ArticleJCI insight2017
Induced haploinsufficiency of Kit receptor tyrosine kinase impairs brain development.
Article in JCI insight, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
9 citing papers in PubMed, 17 citations in OpenAlex.
- Mast Cells in the Developing Brain.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2026Review
- Genetic and molecular factors associated with changes in structural-functional coupling in medication-free obsessive-compulsive disorder.Psychological medicine · 2026Article
- Article
- Metrnl/C-KIT Axis Attenuates Early Brain Injury Following Subarachnoid Hemorrhage by Inhibiting Neuronal Ferroptosis.CNS neuroscience & therapeutics · 2025Article
- Kit Ligand and Kit receptor tyrosine kinase sustain synaptic inhibition of Purkinje cells.eLife · 2024Article
- Immunohistochemistry of Brain Tissues.Methods in molecular biology (Clifton, N.J.) · 2024Article
- Sevoflurane Exposure in Neonates Perturbs the Expression Patterns of Specific Genes That May Underly the Observed Learning and Memory Deficits.International journal of molecular sciences · 2023Article
- Compensatory gene expression potentially rescues impaired brain development in Kit mutant mice.Scientific reports · 2023Article
- Cutting-edge genetics in obsessive-compulsive disorder.Faculty reviews · 2020Review
Corrections and comments
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Kit receptor tyrosine kinase is highly expressed in the developing mammalian brain, yet little is known about its contribution to neural cell development and function. Here we introduced a brain-specific conditional Kit loss-of-function mutation in mice and observed severe hypoplasia of the central nervous system. This was accompanied by an increase in apoptotic cell death in the early embryonic brain and the gradual loss of the self-renewal capacity of neuronal stem/precursor cells. A single copy of the brain-specific conditional Kit loss-of-function allele resulted in the observed phenotype, including impaired in vitro differentiation of neural cells from Kit-haploinsufficient embryonic stem (ES) cells. Our findings demonstrate that Kit signaling is required for the early development of neural cells. This potentially novel Kit-haploinsufficient lethal phenotype may represent an embryonic lethal phenomenon previously unobserved because of its dominantly acting nature.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.