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

Genetic inversion in mast cell-deficient (Wsh) mice interrupts corin and manifests as hematopoietic and cardiac aberrancy.

The American journal of pathology - 1 Dec 2008

Nigrovic Peter A, Gray Daniel H D, Jones Tatiana, Hallgren Jenny, Kuo Frank C, Chaletzky Blair, Gurish Michael, Mathis Diane, Benoist Christophe, Lee David M

Abstract excerpt

Mast cells participate in pathophysiological processes that range from antimicrobial defense to anaphylaxis and inflammatory arthritis. Much of the groundwork for the understanding of mast cells was established in mice that lacked mast cells through defects in either stem cell factor or its receptor, Kit. Among available strains, C57BL/6-Kit(W-sh) (W(sh)) mice are experimentally advantageous because of their...

Read the complete abstract on PubMed

Topics

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

Share to Chromosome Inversion
Share to Heart

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

Share to Heart Defects, Congenital

Share to Hematopoietic System

Share to Mast Cells

Share to Proto-Oncogene Proteins c-kit

Share to Serine Endopeptidases

Share to Spleen

Source

Open in PubMed Open full text

Identifiers

PMID: 18988802
DOI: 10.2353/ajpath.2008.080407
PMCID: PMC2626381

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

Genetic inversion in mast cell-deficient (Wsh) mice interrupts corin and manifests as hematopoietic and cardiac aberrancy.PMID 18988802Read ↗

Mast cell-deficient W-sash c-kit mutant Kit W-sh/W-sh mice as a model for investigating mast cell biology in vivo.Semantic proximity Read ↗

The Wsh, W57, and Ph Kit Expression Mutations Define Tissue-Specific Control Elements Located Between −23 and −154 kb Upstream of KitSemantic proximity Read ↗

Viable c-Kit(W/W) mutants reveal pivotal role for c-kit in the maintenance of lymphopoiesis.Semantic proximity Read ↗

Deletion of JAM-C, a candidate gene for heart defects in Jacobsen syndrome, results in a normal cardiac phenotype in mice.Semantic proximity Read ↗

A novel Kit gene mutation in CF1 mice involved in the extracellular domain of the KIT protein.Semantic proximity Read ↗

Mast cell-deficient Kit(W-sh) "Sash" mutant mice display aberrant myelopoiesis leading to the accumulation of splenocytes that act as myeloid-derived suppressor cells.Semantic proximity Read ↗

Mast cell hyperplasia, B-cell malignancy, and intestinal inflammation in mice with conditional expression of a constitutively active kit.Semantic proximity Read ↗

W(sh)/W(sh) c-Kit mutant mice possess interstitial cells of Cajal in the deep muscular plexus layer of the small intestine.Semantic proximity Read ↗

Cutting Edge: Genetic Variation Influences FcεRI-Induced Mast Cell Activation and Allergic ResponsesSemantic 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 ↗

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

Differential Effects of RASA3 Mutations on Hematopoiesis are Profoundly Influenced by Genetic Background and Molecular VariantSemantic proximity Read ↗

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