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

Impaired glucose homeostasis and neonatal mortality in hepatocyte nuclear factor 3alpha-deficient mice.

Proceedings of the National Academy of Sciences of the United States of America - 31 Aug 1999

Shih D Q, Navas M A, Kuwajima S, Duncan S A, Stoffel M

Abstract excerpt

Hepatocyte nuclear factors 3 (HNF-3) belong to an evolutionarily conserved family of transcription factors that are critical for diverse biological processes such as development, differentiation, and metabolism. To study the physiological role of HNF-3alpha, we generated mice that lack HNF-3alpha by homologous recombination in embryonic stem cells. Mice homozygous for a null mutation in the HNF-3alpha gene...

Read the complete abstract on PubMed

Topics

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

Share to Animals, Newborn
Share to Feeding and Eating Disorders

Methodology Data sources Editorial policy Privacy Delete account & data About Contact Helena Bioinformatics

Share to Feeding Behavior

Share to Hepatocyte Nuclear Factor 3-alpha

Share to Hypoglycemia

Share to Pancreas

Share to Starvation

Share to Triglycerides

Source

Open in PubMed Open full text

Identifiers

PMID: 10468578
DOI: 10.1073/pnas.96.18.10152
PMCID: PMC17858

Provenance

PubMed metadata and Literature Corpus relationships. Corpus snapshot updated 7 Sept 2026. Manifest publication-graph-cohort-2026-09-08.1.

Source receipt: pubmed, retrieved 7 Sept 2026.

Related research

Semantic proximity does not establish scientific evidence. Graph snapshot: 2026-09-29.

Research trail→

Click a neighbor to travelStep 1 · 12 closest

Impaired glucose homeostasis and neonatal mortality in hepatocyte nuclear factor 3alpha-deficient mice.PMID 10468578Read ↗

Regulation of a transcription factor network required for differentiation and metabolism.Semantic proximity Read ↗

Profound defects in pancreatic beta-cell function in mice with combined heterozygous mutations in Pdx-1, Hnf-1alpha, and Hnf-3beta.Semantic proximity Read ↗

Foxa3 (hepatocyte nuclear factor 3gamma ) is required for the regulation of hepatic GLUT2 expression and the maintenance of glucose homeostasis during a prolonged fast.Semantic proximity Read ↗

Beta-cell-targeted expression of a dominant-negative hepatocyte nuclear factor-1 alpha induces a maturity-onset diabetes of the young (MODY)3-like phenotype in transgenic mice.Semantic proximity Read ↗

The human HNF-3 genes: cloning, partial sequence and mutation screening in patients with impaired glucose homeostasis.Semantic proximity Read ↗

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

Elevated levels of hepatocyte nuclear factor 3beta in mouse hepatocytes influence expression of genes involved in bile acid and glucose homeostasis.Semantic proximity Read ↗

A Hepatocyte FOXN3-α Cell Glucagon Axis Regulates Fasting Glucose.Semantic proximity Read ↗

Mutations in the human genes encoding the transcription factors of the hepatocyte nuclear factor (HNF)1 and HNF4 families: functional and pathological consequences.Semantic proximity Read ↗

The maturity-onset diabetes of the young (MODY1) transcription factor HNF4alpha regulates expression of genes required for glucose transport and metabolism.Semantic proximity Read ↗

Hepatocyte nuclear factor 1, a transcription factor at the crossroads of glucose homeostasis.Semantic proximity Read ↗

Hepatocyte nuclear factor-1 beta mutations cause neonatal diabetes and intrauterine growth retardation: support for a critical role of HNF-1beta in human pancreatic development.Semantic proximity Read ↗

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