ArticleGenes & development2006
Critical and distinct roles for key RET tyrosine docking sites in renal development.
Article in Genes & development, 2006. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 78 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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Who cites it
78 citing papers in PubMed, 161 citations in OpenAlex.
- Complete ureteral duplication with occult calculi: A case report.Experimental and therapeutic medicine · 2026Article
- Synthetic budding morphogenesis by optogenetic receptor tyrosine kinase signaling.bioRxiv : the preprint server for biology · 2026Article
- Dose-Dependent and Non-Autonomous Signaling in CAKUT: A Lineage-Specific Framework from Conditional Knockout Studies.Biomolecules · 2026Review
- Modeling development of genitourinary birth defects to understand disruption due to changes in gene dosage.American journal of clinical and experimental urology · 2022Review
- Pulling back the curtain: The hidden functions of receptor tyrosine kinases in development.Current topics in developmental biology · 2022Article
- Intrauterine Low-Protein Diet Exacerbates Abnormal Development of the Urinary System inKidney diseases (Basel, Switzerland) · 2021Article
- A coordinated progression of progenitor cell states initiates urinary tract development.Nature communications · 2021Article
- New imaging tools to measure nephron numberJournal of developmental origins of health and disease · 2021Review
- Review
- Article
- Developmental pathology of congenital kidney and urinary tract anomalies.Clinical kidney journal · 2019Article
- MAPK/ERK Signaling in Regulation of Renal Differentiation.International journal of molecular sciences · 2019Review
- Development of the urogenital system is regulated via the 3'UTR of GDNF.Scientific reports · 2019Article
- FAT4 Fine-Tunes Kidney Development by Regulating RET Signaling.Developmental cell · 2019Article
- MAPK and PI3K signaling: At the crossroads of neural crest development.Developmental biology · 2018Review
- Centrosome amplification disrupts renal development and causes cystogenesis.The Journal of cell biology · 2018Article
- Sox11 gene disruption causes congenital anomalies of the kidney and urinary tract (CAKUT).Kidney international · 2018Article
- Reciprocal Spatiotemporally Controlled Apoptosis Regulates Wolffian Duct Cloaca Fusion.Journal of the American Society of Nephrology : JASN · 2018Article
- Regulation of Renal Differentiation by Trophic Factors.Frontiers in physiology · 2018Review
- The contribution of branching morphogenesis to kidney development and disease.Nature reviews. Nephrology · 2016Review
18 more citing papers are in PubMed but not listed here.
Corrections and comments
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
Abstract
Molecular mechanisms that lead to congenital anomalies of kidneys and the lower urinary tract (CAKUT) are poorly understood. To elucidate the molecular basis for signaling specificity of GDNF-mediated RET signaling in kidney development, we characterized mice that exclusively express either the human RET9 or RET51 isoform, or express these isoforms with individual mutations in docking tyrosines for PTB and SH2-domain-containing adaptors Src (Y981), PLCgamma (Y1015), and Shc (Y1062). Our results provide evidence for differential and isoform-specific roles of these docking sites in murine kidney development. Homozygous Ret(RET9) and Ret(RET51) mice were viable and show normally developed kidneys, indicating redundant roles of human RET isoforms in murine kidney development. In the context of the RET51 isoform, only mutation of the docking Tyr 1015 (Y1015F) resulted in severe renal anomalies. These included bilateral megaureters and multicystic kidneys that were caused by supernumerary ureteric buds that fail to separate from the wolffian duct as well as decreased branching morphogenesis. Similar kidney and ureter defects were observed in RET9(Y1015F) mice that contain the Y1015F mutation in the RET9 isoform. Interestingly, loss of RET9(Y1062)-mediated AKT/MAPK activation resulted in renal agenesis or kidney rudiments, whereas mutation of this residue in RET51 had no obvious effect on AKT/MAPK activity and renal development. These results reveal novel roles of key RET-dependent signaling pathways in embryonic kidney development and provide murine models and new insights into the molecular basis for 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.