Monoclonal Mouse HNF1A Antibody
- Known as:
- Monoclonal Mouse HNF1A Antibody
- Catalog number:
- abx000058
- Product Quantity:
- EUR
- Category:
- -
- Supplier:
- Abbexa
- Gene target:
- Monoclonal Mouse HNF1A Antibody
Related genes to: Monoclonal Mouse HNF1A Antibody
- 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
Related products to: Monoclonal Mouse HNF1A Antibody
Related articles to: Monoclonal Mouse HNF1A Antibody
- Adoptive T cell therapies typically rely on ex vivo CD3/CD28 stimulation, which promotes effector differentiation and limits the persistence of transferred cells. Stem cell-like memory T cells (Tscm), with their capacity for self-renewal and multipotency, represent an ideal therapeutic subset but remain difficult to generate at scale. Here, we present a CD3-independent strategy using artificial antigen-presenting cells expressing a membrane-bound CD28 superagonist (αCD28-aAPCs) to expand CD8 T cells with Tscm-like features. In naïve CD8 T cells, αCD28-aAPC stimulation initiates a distinct transcriptional and epigenetic program, marked by high TCF1 expression, metabolic fitness, and resistance to exhaustion-key hallmarks of the Tscm phenotype. Mechanistically, this approach circumvents canonical CD3/TCR signaling and notably avoids induction of IRF4, a key transcription factor that drives BLIMP1 upregulation, TCF1 downregulation, and glycolytic commitment during effector differentiation. Instead, sustained CD28 signaling alone reprograms T cells toward a Tscm-like state. Upon subsequent antigen encounter and CD3 engagement, these αCD28-aAPC-expanded T cells mount robust effector responses while retaining superior persistence and antitumor activity in preclinical models. Our findings reveal an underappreciated role of CD28 signaling in guiding Tscm-like fate through IRF4 suppression and establish a platform for generating durable and functionally potent T cell therapies. - Source: PubMed
Publication date: 2026/04/21
Ihara FumieOhashi YotaZheng Evey Y FFukao SaoriRodrigo RowenaNoamani BabakBoukhaled Giselle MWang Ben XHan Dong-HoonWei XinyuBurt Brian DSaso KayokoMatsunaga YukikoLy DalamKagoya YukiButler Marcus OMak Tak WSaibil Samuel DHirano Naoto - Cytokines and chemokines are central mediators of inflammation and immune dysregulation in diabetes mellitus, linking metabolic stress to tissue injury across diverse disease types and complications. In type 1 diabetes (T1D), pro-inflammatory cytokines such as IL-1β, TNF-α, and IFN-γ drive autoimmune β-cell destruction, amplified by chemokines like CXCL10 that recruit autoreactive T cells. In type 2 diabetes (T2D), obesity-associated metaflammation is characterized by chronic low-grade elevations in IL-6, IL-1β, TNF-α, and chemokines, including CCL2, which promote insulin resistance and β-cell stress. Gestational diabetes (GDM) reflects heightened placental cytokine and chemokine signaling, particularly TNF-α, IL-6, and CCL2, impacting maternal metabolism and fetal programming. While monogenic diabetes (MODY) generally lacks a strong inflammatory signature, emerging evidence suggests that specific subtypes (e.g., HNF1A-MODY) may engage unique cytokine axes. Across complications, including diabetic retinopathy, nephropathy, neuropathy, cardiomyopathy, and macrovascular disease, distinct cytokine/chemokine networks orchestrate fibrosis, leukocyte infiltration, neovascularization, and endothelial dysfunction. Therapeutic interventions targeting these pathways (e.g., IL-1β antagonists, CCR2 inhibitors, IL-17/IL-23 blockade) show promise, yet translation to routine clinical use remains limited by modest efficacy and safety concerns. This review synthesizes current evidence, highlights cytokine/chemokine-driven mechanisms across diabetes forms and complications, and discusses emerging therapeutic strategies and biomarker opportunities for precision medicine. - Source: PubMed
Publication date: 2026/04/08
Lu TinglinQiang WeidongYe Qingqing - Congenital hyperinsulinism (CHI) is the commonest cause of persistent hypoglycaemia in neonates and infants (blood glucose <3.0 mmol/L in first 2-3 days of life; <3.5 mmol/L after 3 days of life). Diazoxide demonstrates variable efficacy depending on the underlying genetic variant and clinical phenotype. Diazoxide has been associated with side effects that are likely dose dependent. This narrative review synthesizes current evidence on diazoxide's pharmacokinetics and side effect profile to support the development of individualised dosing strategies guided by genotype and patient-specific risk factors, with the aim of optimizing therapeutic outcomes and minimizing adverse effects. - Source: PubMed
Publication date: 2026/03/30
Wong TeresaChan DanielChua CherieCher WenqiLim SelinaChandran SureshYap Fabian - The TITANIA (mulTi omIcs daTa cANcer dIagnostics therApies) study is an international collaboration to generate high-quality multi-omics cancer profiles. We conducted an exploratory investigation within this framework to understand the molecular basis of lymphovascular invasion (LVI), a critical determinant of metastatic potential in clear cell renal cell carcinoma (ccRCC). We analyzed 31 ccRCC specimens (11 LVI+, 20 LVI-) from the National Cancer Center Hospital East using whole-genome sequencing, RNA sequencing, and proteomic profiling. Our findings were integrated with public single-cell RNA sequencing (GSE159115) and spatial transcriptomics (GSE175540) datasets to provide a broader biological context. LVI+ tumors consistently showed a distinctive hepatic-lineage gene expression signature, with significant upregulation of aldolase B (ALDOB) and other liver-specific metabolism genes at both the RNA and protein levels. Single-cell analysis identified a previously unrecognized hepatic-differentiated tumor subpopulation expressing master transcription factors HNF1A and HNF4A, which was positioned at the terminal stages of tumor evolution. Comparison with established hepatocyte gene signatures from three independent databases confirmed enrichment of hepatic metabolic programs in this subpopulation. Spatial transcriptomics revealed preferential localization within hypoxic tumor regions. A metabolic program resembling hepatic lineage differentiation, associated with aggressive disease features including LVI and hypoxic microenvironments, offers preliminary insights into renal cancer progression and potential biomarker development. This is a discovery-based, hypothesis-generating study; all findings require independent functional validation before clinical application. - Source: PubMed
Yajima ShugoTsukada YuichiroYamashita RiuFujisawa TakaoKuwata TakeshiWatanabe ReikoIshii GenichiroGabelia NinaJuhl HartmutKoga YoshikatsuYoshino TakayukiIto MasaakiMasuda Hitoshi - Maturity-onset diabetes of the young (MODY) is a monogenic type of diabetes caused by different pathogenic genetic variants in glucose metabolism-related genes, with GCK-MODY and HFN1A-MODY subtypes being the most frequent. Diagnosing the specific MODY subtype is essential for correct treatment and follow-up, but it requires gene sequencing, a time-consuming and costly process that depends on highly skilled professionals. Therefore, it is mandatory to develop tools that allow to correctly determine in which order to study the involved genes, reducing the number of sequencing procedures to find the causal variant and making the diagnostic process more efficient. This proof-of-concept study evaluates machine learning as a complement to clinical characterization and genetic testing, by optimizing binary classification models for explainable prediction of MODY subtypes, with a focus on GCK-MODY and HFN1A-MODY. - Source: PubMed
Publication date: 2026/03/26
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