ArticleThe Journal of clinical investigation2010
Organotypic specificity of key RET adaptor-docking sites in the pathogenesis of neurocristopathies and renal malformations in mice.
Article in The Journal of clinical investigation, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 34 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.
The trial behind it
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
34 citing papers in PubMed, 58 citations in OpenAlex.
- GFRA4 improves the neurogenic potential of enteric neural crest stem cells via hedgehog pathway.Pediatric research · 2024Article
- RET signaling in breast cancer therapeutic resistance and metastasis.Breast cancer research : BCR · 2023Review
- A Single RET Mutation in Hirschsprung Disease Induces Intestinal Aganglionosis Via a Dominant-Negative Mechanism.Cellular and molecular gastroenterology and hepatology · 2023Article
- Hirschsprung's disease: key microRNAs and target genes.Pediatric research · 2022Article
- Expanding the novel MAPKAPK5-related developmental disorder's genotype-phenotype correlation: Patient report and 19 months of follow-up.Clinical genetics · 2022Article
- Multidisciplinary approaches for elucidating genetics and molecular pathogenesis of urinary tract malformations.Kidney international · 2022Review
- Multiple Roles of Ret Signalling During Enteric Neurogenesis.Frontiers in molecular neuroscience · 2022Article
- A coordinated progression of progenitor cell states initiates urinary tract development.Nature communications · 2021Article
- MiR-195-5p inhibits proliferation and invasion of nerve cells in Hirschsprung disease by targeting GFRA4.Molecular and cellular biochemistry · 2021Article
- ChIP-Seq-Based Approach in Mouse Enteric Precursor Cells Reveals New Potential Genes with a Role in Enteric Nervous System Development and Hirschsprung Disease.International journal of molecular sciences · 2020Article
- Article
- MAPK/ERK Signaling in Regulation of Renal Differentiation.International journal of molecular sciences · 2019Review
- The GDNF Family: A Role in Cancer?Neoplasia (New York, N.Y.) · 2018Review
- Regulation of Renal Differentiation by Trophic Factors.Frontiers in physiology · 2018Review
- Article
- 7-dehydrocholesterol efficiently supports Ret signaling in a mouse model of Smith-Opitz-Lemli syndrome.Scientific reports · 2016Article
- miRNA Profiling Reveals Dysregulation of RET and RET-Regulating Pathways in Hirschsprung's Disease.PloS one · 2016Article
- Yap and Taz are required for Ret-dependent urinary tract morphogenesis.Development (Cambridge, England) · 2015Article
- Receptor tyrosine kinase signaling: regulating neural crest development one phosphate at a time.Current topics in developmental biology · 2015Review
- To bud or not to bud: the RET perspective in CAKUT.Pediatric nephrology (Berlin, Germany) · 2014Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
7 authors at 3 institutions in 1 country.
Funding
Abstract
The receptor tyrosine kinase ret protooncogene (RET) is implicated in the pathogenesis of several diseases and in several developmental defects, particularly those in neural crest-derived structures and the genitourinary system. In order to further elucidate RET-mediated mechanisms that contribute to these diseases and decipher the basis for specificity in the pleiotropic effects of RET, we characterized development of the enteric and autonomic nervous systems in mice expressing RET9 or RET51 isoforms harboring mutations in tyrosine residues that act as docking sites for the adaptors Plcgamma, Src, Shc, and Grb2. Using this approach, we found that development of the genitourinary system and the enteric and autonomic nervous systems is dependent on distinct RET-stimulated signaling pathways. Thus, mutation of RET51 at Y1062, a docking site for multiple adaptor proteins including Shc, caused distal colon aganglionosis reminiscent of Hirschsprung disease (HSCR). On the other hand, this mutation in RET9, which encodes an isoform that lacks the Grb2 docking site present in RET51, produced severe abnormalities in multiple organs. Mutations that abrogate RET-Plcgamma binding, previously shown to produce features reminiscent of congenital anomalies of kidneys or urinary tract (CAKUT) syndrome, produced only minor abnormalities in the nervous system. Abrogating RET51-Src binding produced no major defects in these systems. These studies provide insight into the basis of organotypic specificity and redundancy in RET signaling within these unique systems and in diseases such as HSCR and CAKUT.
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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.