Ask about this productRelated genes to: HNF4G antibody
- Gene:
- HNF4G NIH gene
- Name:
- hepatocyte nuclear factor 4 gamma
- Previous symbol:
- -
- Synonyms:
- NR2A2
- Chromosome:
- 8q21.13
- Locus Type:
- gene with protein product
- Date approved:
- 1998-04-20
- Date modifiied:
- 2016-10-05
Related products to: HNF4G antibody
Related articles to: HNF4G antibody
- - Source: PubMed
Publication date: 2026/07/08
- Pancreatic cancer remains a highly lethal malignancy, primarily due to late-stage diagnosis. Current screening paradigms, which focus exclusively on high-risk individuals, leave the vast "low-risk" population unscreened. This conventional binary risk stratification, based predominantly on family history and known genetic syndromes, fails to incorporate emerging risk dimensions such as polygenic risk scores, lifestyle factors, and novel biomarkers. We propose a paradigm shift from this static model towards a dynamic, multidimensional risk stratification framework. By integrating genetic susceptibility (, newly identified variants in , ), lifestyle metrics (, new-onset diabetes), and liquid biopsy biomarkers (, circulating tumor DNA, carbohydrate antigen 19-9 dynamics), we can reclassify a subset of "low-risk" individuals who may benefit from targeted screening. The integration of artificial intelligence for prospective validation, as seen in ongoing trials, is crucial for implementing this approach. - Source: PubMed
Wang Rui-Gang - Obesity is an epidemic with myriad health effects, but little is understood regarding individual obese phenotypes and how they may respond to therapy. Epigenetic changes associated with obesity have been detected in blood, liver, pancreas, and adipose tissues. Previous work using human organoids found that dietary glucose hyperabsorption is a steadfast trait in cultures derived from some obese subjects, but detailed transcriptional or epigenomic features of the intestinal epithelia associated with this persistent phenotype are unknown. This study evaluated differentially expressed genes and relative chromatin accessibility in intestinal organoids established from donors classified as non-obese, obese, or obese hyperabsorptive by body mass index and glucose transport assays. Transcriptomic analysis indicated that obese hyperabsorptive subject organoids have significantly upregulated dietary nutrient absorption transcripts and downregulated type I interferon targets. Chromatin accessibility and transcription factor footprinting predicted that enhanced HNF4G binding may promote the obese hyperabsorption phenotype. Quantitative RT-PCR assessment in organoids representing a larger subject cohort suggested that intestinal epithelial expression of CUBN, GIP, SLC5A11, and SLC2A5 were highly correlated with hyperabsorption. Thus, the obese hyperabsorption phenotype was characterized by transcriptional changes that support increased nutrient uptake by intestinal epithelia, potentially driven by differentially accessible chromatin. Recognizing unique intestinal phenotypes in obesity provides a new perspective in considering therapeutic targets and options with which to manage the disease. - Source: PubMed
Publication date: 2025/10/08
Badurdeen Dilhana SLi ZhenLee Jeong-HeonMa TaoBhagwate Aditya VijayLatanich RachelDogiparthi ArjitOrdog TamasKovbasnjuk OlgaKumbhari VivekFoulke-Abel Jennifer - Objective of this study is to conduct a genome-wide association study (GWAS) of first-parity reproductive traits in Suzi pigs to identify significant single-nucleotide polymorphisms (SNPs) or candidate genes influencing these traits. - Source: PubMed
Publication date: 2025/11/06
Fu YanfengLi WeiningDai ChaohuiLiao ChaoCheng JinhuaLi HuiZhao Weimin - Emerging evidence suggests that lineage-specifying transcription factors control the progression of pancreatic ductal adenocarcinoma (PDAC). We have discovered a transcription factor switching mechanism involving the poorly characterized orphan nuclear receptor HNF4G and the putative pioneer factor FOXA1, which drives PDAC progression. Using our unbiased protein interactome discovery approach, we identified HNF4A and HNF4G as reproducible, FOXA1-associated proteins, in both preclinical models and Whipple surgical samples. In the primary tumor context, we consistently find that the dominant transcription factor is HNF4G, where it functions as the driver. A molecular switch occurs in advanced disease, whereby HNF4G expression or activity decreases, unmasking FOXA1's transcriptional potential. Derepressed FOXA1 drives late-stage disease by orchestrating metastasis-specific enhancer-promoter loops to regulate the expression of metastatic genes. Overall survival is influenced by HNF4G and FOXA1 activity in primary tumor growth and in metastasis, respectively. We suggest that the existence of stage-dependent transcription factor activity, triggered by molecular compartmentalization, mediates the progression of PDAC. - Source: PubMed
Publication date: 2025/10/30
Rao Shalini VYoung LisaCheeseman DanyaFlynn SeanKrebs NiklasCouturier Dominique-LaurentMack StephanieBrais RebeccaTemple JillSmith AmyPapachristou EvangeliaPelicano CatarinaChilamakuri Chandra Sekhar ReddyHerka KrzysztofBaba HideoFarah LuayCheung Phyllis FSiveke JensGuerrier StéphaneInsolia LucaGill MichaelArcher Goode EmilyKupczak StevenCheng YiBorsari GiacomoJodrell DuncanD'Santos CliveRussell AlasdairGrünwald Barbara TSerrao EvaChernukhin IgorCarroll Jason S