HNF4
- Known as:
- HNF4
- Catalog number:
- E021043-2
- Product Quantity:
- 100ug
- Category:
- -
- Supplier:
- EnoGene
- Gene target:
- HNF4
Related genes to: HNF4
- Gene:
- HNF4A NIH gene
- Name:
- hepatocyte nuclear factor 4 alpha
- Previous symbol:
- TCF14, MODY, MODY1
- Synonyms:
- NR2A1, HNF4
- Chromosome:
- 20q13.12
- Locus Type:
- gene with protein product
- Date approved:
- 1998-04-20
- Date modifiied:
- 2019-04-23
Related products to: HNF4
Related articles to: HNF4
- Hepatocellular carcinoma (HCC) commonly develops in the context of chronic liver injury, viral hepatitis, metabolic dysfunction, alcohol-related liver disease and cirrhosis. Although immune checkpoint inhibitor-based combination therapies have improved the treatment of unresectable HCC, primary and acquired resistance and the lack of reliable predictive biomarkers continue to limit precision treatment. Transposable elements (TEs) and TE-derived sequences represent a regulatory layer linking epigenetic disruption, aberrant transcription and immune remodelling. In HCC, DNA hypomethylation, altered repressive histone modifications, dysfunction of TE-silencing machinery and dysregulated RNA-level control may promote the reactivation of LINE-1, HERV/ERV and other TE-derived sequences. Reactivated TEs may influence tumour-cell states and the immune microenvironment through cryptic promoter or enhancer activity, TE-derived transcripts, viral mimicry, innate immune sensing and potential tumour-associated antigens. HCC-specific evidence includes clinical associations of LINE-1 hypomethylation and mechanistic findings involving the TE/KDM1A/HNF4A axis and SETDB1-mediated HERV/ERV silencing and viral mimicry. Using a structured narrative literature search that emphasised studies published during the past five years while retaining relevant landmark studies, this review integrates the epigenetic, transcriptional, immune and translational dimensions of TE dysregulation in HCC. A five-level evidence framework is applied to distinguish HCC-specific mechanistic and in vivo evidence, HCC functional and cell-based findings, HCC clinical and omics associations, pan-cancer or non-HCC evidence, and hypothesis-generating candidates. This framework highlights the uneven maturity of the field and the need for locus-specific functional studies and independent clinical validation. TIGD family members are discussed as a hypothesis-generating example of TE-derived protein-coding candidates rather than as established HCC regulators, biomarkers or therapeutic targets. - Source: PubMed
Publication date: 2026/09/29
Chen XiaopengLi BaodingChai HaoYang ChengweiBai RuiMa WenxiaoLi Minghao - Uridine 5'-diphospho-glucuronosyltransferase (UGT) enzymes play a critical role in hepatic and other metabolism of endogenous and exogenous small molecules. The addition of glucuronic acid via UGT increases the polarity and subsequent solubility of small molecules, helping direct them for biliary excretion and renal excretion by organic anion transporter OAT3 (SLC22A8). Mutations in UGTs are associated with disorders in biliary metabolism (e.g., Gilbert's syndrome, Crigler-Najjar syndrome). Here, we used comprehensive serum metabolomic profiling of pan -knockout ( ) mice to define the metabolic consequences of UGT deficiency. All 7 knockout mice exhibited markedly elevated bilirubin (mean = 5.96 mg/dL). Partial Least Squares Discriminant Analysis (PLS-DA) showed clear separation between and wild type (WT), and volcano plots revealed significant endogenous metabolite alterations. These included upregulation of numerous bilirubin degradation products as well as major disturbances in lipid and amino acid metabolism. In particular, pathway enrichment analyses identified disruptions in fatty acid biosynthesis, glycine-serine metabolism, heme breakdown, porphyrin metabolism, and β-oxidation of fatty acids. Thus, the UGT1 proteins regulate different aspects of endogenous metabolism and signaling. Consistent with this notion, there were increases in liver expression of several nuclear receptors (e.g., HNF4a, PPARa, PXR) involved in metabolic signaling. These results support the remote sensing and signaling theory (RSST), which proposes that UGT1 proteins play a key role in organ crosstalk via routing small molecules between the liver and kidney, with glucuronidated molecules being mainly directed to the multispecific SLC kidney transporter OAT3. We propose that this glucuronidation-regulated RSST loop is essential to signaling along the gut-liver-kidney axis. - Source: PubMed
Publication date: 2026/08/15
Falah KianLiu JiarunNguyen NghiaChen ShujuanTukey Robert HNigam Sanjay K - Mechanical ventilation is associated with acute and long-term cognitive dysfunction, yet the molecular pathways linking ventilator-induced lung injury (VILI) to brain injury remain poorly characterized. We previously demonstrated that peripheral IL-6 signaling mediates delirium-like phenotypes in a murine VILI model. Here, we use unbiased aptamer-based proteomics to determine whether this model exhibits proteomic signatures consistent with neurodegenerative processes in the brain and plasma. - Source: PubMed
Publication date: 2026/09/29
Winzey Kevin DGuzman SamuelYang EdwardMoreira DebbieWang XingyuGu XuesongDillon Simon TEly E WesleyKarumanchi S AnanthLibermann Towia ALahiri Shouri - Sepsis induces profound alterations in liver function that contribute to disease progression. We previously demonstrated that peritoneal sepsis is associated with marked disruption of hepatic transcriptional programs, including loss-of-function of Hepatocyte Nuclear Factor 4 alpha (HNF4α), a master regulator of hepatic identity and metabolism. Using hepatocyte-specific HNF4α knockout mice, we further showed that loss of HNF4α is detrimental during peritoneal sepsis. Here, we investigated whether this response is conserved in pneumonia-induced sepsis and assessed its functional significance. Bulk liver RNA sequencing revealed that suppression of hepatic metabolic pathways and HNF4α target genes are conserved features of both peritoneal and -induced sepsis. Unexpectedly, hepatocyte-specific HNF4α deficiency was associated with lower bacterial burden and increased survival during pneumococcal sepsis. Mechanistically, this protective effect was dependent on neutrophils and not macrophages. These findings demonstrate that sepsis-induced hepatic HNF4α dysregulation is conserved across distinct infectious etiologies but exerts context-dependent effects on disease outcome. - Source: PubMed
Publication date: 2026/09/15
Vandewalle JolienHeyerick MarahTimmermans StevenLibert Claude - Air pollutants are implicated in carcinogenesis, but their relevance to gastric cancer (GC) across prognosis, tumor organization and cell behavior remains unclear. We integrated evidence to evaluate pollutant-prioritized GC candidates. - Source: PubMed
Publication date: 2026/09/10
Zhao LumingHu NanXu YimengMao ChenxiHong YidongZhang JingzhouZhou KangjieWu Fenglei