HNF1a _ HNF1b _ HNF1c EMSA Kit
- Known as:
- HNF1a _ HNF1b _ HNF1c EMSA Kit
- Catalog number:
- AY1323
- Product Quantity:
- 25 rxn
- Category:
- -
- Supplier:
- Panomics
- Gene target:
- HNF1a _ HNF1b HNF1c EMSA Kit
Related genes to: HNF1a _ HNF1b _ HNF1c EMSA Kit
- Gene:
- HNF1A NIH gene
- Name:
- HNF1 homeobox A
- Previous symbol:
- MODY3, TCF1
- Synonyms:
- HNF1, LFB1
- Chromosome:
- 12q24.31
- Locus Type:
- gene with protein product
- Date approved:
- 1990-02-12
- Date modifiied:
- 2019-04-23
- Gene:
- HNF1B NIH gene
- Name:
- HNF1 homeobox B
- Previous symbol:
- TCF2
- Synonyms:
- LFB3, VHNF1, HNF1beta, MODY5
- Chromosome:
- 17q12
- Locus Type:
- gene with protein product
- Date approved:
- 1990-05-28
- Date modifiied:
- 2015-09-07
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- Evidence regarding the efficacy and safety of sodium-glucose cotransporter 2 inhibitors (SGLT2i) in monogenic diabetes is limited. We evaluated real-world metabolic, renal, and safety outcomes of SGLT2i therapy in adults with monogenic diabetes. - Source: PubMed
Publication date: 2026/08/06
Audrain EstelleBel Lassen PierreBellanné-Chantelot ChristineVantyghem Marie ChristineDupuis HippolyteVidal-Trecan TiphaineChevalier NicolasDubois-Laforgue DanièleLamothe SophieVatier CamilleVillard OrianneValéro RenéBriet ClaireVigouroux CorinneCiangura CécileAmouyal Chloé - This discovery study investigated the impact of MODY-associated mutations in hepatocyte nuclear factors HNF1A and HNF1B on the cellular proteome, aiming to identify affected pathways and advance understanding of diabetes pathogenesis. Human induced pluripotent stem cells (hiPSCs) carrying the HNF1A frameshift mutation (p.Pro291fsinsC) were differentiated into pancreatic progenitors, and renal proximal tubule epithelial cells (RPTECs) were engineered to overexpress HNF1B with the S148L point mutation. Label-free quantitative proteomics was performed using data-dependent and data-independent acquisition on Orbitrap and timsTOF mass spectrometers. Pathway enrichment was analyzed using Qiagen IPA, Hallmark gene sets, and STRING networks. Comprehensive proteome coverage (over 7000 proteins) revealed consistent downregulation of oxidative phosphorylation, mitochondrial function, and interferon signaling pathways. Both models exhibited suppression of innate immune responses, with overlapping downregulated proteins, including members of the OAS, IFIT, and MX1 families. Using label-free proteomics, we show that MODY-associated mutations in HNF1A and HNF1B suppress mitochondrial function and interferon signaling and are additionally associated with reduced abundance of predicted targets such as A1CF as well as diabetes-related proteins including SCGN, supporting their role in diabetes pathogenesis. - Source: PubMed
Publication date: 2026/08/05
Kuznetsova Ksenia GVašíček JakubSkiadopoulou DafniUnger LucasNethala Rachel AnandWierer MichaelGhila LuizaJohansson StefanNjølstad Pål RasmusChera SimonaJohansson Bente BergManning AlisaVaudel Marc - Maturity-onset diabetes of the young (MODY) is a heterogeneous monogenic diabetes category caused by defects in genes involved in pancreatic β-cell development, glucose sensing, or insulin secretion. In children, adolescents, and young adults, its clinical presentation may overlap with type 1 diabetes (T1D) or early-onset type 2 diabetes (T2D), which can complicate etiological classification. - Source: PubMed
Publication date: 2026/07/14
Rouzimaimaiti AibibaiZaiyinati JiazireyaMa YanrongMa FuhuiMa RuiHu YanGuo Yanying - Monogenic diabetes covers single-variant inherited subtypes of diabetes, of which the most prevalent are HNF4A-MODY (MODY1), GCK-MODY (MODY2), HNF1A-MODY (MODY3), HNF1B-MODY (MODY5) and mitochondrial diabetes. Together, they account for about 1% of diabetes cases, but more than 70% of affected individuals are classified with other forms of diabetes. The classical phenotype is young-onset, non-autoimmune diabetes with partially preserved insulin secretion and a family history of diabetes. Correct genetic diagnosis is crucial for family counselling and optimal diabetes management, as reviewed in this article. - Source: PubMed
Publication date: 2026/06/22
Svendstrup MathildeJensen Johanne SkovThuesen Anne Cathrine BaunMaagensen HenrikHansen TorbenStøy JulieVilsbøll Tina - Maturity-onset diabetes of the young (MODY) is a rare monogenic form of diabetes characterized by impaired insulin secretion and genetic and clinical heterogeneity. Accurate molecular diagnosis enables precision medicine by guiding gene-specific treatment, improving glycemic control, and avoiding unnecessary therapies. Since our previous systematic review in 2020, new studies have further clarified therapeutic strategies and emerging treatment options. This review updates the evidence on pharmacological management of MODY and its clinical implications. - Source: PubMed
Publication date: 2026/06/15
Zagaroli LucaDi Berardino AlessioPetragnano FrancescoLustri SerenaFasciani IreneRossi MarioBaroni Marco GDelvecchio Maurizio