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genetic association studies in population of children in Japan: Data suggest that mutations in INS (show INS Proteins), HNF1A, HNF4A (show HNF4A Proteins), and HNF1B (show HNF1B Proteins) likely play critical roles in children with insulin (show INS Proteins)-requiring autoantibody-negative type 1 diabetes in the population studied. (INS (show INS Proteins) = insulin (show INS Proteins); HNF1A = HNF1 homeobox A; HNF4A (show HNF4A Proteins) = hepatocyte nuclear factor 4 alpha (show HNF4A Proteins); HNF1B (show HNF1B Proteins) = HNF1 homeobox B (show HNF1B Proteins))
Carriers of variant p.E508K in HNF1A have a reduced insulin response rather than the increased sensitivity to sulfonylureas seen in patients with MODY3.
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 (show HNF4A Proteins), specifically in subset of individuals with PTV. (MODY (show HNF4A Proteins) = 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 (show INS Proteins) 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 (show SOX9 Proteins) axis.
Twenty-five different variants were identified in GCK (show GCK Proteins) gene (30 probands-61% of positivity), and 7 variants in HNF1A (10 probands-17% of positivity). Fourteen of them were novel (12- GCK (show GCK Proteins) /2- HNF1A ). ACMG guidelines were able to classify a large portion of variants as pathogenic (36%- GCK (show GCK Proteins) /86%- HNF1A ) and likely pathogenic (44%- GCK (show GCK Proteins) /14%- HNF1A ), with 16% (5/32) as uncertain significance.
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 (show SPHK2 Proteins), neutral ceramidase, and ceramide synthase-5 (show LASS5 Proteins).
This is attributed in part to ineffective repression of Tcf1 expression in knockout T cells, as DNMT3a (show DNMT3A Proteins) localizes to the Tcf7 (show TCF7 Proteins) promoter and catalyzes its de novo methylation in early effector WT CD8 (show CD8A Proteins)(+) T cells. These data identify DNMT3a (show DNMT3A Proteins) as a crucial regulator of CD8 (show CD8A Proteins)(+) early effector cell differentiation and effector versus memory fate decisions.
We identified PD-1 (show PDCD1 Proteins) to be specifically expressed in PLZF (show ZBTB16 Proteins)(+) ILCp and revealed that the timing and order of expression of the transcription factors NFIL3 (show NFIL3 Proteins), ID2, and TCF-1 was critical. Importantly, induction of ILC (show CCL27 Proteins) lineage commitment required only transient expression of NFIL3 (show NFIL3 Proteins) prior to ID2 and TCF-1 expression.
Knockdown of MACF1 in osteoblastic cells inhibits osteoblast differentiation through suppressing the beta-catenin (show CTNNB1 Proteins)/TCF1-Runx2 (show RUNX2 Proteins) axis.
Lef1 (show LEF1 Proteins) 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 (show CD8A Proteins)(+) 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 (show MLXIP Proteins)-24-TCF1 pathway in controlling effector cytokine production by T cells and further suggest miR (show MLXIP Proteins)-24 could function as a key upstream molecule regulating TCF1-mediated immune responses.
HNF1alpha plays a crucial role in hepatocyte lipid metabolism and hepatocarcinogenesis
pigs harboring the dominant-negative mutant human MODY3 gene showed reproducible and distinct glomerular nodules.
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