ArticleJournal of the American Society of Nephrology : JASN2009
Loss of Sprouty1 rescues renal agenesis caused by Ret mutation.
Article in Journal of the American Society of Nephrology : JASN, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers.
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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
28 citing papers in PubMed, 53 citations in OpenAlex.
- SPRY1 Interaction with CBL Promotes Vimentin Stabilization to Enhance Malignant Progression and Metastasis in Wilms Tumor.Annals of surgical oncology · 2025Article
- Sprouty1 is a broad mediator of cellular senescence.Cell death & disease · 2024Article
- Regulation of nephron progenitor cell lifespan and nephron endowment.Nature reviews. Nephrology · 2022Review
- A dominant negative mutation uncovers cooperative control of caudal Wolffian duct development by Sprouty genes.Cellular and molecular life sciences : CMLS · 2022Article
- The biomechanical basis of biased epithelial tube elongation in lung and kidney development.Development (Cambridge, England) · 2021Article
- Review
- Organ-Specific Branching Morphogenesis.Frontiers in cell and developmental biology · 2021Review
- Expression Analysis of GDNF/RET Signaling Pathway in Human AD-MSCs Grown in HEK 293 Conditioned Medium (HEK293-CM).Cell biochemistry and biophysics · 2020Article
- Identification of a five-mRNA signature as a novel potential prognostic biomarker in pediatric Wilms tumor.Molecular genetics & genomic medicine · 2020Article
- Sprouty1 Controls Genitourinary Development via its N-Terminal Tyrosine.Journal of the American Society of Nephrology : JASN · 2019Article
- MAPK/ERK Signaling in Regulation of Renal Differentiation.International journal of molecular sciences · 2019Review
- FAT4 Fine-Tunes Kidney Development by Regulating RET Signaling.Developmental cell · 2019Article
- Regulation of Renal Differentiation by Trophic Factors.Frontiers in physiology · 2018Review
- Nephron number, hypertension, and CKD: physiological and genetic insight from humans and animal models.Physiological genomics · 2017Review
- 7-dehydrocholesterol efficiently supports Ret signaling in a mouse model of Smith-Opitz-Lemli syndrome.Scientific reports · 2016Article
- NEDL2 regulates enteric nervous system and kidney development in its Nedd8 ligase activity-dependent manner.Oncotarget · 2016Article
- Glial cell line-derived neurotrophic factor induces cell proliferation in the mouse urogenital sinus.Molecular endocrinology (Baltimore, Md.) · 2015Article
- To bud or not to bud: the RET perspective in CAKUT.Pediatric nephrology (Berlin, Germany) · 2014Review
- Article
- Article
Corrections and comments
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Authors and funding
6 authors at 2 institutions in 3 countries.
Funding
Abstract
Renal morphogenesis requires a balance between positive and negative signals, which are provided in part by the receptor tyrosine kinase Ret and the putative tumor suppressor Sprouty1, respectively. Tyrosine 1062 of Ret is a binding site for several adaptor and effector proteins, such as Grb2/Sos/Ras, which activate the ERK pathway. Mice lacking Ret tyrosine 1062 nearly mimic the phenotype of Ret-knockout mice, which includes renal agenesis. Sprouty1 regulates Ret activity by modulating the ERK pathway, but the mechanism by which this occurs is uncertain. Here, we show that loss of Sprouty1 rescues the renal agenesis and early postnatal lethality caused by lack of Ret tyrosine 1062. The kidneys and lower urinary tracts of double-mutant mice developed normally. This effect was specific to the urinary system, because loss of Sprouty1 did not rescue the defects in the enteric nervous system characteristic of animals lacking Ret tyrosine 1062. These results suggest that Sprouty1 can modulate ERK signaling downstream of Ret, independent of Grb2/Sos/Ras, during renal morphogenesis.
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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.