Discover Community Create You

Loading publication...

Noodle always counts identifier-free feature events for service operation. With your permission, Google Analytics can also estimate audience and engagement. Search text, publication identifiers, cookies, IP addresses and browser fingerprints are never included in Noodle's first-party event counters.

Privacy details

Article

Overexpression of dominant negative mutant hepatocyte nuclear factor (HNF)-1alpha inhibits arginine-induced insulin secretion in MIN6 cells.

Diabetologia - 1 Jul 1999

Tanizawa Y, Ohta Y, Nomiyama J, Matsuda K, Tanabe K, Inoue H, Matsutani A, Okuya S, Oka Y

Abstract excerpt

AIMS/HYPOTHESIS: To explain the mechanisms whereby mutations in the HNF-1alpha gene cause insulin secretory defects. METHODS: A truncated mutant HNF-1alpha (HNF-1alpha288t) was overexpressed in hepatoma cells (HepG2) and murine insulinoma cells (MIN6) using a recombinant adenovirus system and expression of the HNF-1alpha target genes and insulin secretion were examined. RESULTS: Expression of phenylalanine...

Read the complete abstract on PubMed

Topics

Share this publication in a Topic to start or enrich a Post.

Share to Arginine
Share to Hepatocyte Nuclear Factor 1

Methodology Data sources Editorial policy Privacy About Contact Helena Bioinformatics

Share to Hepatocyte Nuclear Factor 1-alpha

Share to Hepatocyte Nuclear Factor 1-beta

Share to Insulin

Share to Insulin Secretion

Share to Nuclear Proteins

Share to Tumor Cells, Cultured

Source

Identifiers

PMID: 10440133
DOI: 10.1007/s001250051242

Provenance

PubMed metadata and Literature Corpus relationships. Corpus snapshot updated 7 Sept 2026. Manifest publication-graph-cohort-2026-09-07.1.

Source receipt: pubmed, retrieved 7 Sept 2026.

Related research

Semantic proximity does not establish scientific evidence.

Research trail→

Click a neighbor to travelStep 1 · 12 closest

Overexpression of dominant negative mutant hepatocyte nuclear factor (HNF)-1alpha inhibits arginine-induced insulin secretion in MIN6 cells.PMID 10440133Read ↗

Molecular targets of a human HNF1 alpha mutation responsible for pancreatic beta-cell dysfunction.Semantic proximity Read ↗

Common variants in HNF-1 alpha and risk of type 2 diabetes.Semantic proximity Read ↗

Hepatocyte nuclear factor-4alpha is essential for glucose-stimulated insulin secretion by pancreatic beta-cells.Semantic proximity Read ↗

Hepatocyte nuclear factor-1alpha modulates pancreatic beta-cell growth by regulating the expression of insulin-like growth factor-1 in INS-1 cells.Semantic proximity Read ↗

Conditional expression of hepatocyte nuclear factor-1beta, the maturity-onset diabetes of the young-5 gene product, influences the viability and functional competence of pancreatic beta-cells.Semantic proximity Read ↗

Roles of HNF1α and HNF4α in pancreatic β-cells: lessons from a monogenic form of diabetes (MODY).Semantic proximity Read ↗

Regulation of human insulin, IGF-I, and multidrug resistance protein 2 promoter activity by hepatocyte nuclear factor (HNF)-1beta and HNF-1alpha and the abnormality of HNF-1beta mutants.Semantic proximity Read ↗

Mutation P291fsinsC in the Transcription Factor Hepatocyte Nuclear Factor-1α is Dominant NegativeSemantic proximity Read ↗

Mitochondrial dysfunction contributes to impaired insulin secretion in INS-1 cells with dominant-negative mutations of HNF-1alpha and in HNF-1alpha-deficient islets.Semantic proximity Read ↗

Contrasting insulin sensitivity of endogenous glucose production rate in subjects with hepatocyte nuclear factor-1beta and -1alpha mutations.Semantic proximity Read ↗

Novel MODY3 mutations in the hepatocyte nuclear factor-1alpha gene: evidence for a hyperexcitability of pancreatic beta-cells to intravenous secretagogues in a glucose-tolerant carrier of a P447L mutation.Semantic proximity Read ↗

A missense mutation in hepatocyte nuclear factor-4 alpha, resulting in a reduced transactivation activity, in human late-onset non-insulin-dependent diabetes mellitus.Semantic proximity Read ↗

⌁Select a neighboring publication to make it the new centre.