Developmental abnormalities in Steel17H mice result from a splicing defect in the steel factor cytoplasmic tail.

doi:10.1101/gad.6.10.1832

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Article

Developmental abnormalities in Steel17H mice result from a splicing defect in the steel factor cytoplasmic tail.

Genes & development - 1 Oct 1992

Brannan C I, Bedell M A, Resnick J L, Eppig J J, Handel M A, Williams D E, Lyman S D, Donovan P J, Jenkins N A, Copeland N G

Abstract excerpt

The murine dominant White spotting (W) and Steel (Sl) loci encode the c-kit tyrosine kinase receptor and its cognate ligand steel factor (SLF), respectively. Mutations at either locus produce deficiencies in the same three migratory cell populations--those giving rise to pigment cells, germ cells, and blood cells. The identification of the gene products of these two loci combined with the plethora of W and Sl...

Topics

Amino Acid Sequence
Animals
Base Sequence
Blotting, Northern
Cytoplasm
DNA
Embryonic and Fetal Development
Female
Hematopoietic Cell Growth Factors
Homozygote
Male

Methodology Data sources Editorial policy Privacy About Contact Helena Bioinformatics

Mice

Mice, Mutant Strains

Molecular Sequence Data

Mutation

Plasmids

Proto-Oncogene Proteins

Proto-Oncogene Proteins c-kit

Source

Open in PubMed

Identifiers

PMID: 1383087
DOI: 10.1101/gad.6.10.1832

Provenance

PubMed metadata and Literature Corpus relationships. Corpus snapshot updated 29 Aug 2026. Prepared record publication-1383087-2026-08-29.1. Manifest publication-graph-cohort-2026-08-29.1.

Source receipt: PubMed via Helena Literature Corpus, retrieved 29 Aug 2026.

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Developmental abnormalities in Steel17H mice result from a splicing defect in the steel factor cytoplasmic tail.PMID 1383087Read ↗

DNA rearrangements located over 100 kb 5' of the Steel (Sl)-coding region in Steel-panda and Steel-contrasted mice deregulate Sl expression and cause female sterility by disrupting ovarian follicle development.Semantic proximity Read ↗

Altered cell-surface targeting of stem cell factor causes loss of melanocyte precursors in Steel17H mutant mice.Semantic proximity Read ↗

The kit-ligand (steel factor) and its receptor c-kit/W: pleiotropic roles in gametogenesis and melanogenesis.Semantic proximity Read ↗

The presence of novel amino acids in the cytoplasmic domain of stem cell factor results in hematopoietic defects in Steel(17H) mice.Semantic proximity Read ↗

W-sash affects positive and negative elements controlling c-kit expression: ectopic c-kit expression at sites of kit-ligand expression affects melanogenesis.Semantic proximity Read ↗

Role of dimerization of the membrane-associated growth factor kit ligand in juxtacrine signaling: the Sl17H mutation affects dimerization and stability-phenotypes in hematopoiesis.Semantic proximity Read ↗

The kit ligand encoded at the murine Steel locus: a pleiotropic growth and differentiation factor.Semantic proximity Read ↗

A rare complex DNA rearrangement in the murine Steel gene results in exon duplication and a lethal phenotype.Semantic proximity Read ↗

Steel factor and c-kit protooncogene: genetic lessons in signal transduction.Semantic proximity Read ↗

The murine W/c-kit and Steel loci and the control of hematopoiesis.Semantic proximity Read ↗

Loss of the transmembrane but not the soluble kit ligand isoform increases testicular germ cell tumor susceptibility in mice.Semantic proximity Read ↗

Steel-Dickie mutation encodes a c-kit ligand lacking transmembrane and cytoplasmic domains.Semantic proximity Read ↗

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