dennd1a as an example revealed that its neuron-specific downregulation impaired the oxytocin receptor-extracellular signal-regulated kinase pathway and induced depressive-like behaviors in mice. Pharmacological enhancement of this pathway alleviated depressive-like phenotypes in Dennd1a-deficient mice and restored oxytocin signaling in DENND1A-deficient human neurons, highlighting the importance of patient stratification for targeted treatment in complex diseases such as psychiatric disorders. - Source: PubMed
Publication date: 2026/06/10
Zhang LianshengKong XiangruiMa QiHu XindeCai ShichengWang BoZou WeijuanBai TaoZhang MeimeiFan LiuTan RunlinDai ZijiJia ZhihengLi TianwenLiu XingyuXu HuataiWu JianrongZheng YuanyiXu ZhengzhengZhou Haibo - To investigate the protective mechanism of Astragaloside IV (AS-IV) in diabetic retinopathy(DR).A streptozotocin-induced diabetic rat model was established and divided in to three groups: control, DR, and DR + AS-IV. Retinal injury was assessed using optical coherence tomography (OCT). Retinal proteomes were profiled using 4D-DIA proteomics. Candidate genes were validated using quantitative PCR (qPCR).302 differentially expressed proteins were detected. Venn diagram analysis revealed three down-regulated proteins in the DR group: Gnal, Dennd1a, and Snx13, and two up-regulated proteins: Ogn and Mylpf. AS-IV treatment reversed the expression of Dennd1a and Gnal while downregulating Ogn, Mylpf, and Snx13. PPI analysis revealed limited direct connectivity among the five proteins but identified 10 additional interactors, including MYLK, ADCY9, and RAB35. GO analysis indicated involvement in muscle contraction, muscle myosin complex, and phosphatidylinositol phosphate binding and structural molecule activity. KEGG analysis highlighted calcium signalling as a key pathway. Molecular docking demonstrated stable interactions between AS-IV and Dennd1a, Ogn, and Snx13 proteins. qPCR confirmed significant regulation of Dennd1a and Ogn, while Snx13 and Mylpf changes were not significant.AS-IV exhibited protective effects against diabetic retinal injury by modulating Dennd1a and Ogn, implicating calcium signalling and structural pathways in its therapeutic mechanism. - Source: PubMed
Publication date: 2026/01/25
Zhang XingyiLiu Hua - Polycystic ovary syndrome (PCOS) is a complex disorder characterized by reproductive abnormalities such as hyperandrogenism, ovulatory dysfunction, and polycystic ovarian morphology, and is frequently accompanied by metabolic disturbances such as insulin resistance, obesity and dyslipidemia. Genome-wide association studies (GWASs) have identified several susceptibility loci, yet little is known about their functional implications. Clustered regularly interspaced short palindromic repeats (CRISPR)/CRISPR-associated protein 9 (CRISPR/Cas9) has emerged as a powerful gene editing tool in bridging this gap by allowing researchers to directly target candidate genes in ovarian and metabolic pathways. For instance, experimental models have highlighted the role of and in androgen excess, anti-Müllerian hormone (AMH) in follicular arrest, and insulin receptor substrate 1 (IRS1) and PPARγ in insulin signaling and adipogenesis. To highlight the multifactorial nature of PCOS, animal models, including zebrafish and rodents, have been used to reveal interactions between reproductive and metabolic phenotypes. Nevertheless, most studies remain restricted to single-gene models, and dual-gene models or combined gene editing and hormonal induction models remain underexplored. Future research integrating precision editing, multi-omic platforms, and patient-derived organoids may provide more accurate disease models and novel therapeutic strategies. - Source: PubMed
Publication date: 2025/11/12
Bucheeri ShahdAlcibahy YasmineBucheeri YaraBucheeri SarahAlhermi AbrarButler Alexandra E - To evaluate whether genetic variants in genes involved in folliculogenesis and steroidogenesis are associated with ovarian response in Vietnamese and Caucasian women undergoing IVF/ICSI. - Source: PubMed
Publication date: 2025/10/20
Neves Ana RaquelCasarini LivioCarretta ChiaraManfredini RossellaGarcía Martínez SandraVuong Ngoc LanBlockeel ChristopheSimoni ManuelaPolyzos Nikolaos P - This review examines the nature of the relationship of increased adiposity to hyperandrogenic oligo-anovulatory polycystic ovary syndrome (PCOS). Most PCOS results from a "functionally typical" form of ovarian hyperandrogenism characterized by a unique pattern of ovarian steroidogenic hyperresponsiveness to gonadotropin stimulation that seems explainable by gene variants that cause overexpression of an activating variant of DENND1A (differentially expressed in normal and neoplastic development). However, one-third of PCOS is "functionally atypical," lacking this ovarian response. These 2 forms of PCOS share clinical traits with the respective "reproductive" and "metabolic" subtypes of PCOS that have been recently distinguished by cluster analysis, with DENND1A gene variants present in significantly more of the former. This review suggests that severe adiposity causes "metabolic/functionally atypical" PCOS by enhancing ovarian steroidogenesis through hyperinsulinism and adipose- and gut-dependent proinflammatory adipokines in genetically predisposed individuals, plus amplifying the ability of adipose tissue to generate testosterone and adrenal-derived 11ß-hydroxytestosterone from circulating precursors. This review furthermore indicates that preferential abdominal fat accumulation, often subclinical, is a central feature of PCOS that also affects metabolic function. The hyperandrogenic environment created within adipose tissue by adiposity-dependent and independent insulin-resistant hyperinsulinism, intra-adipose steroidogenesis, and PCOS-related hyperandrogenemia also appears to restrict the capacity of subcutaneous adipose to safely store fat, predisposing to ectopic fat deposition and lipotoxicity with weight gain. We conclude that excess total and/or abdominal fat seems to be a nearly constant feature of PCOS, either as the cause of hyperandrogenism or as the result of hyperandrogenism contributing to the adipogenic endocrine milieu. - Source: PubMed
Rosenfield Robert LDumesic Daniel A