Use your antibodies-online credentials, if available.
No Products on your Comparison List.
Your basket is empty.
Find out more
Show all synonyms
Select your origin of interest
Our data revealed that HNF1A-AS1 is a direct transactivation target of HNF1alpha in HCC cells and involved in the anti-HCC effect of HNF1alpha. HNF1A-AS1 functions as phosphatase activator through the direct interaction with SHP-1.
The results show that individuals with the HNF1A allele might achieve greater benefit with regard to weight loss and improvement of insulin resistance by choosing a hypocaloric and high-fat weight-loss diet than a low-fat diet.
These findings show that HNF4A methylation status in the blood of children is associated with metabolic profiles. Therefore, we suggest that the DNA methylation status might serve as a potential epigenetic biomarkers of metabolic syndrome.
Lower serum miR-122 is a unique feature of HNF1A-diabetes mellitus patients and might partially explain the increased risk for liver neoplasm and abnormal lipid metabolism in HNF1A-DM patients.
HNF1A and ABCC8 are among the most frequently mutated maturity-onset diabetes of the young genes in south India.
genetic association studies in population of children in Japan: Data suggest that mutations in INS, HNF1A, HNF4A, and HNF1B likely play critical roles in children with insulin-requiring autoantibody-negative type 1 diabetes in the population studied. (INS = insulin; HNF1A = HNF1 homeobox A; HNF4A = hepatocyte nuclear factor 4 alpha; HNF1B = HNF1 homeobox B)
Carriers of variant p.E508K in HNF1A have a reduced insulin response rather than the increased sensitivity to sulfonylureas seen in patients with MODY3.
no association of rs7305618 or rs2393791 with polycystic ovary syndrome
genetic association studies in populations in England and France: Data suggest that SNPs (27L allele) in HNF1A are associated with 1.6-year decrease in age at diagnosis of MODY, specifically in subset of individuals with PTV. (MODY = maturity-onset diabetes of the young; PTV = protein-truncating variant) [META-ANALYSIS]
SNPs rs1169288 and rs2464196 of HNF1A gene were significantly associated with metabolic syndrome in a Morrocan population.
The prevalence of maturity onset diabetes of the young due to HNF1A variants in Croatia has been determined.
Germline HNF1A mutations were identified as the cause of autosomal dominant maturity-onset diabetes of the young type 3 (MODY3), a genetic type 2 diabetes occurring in young patients in a familial context. Liver Adenomatosis associated with MODY3 owing to a germline mutation of HNF1A.
HNF1A mutations are associated with MODY 3 phenotype.
Genetic variants in HNF1A gene had significantly decreased pancreas weight and insulin mass similar to that of type 1 diabetes.
In conclusion, these results highlight the potential therapeutic effects of Andro in treatment of chondrosarcoma via targeting the TCF-1/SOX9 axis.
Twenty-five different variants were identified in GCK gene (30 probands-61% of positivity), and 7 variants in HNF1A (10 probands-17% of positivity). Fourteen of them were novel (12- GCK /2- HNF1A ). ACMG guidelines were able to classify a large portion of variants as pathogenic (36%- GCK /86%- HNF1A ) and likely pathogenic (44%- GCK /14%- HNF1A ), with 16% (5/32) as uncertain significance.
HNF-1A plays a critical role in lipid and glucose homeostasis in second trimester of pregnancy
The HNF1A variant p.Ala180Val does not seem to cause MODY3, although it may confer risk for type 2 diabetes mellitus.
the contribution of the Maturity Onset Diabetes of the Young gene HNF1A in the etiology of 23 unrelated Tunisian families
genetic association studies in population in Japan: Data suggest that HNF1A diplotype of three genetic risk variants (SNPs rs1169288-C, rs1183910-A, rs2464196-A) may be independent risk factor for development of diabetic retinopathy resulting from poor glycemic control in normal-weight patients with type 2 diabetes in the population studied.
TCF-1 controls T cell fate is through its widespread ability to target silent chromatin and establish the epigenetic identity of T cells.
Tcf1 binding reduced the activity of a Gzmb-associated regulatory element, and this accounted for the reduced Gzmb expression in Tcf1-expressing NK cells.
Transcriptional analysis revealed 4 important genes involved in sphingolipid metabolism to be deregulated in HNF1A deficiency: Ormdl1, sphingosine kinase-2, neutral ceramidase, and ceramide synthase-5.
