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

NSCL-1 and NSCL-2 synergistically determine the fate of GnRH-1 neurons and control necdin gene expression.

The EMBO journal - 27 Oct 2004

Krüger Marcus, Ruschke Karen, Braun Thomas

Abstract excerpt

To study the role of the bHLH genes NSCL-1 and NSCL-2 in the development of GnRH-1 neurons, we have generated compound mutant mice. Mutant animals die at birth and show a virtually complete absence of GnRH-1 neurons in the posterior parts of the brain at E18.5 and an aberrant morphology of the re...

Read the complete abstract on PubMed

Topics

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

Share to Basic Helix-Loop-Helix Transcription Factors
Share to Cell Movement
Share to Embryo, Mammalian

Methodology Data sources Editorial policy Privacy About Contact Helena Bioinformatics

Share to Gene Silencing

Share to Gestational Age

Share to Gonadotropin-Releasing Hormone

Share to Hypothalamus

Share to In Situ Hybridization

Source

Open in PubMed Open full text

Identifiers

PMID: 15470499
DOI: 10.1038/sj.emboj.7600431
PMCID: PMC524395

Provenance

PubMed metadata and Literature Corpus relationships. Corpus snapshot updated 4 Sept 2026. Prepared record publication-15470499-2026-09-04.2. Manifest publication-graph-cohort-2026-09-04.2.

Source receipt: PubMed via Helena Literature Corpus, retrieved 4 Sept 2026.

Related research

Semantic proximity does not establish scientific evidence.

Research trail→

Click a neighbor to travelStep 1 · 12 closest

NSCL-1 and NSCL-2 synergistically determine the fate of GnRH-1 neurons and control necdin gene expression.PMID 15470499Read ↗

Necdin, a Prader-Willi syndrome candidate gene, regulates gonadotropin-releasing hormone neurons during developmentSemantic proximity Read ↗

Loss of the Prader-Willi syndrome protein necdin causes defective migration, axonal outgrowth, and survival of embryonic sympathetic neurons.Semantic proximity Read ↗

Necdin promotes GABAergic neuron differentiation in cooperation with Dlx homeodomain proteins.Semantic proximity Read ↗

Expression and imprinting of MAGEL2 suggest a role in Prader-willi syndrome and the homologous murine imprinting phenotype.Semantic proximity Read ↗

Temporal requirements for ISL1 in sympathetic neuron proliferation, differentiation, and diversificationSemantic proximity Read ↗

Necdin-deficient mice do not show lethality or the obesity and infertility of Prader-Willi syndromeSemantic proximity Read ↗

The mouse Necdin gene is expressed from the paternal allele only and lies in the 7C region of the mouse chromosome 7, a region of conserved synteny to the human Prader-Willi syndrome region.Semantic proximity Read ↗

The Necdin Gene is Deleted in Prader-Willi Syndrome and is Imprinted in Human and MouseSemantic proximity Read ↗

The human necdin gene, NDN, is maternally imprinted and located in the Prader-Willi syndrome chromosomal regionSemantic proximity Read ↗

Disruption of the mouse necdin gene results in early post-natal lethality.Semantic proximity Read ↗

Differentiation and localization of interneurons in the developing spinal cord depends on DOT1L expressionSemantic proximity Read ↗

Type I bHLH Proteins Daughterless and Tcf4 Restrict Neurite Branching and Synapse Formation by Repressing Neurexin in Postmitotic Neurons.Semantic proximity Read ↗

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