ArticleThe Journal of biological chemistry2011
RET modulates cell adhesion via its cleavage by caspase in sympathetic neurons.
Article in The Journal of biological chemistry, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 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
10 citing papers in PubMed, 22 citations in OpenAlex.
- Targeting the RET tyrosine kinase in neuroblastoma: A review and application of a novel selective drug design strategy.Biochemical pharmacology · 2023Review
- Caspase Cleavage of Receptor Tyrosine Kinases in the Dependence Receptor Family.Biomolecules & therapeutics · 2023Review
- Role of Glycans on Key Cell Surface Receptors That Regulate Cell Proliferation and Cell Death.Cells · 2021Review
- Proteolytic Cleavage of Receptor Tyrosine Kinases.Biomolecules · 2021Review
- Key genes of renal tubular necrosis: a bioinformatics analysis.Translational andrology and urology · 2020Article
- Brain ischemia downregulates the neuroprotective GDNF-Ret signaling by a calpain-dependent mechanism in cultured hippocampal neurons.Cell death & disease · 2015Article
- Promoter CpG island methylation of RET predicts poor prognosis in stage II colorectal cancer patients.Molecular oncology · 2014Article
- Receptor tyrosine kinases in the nucleus.Cold Spring Harbor perspectives in biology · 2013Review
- Segmental aganglionosis (zonal aganglionosis or "skip" lesions) in Hirschsprungs disease: a report of 2 unusual cases.Pediatric surgery international · 2013Article
- Mitochondria-targeted nitroxide, Mito-CP, suppresses medullary thyroid carcinoma cell survival in vitro and in vivo.The Journal of clinical endocrinology and metabolism · 2013Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
4 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
RET is a tyrosine kinase receptor involved in numerous cellular mechanisms including proliferation, neuronal navigation, migration, and differentiation upon binding with glial cell derived neurotrophic factor family ligands. RET is an atypical tyrosine kinase receptor containing four cadherin domains in its extracellular part. Furthermore, it has been shown to act as a dependence receptor. Such a receptor is active in the absence of ligand, triggering apoptosis through a mechanism that requires receptor intracellular caspase cleavage. However, different data suggest that RET is not always associated with the cell death/survival balance but rather provides positional information. We demonstrate here that caspase cleavage of RET is involved in the regulation of adhesion in sympathetic neurons. The cleavage of RET generates an N-terminal truncated fragment that functions as a cadherin accessory protein, modifying cadherin environment and potentiating cadherin-mediated cell aggregation. Thus, the caspase cleavage of RET generates two RET fragments: one intracellular domain that can trigger cell death in apoptotic permissive settings, and one membrane-anchored ectodomain with cadherin accessory activity. We propose that this latter function may notably be important for the adequate development of the superior cervical ganglion.
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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.