HNF4A Antibody - N-terminal region (ARP31946_P050)
- Known as:
- HNF4A Antibody - N-terminal region (ARP31946_P050)
- Catalog number:
- arp31946_p050
- Product Quantity:
- USD
- Category:
- -
- Supplier:
- Aviva Systems Biology
- Gene target:
- HNF4A Antibody - N-terminal region (ARP31946_P050)
Related genes to: HNF4A Antibody - N-terminal region (ARP31946_P050)
- 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: HNF4A Antibody - N-terminal region (ARP31946_P050)
Related articles to: HNF4A Antibody - N-terminal region (ARP31946_P050)
- Glioblastoma multiforme (GBM), the most aggressive primary central nervous system malignancy in adults, is hallmarked by robust angiogenesis and pronounced heterogeneity, with the mesenchymal subtype linked to the poorest prognosis. The median survival of GBM patients is merely ~ 14 months, and approved anti-angiogenic agents like bevacizumab only yield short-term benefits without improving overall survival, highlighting the urgent need for novel anti-angiogenic targets. FAM135B, a brain-enriched protein-coding gene, is implicated in tumorigenesis and chemoresistance in other cancers, but its role and underlying mechanism in GBM angiogenesis remain unelucidated. - Source: PubMed
Publication date: 2026/06/08
Wang ChuangyuanZhang FabingHao LiweiZhang YujieFeng ChenyaWeng NuozhouHu PeiqianLin WanmeiChen TaoliangWang TianweiZhang YinianKe YiquanZhao LiangChen Zetao - The intestinal epithelial barrier maintains gut homeostasis, and its disruption contributes to inflammatory diseases such as Inflammatory Bowel Diseases (IBD). Although barrier restoration is a promising therapeutic strategy, most current approaches target immune responses rather than epithelial function. Since barrier injury and repair progress through discrete phases, this study aimed to define time-resolved epithelial transcriptional programs and identify candidate regulatory nodes for barrier-focused therapeutic intervention. - Source: PubMed
Publication date: 2026/06/08
Yoon Hyo ShinMa ShiningKanke MattWu Wan-JungHoang UyenTan Jessica AWilks AlexPatel PriyankaChandra SundeepLuo XinLu DanielMartin ScottWilson MarkVan Lookeren Campagne MennoLi Chi-MingKao Cheng-Yuan - Type 2 diabetes (T2D) is a common and complex metabolic condition with significant heterogeneity within and across ancestries . Compared with individuals of European ancestry (EUR), people of south Asian ancestry (SAS) have two to four-fold higher risk of T2D, develop the disease at younger ages and lower body mass index (BMI), and experience more rapid progression to complications . Understanding the genetic basis of this is hindered by low representation of south Asians in genetic studies. Here, we perform an exome-wide association study of T2D in 13,674 cases and 41,024 controls from the Genes & Health study of British Pakistani and Bangladeshi individuals. We identify a novel rare variant in - a canonical monogenic diabetes / MODY gene, in which missense variants would be expected to increase T2D risk. Surprisingly, Pro437Ser is associated with a halved risk of T2D and reduced risk of diabetes-related complications but increased non-HDL cholesterol. We additionally characterise a T2D risk-increasing variant which is common only in South and East Asian ancestral groups ( Val429Met), which is associated with lower BMI and phenotypic and genetic markers of insulin deficiency. We validate our findings through replication in independent multi-ancestry cohorts, functional assays, and integration of proteogenomic analysis. These findings highlight how the study of under-represented populations can identify biological mechanisms associated with disease phenotypes enriched in those populations. - Source: PubMed
Publication date: 2026/05/19
Hodgson SamBui ViHu SiqiMaroteau CyrielleBigossi MargheritaHuerta-Chagoya AliciaNguyen TrangDawed Adem YKoesterer RyanVora MaheakStow DanielWilliamson AliceBlee Alexandra MCarrasco-Zanini Sanchez JuliaBaskar ViswanathanJebarani SaravananJacobs Benjamin MKalantzis GeorgiosRison StuartWalter KlaudiaPennarun ErwanTaylor KatherineHsu Sarah Manning AlisaUdler MiriamMartin Hilary CBarroso InêsFlannick JasonFumagalli MatteoRadha VenkatesanPradeepa RajendraLangenberg ClaudiaMohan ViswanathanAnjana Ranjit Mohanvan Heel David AMercader Josep MJamshidi YaldaFiner SarahMajithia Amit RSiddiqui Moneeza K - - Source: PubMed
Publication date: 2026/03/31
Dubois-Laforgue DanièleDonadille BrunoCiangura CécileAmouyal ChloéArnoux Jean-BaptisteBarat PascalBaron SabineBeltrand JacquesBismuth EliseBouché ClaraCarel Jean-ClaudeCavé HélèneChristin-Maitre SophieCollin-Chavagnac DelphineDamgé ChristianeDelemer BrigitteGourdy PierreJacqueminet SophieJanmaat Sonjade Kerdanet MarcKessler LaurenceLangin DominiqueNault Jean-CharlesNizard JackyPolak MichelReynaud RachelSaint-Martin CécileTauveron IgorValéro RenéVambergue AnneVantyghem Marie-ChristineVatier CamilleNicolino MarcBellanné-Chantelot ChristineVigouroux Corinne - Drug-induced liver injury is the most common cause of acute liver failure in Western countries, but the choice of effective antidotes is restricted in most conditions. Glycine-N-acyltransferase (GLYAT) catalyzes the conjugation of glycine to acyl-CoA, serving as a crucial phase II metabolic enzyme for hepatic detoxification. However, few studies have clarified the role of GLYAT in drug-induced liver injury. Our study showed that hepatic glycine level and Glyat expression were reduced upon APAP exposure, but restored within 12 h, similar to the change of hepatic glutathione (GSH). This dynamic expression pattern may be regulated by liver-enriched transcription factors such as HNF4A identified through promoter analysis. Glyat knockout in female mice reduced circulating alanine transaminase (ALT), aspartate transaminase (AST), hepatic reactive oxygen species (ROS) and phosphorylated c-Jun N-terminal kinase (JNK) / extracellular regulated protein kinases (ERK) levels. Conversely, overexpression of Glyat by injection of adeno-associated virus 8 (AAV8) in female mice displayed exacerbated phenotypes, including elevated serum transaminases, increased oxidative stress, enhanced mitogen-activated protein kinase (MAPK) signaling and aggravated hepatocellular necrosis. However, neither Glyat deletion nor overexpression in male mice had effects on APAP toxicity. These protective effects were associated with increased hepatic glycine and GSH levels, as well as attenuated oxidative stress and inflammatory responses. In addition, glycine supplementation had similar hepatoprotective effects to Glyat deficiency in female mice. Taken together, these findings identify GLYAT as a potential therapeutic target and suggest that glycine supplementation may serve as an adjuvant therapy for APAP-induced liver damage, particularly in females. - Source: PubMed
Publication date: 2026/05/19
Zhao JunLiu QinhuiXie LuyueWang CuitongXiong YiminLiang XinqiSun YingXu YingSong HaiyingXu MingzhuJing XiandanXu YiningLi YanpingMo LiPang JuanHe Jinhan