This is attributed in part to ineffective repression of Tcf1 expression in knockout T cells, as DNMT3a localizes to the Tcf7 promoter and catalyzes its de novo methylation in early effector WT CD8(+) T cells. These data identify DNMT3a as a crucial regulator of CD8(+) early effector cell differentiation and effector versus memory fate decisions.
We identified PD-1 to be specifically expressed in PLZF(+) ILCp and revealed that the timing and order of expression of the transcription factors NFIL3, ID2, and TCF-1 was critical. Importantly, induction of ILC lineage commitment required only transient expression of NFIL3 prior to ID2 and TCF-1 expression.
Knockdown of MACF1 in osteoblastic cells inhibits osteoblast differentiation through suppressing the beta-catenin/TCF1-Runx2 axis.
Lef1 and Tcf1 showed oncogenic effect in colonic carcinogenesis. Cellular context of miRNAs might play important roles in carcinogenesis by altering the expression pattern of Lef/Tcfs members.
this study found that virus-specific CD8(+) T cells that sustained the T cell response during chronic viral infection are defined by, and depended on, the expression of Tcf1
data demonstrate a novel miR-24-TCF1 pathway in controlling effector cytokine production by T cells and further suggest miR-24 could function as a key upstream molecule regulating TCF1-mediated immune responses.
HNF1alpha plays a crucial role in hepatocyte lipid metabolism and hepatocarcinogenesis
Data show that TCF1 proteindeficiency relieved most manifestations of autoimmune lymphoproliferative syndrome (ALPS)-like phenotype, which were caused by Fas protein mutation in TCF1(-/-) lpr/lpr mice.
Data show that the Wnt-effector hepatocyte nuclear factor 1-alpha (Tcf1) is recruited to and triggers transcription of the Ink4/Arf tumor suppressor locus, such as as p15Ink4b, p16Ink4a and p19Arf.
this study shows that distinct, asynchronous and stage-specific transcription factors (TCF-1, GATA-3 and Runx1) activate Bcl11b for T cell commitment
this study shows that the transcription factors Tcf1 and Lef1 suppress CD4+ T lineage genes in CD8+ T cells through intrinsic histone deacetylase activity
Results show that Tcf1 binding to Zfp703 inhibits beta-catenin/Tcf1 complex formation.
this study shows that Tcf1 short isoforms are adequate in supporting developing thymocytes to traverse through maturation steps and in regulating the expression of most Tcf1 target genes
HNF1alpha plays a key role in the constitutive expression of megalin and cubilin, hence regulating endocytosis in the proximal tubule of the kidney.
leukemic stem cells are therefore more sensitive to loss of Tcf1 and Lef1 than Hematopoietic Stem Cells in their self-renewal capacity.
Sp5/8 bind directly to GC boxes in Wnt target gene enhancers and to adjacent, or distally positioned, chromatin-bound T-cell factor (Tcf) 1/lymphoid enhancer factor (Lef) 1 to facilitate recruitment of beta-catenin to target gene enhancers.
TCF1 is required for the T follicular helper cell response to viral infection functioning through negative feedback loops with IL-2 and Blimp1.
pigs harboring the dominant-negative mutant human MODY3 gene showed reproducible and distinct glomerular nodules.
the g.8260 A>G polymorphism significantly associated with pH 24(H), meat percentage and muscle area in the F Duroc x Pietrain (DuPi, n=313) and with pH 24(L), fat area and backfat thickness in the Pietrain (Pi, n=110) population.
The protein encoded by this gene is a transcription factor required for the expression of several liver-specific genes. The encoded protein functions as a homodimer and binds to the inverted palindrome 5'-GTTAATNATTAAC-3'. Defects in this gene are a cause of maturity onset diabetes of the young type 3 (MODY3) and also can result in the appearance of hepatic adenomas.
HNF1 homeobox A
, albumin proximal factor
, hepatic nuclear factor 1
, hepatocyte nuclear factor 1-alpha
, interferon production regulator factor
, liver-specific transcription factor LF-B1
, transcription factor 1, hepatic
, hepatic nuclear factor (HNF1)
, transcription factor 1, hepatic; LF-B1, hepatic nuclear factor (HNF1), albumin proximal factor
, hepatocyte nuclear factor 1
, transcription factor 1
, LF-B1 hepatic nuclear factor (HNF1): albumin proximal factor also TCF1
, LF-B1, hepatic nuclear factor (HNF1): albumin proximal factor, also TCF1
, Transcription factor 1 hepatic
, Transcription factor 1, hepatic
, hepatic nuclear factor-1-alpha
, hepatocyte nuclear factor 1 alpha