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analysis of KRT81 and HNF1A expression by IHC is a reliable way to identify biologically relevant subtypes of PDAC that could easily be integrated into common pathologic practice.
HNF1A MODY is the probable etiology of diabetes in this case while highlighting the complex clinical and genetic interplay involved in accurately identifying a diabetes phenotype in ethnic minority populations.
In 263 Japanese partients with suspected maturity-onset diabetes of the young, mutations were identified in 103 (39.2%) patients: 57 mutations in GCK; 29, HNF1A; 7, HNF4A; and 10, HNF1B.
heterogeneous clinical phenotypes of hyperinsulinism
The prevalence of HNF1A mutation was relatively lower in Mainland China and HNF4A mutation was rare in a population of maturity-onset diabetes of the Young.
Maturity Onset Diabetes of the Young due to Glucokinase, HNF1-A, HNF1-B, and HNF4-A Mutations in a Cohort of Turkish Children Diagnosed as Type 1 Diabetes Mellitus.
TCF1 expression marks self-renewing human CD8(+) T cells.
This can be seen with dramatic impact on clinical care, in patients with genetic forms of diabetes such as Maturity Onset Diabetes of the Young caused by HNF1A mutations, and Neonatal diabetes due to activating mutations in ABCC8 or KCNJ11
HNF1A genetic variants were associated with both Diabetes and Coronary Artery Disease .
we established an HNF1A-dependent gene signature in PDA cells that significantly correlated with reduced survivability in patients. These findings identify HNF1A as a central transcriptional regulator of PCSC properties and novel oncogene in PDA
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.
Ezh2 is recruited by Tcf1 to directly activate Bcl6 transcription, with this function requiring Ezh2 phosphorylation at Ser21.
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.
HNF1alpha plays a crucial role in hepatocyte lipid metabolism and hepatocarcinogenesis
HNF1alpha plays a key role in the constitutive expression of megalin and cubilin, hence regulating endocytosis in the proximal tubule of the kidney.
Our data demonstrate that HNF1A is an important cell-intrinsic transcription factor in adult B lymphopoiesis
HNF1alpha, but not HNF1beta, is the primary positive regulator of PCSK9 transcription in mouse liver
Deletion of intestinal SIRT1 impairs DCoH2-HNF-1alpha-FXR signaling and alters systemic bile acid homeostasis.
the data strongly supports a critical role for HNF4a and Hnf1a in the tissue-specific regulation of drug handling and differentiation toward a PT-like cellular identity.
Among all Muc5ac regulators, only GATA-6 and HNF-4a expression was concomitant to that of Muc5ac in the developing stomach.
HNF1alpha might regulate beta-cell mass or function at least partly by modulating Hgfac expression.
Dynamic changes in gene expression occur on pancreatitis induction, determining altered exocrine and endocrine function. This analysis uncovers roles for Hnf1alpha in the regulation of acinar cell determination and function.
Sp1, CREB, HNF-1, and NF-Y, known to be responsive to hormones and diet, regulate NAGS transcription
The miR-192/-194 cluster was markedly down-regulated in liver of Tcf1(-/-) mice.
Hepatic nuclear factor 1alpha (HNF1alpha) dysfunction down-regulates X-box-binding protein 1 (XBP1) and sensitizes beta-cells to endoplasmic reticulum stress.
a critical link between HNF1A-MODY-induced alterations in Bmp-3 expression and insulin gene levels
Hnf1-alpha regulates MafA in beta-cells and compromised MafA expression contributes to beta-cell dysfunction in maturity onset diabetes of young mice.
These findings reveal a novel nutrient-dependent interaction between Sirt1 and HNF-1alpha which results in regulation of Crp expression.
Data indicate that HNF1alpha is a more potent activator of AFM promoter than is HNF1beta.
Although the phenotype of the Hnf1a-null mouse is complex, metabolomics has opened the door to investigation of several physiological systems in which Hnf1alpha may be a critical regulatory component.
HNF1alpha directly regulates the expression of ClC-5 in the renal proximal tubule
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