ArticleHuman mutation2014
Mutational and functional analysis of the tumor-suppressor PTPRD in human melanoma.
Article in Human mutation, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers, 1 of them a synthesis that pooled it.
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
22 citing papers in PubMed, 1 synthesis or guideline pooled it, 39 citations in OpenAlex.
- Genetic overlap between endometriosis and endometrial cancer: evidence from cross-disease genetic correlation and GWAS meta-analyses.Cancer medicine · 2018Pooled it
- Glucagon-like peptide-1 receptor (GLP-1R) overexpression defines a distinct immunogenetic subset in primary and metastatic thyroid cancer: implications for GLP-1R agonist therapy.Frontiers in oncology · 2026Article
- Targeted DNA Sequencing of Cutaneous Melanoma Identifies Prognostic and Predictive Alterations.Cancers · 2024Article
- Epigenetic germline variants predict cancer prognosis and risk and distribute uniquely in topologically associating domains.F1000Research · 2023Article
- Seed sequence polymorphism rs2168518 and allele-specific target gene regulation of hsa-miR-4513.Human molecular genetics · 2022Article
- Eight gene mutation-based polygenic hazard score as a potential predictor for immune checkpoint inhibitor therapy outcome in metastatic melanoma.Frontiers in molecular biosciences · 2022Article
- Integration of genome-wide association study and expression quantitative trait locus mapping for identification of endometriosis-associated genes.Scientific reports · 2021Article
- Profile of Basal Cell Carcinoma Mutations and Copy Number Alterations - Focus on Gene-Associated Noncoding Variants.Frontiers in oncology · 2021Article
- IL-6 induces tumor suppressor protein tyrosine phosphatase receptor type D by inhibiting miR-34a to prevent IL-6 signaling overactivation.Molecular and cellular biochemistry · 2020Article
- Protein tyrosine phosphatase receptor type D (PTPRD)-mediated signaling pathways for the potential treatment of hepatocellular carcinoma: a narrative review.Annals of translational medicine · 2020Review
- Article
- PTPRD: neurobiology, genetics, and initial pharmacology of a pleiotropic contributor to brain phenotypes.Annals of the New York Academy of Sciences · 2019Review
- Mapping the protein-protein and genetic interactions of cancer to guide precision medicine.Current opinion in genetics & development · 2019Review
- Negative regulators of STAT3 signaling pathway in cancers.Cancer management and research · 2019Review
- Protein Tyrosine Phosphatases as Potential Regulators of STAT3 Signaling.International journal of molecular sciences · 2018Review
- RAS at the Golgi antagonizes malignant transformation through PTPRκ-mediated inhibition of ERK activation.Nature communications · 2018Article
- Somatic inactivating PTPRJ mutations and dysregulated pathways identified in canine malignant melanoma by integrated comparative genomic analysis.PLoS genetics · 2018Article
- Review
- Phosphatidylinositol 3-Kinase-DNA Methyltransferase 1-miR-1281-Histone Deacetylase 4 Regulatory Axis Mediates Platelet-Derived Growth Factor-Induced Proliferation and Migration of Pulmonary Artery Smooth Muscle Cells.Journal of the American Heart Association · 2018Article
- Protein tyrosine phosphatase receptor-type δ acts as a negative regulator suppressing breast cancer.Oncotarget · 2017Article
Corrections and comments
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Authors and funding
11 authors at 7 institutions in 2 countries.
Funding
Abstract
Protein tyrosine phosphatases (PTPs) tightly regulate tyrosine phosphorylation essential for cell growth, adhesion, migration, and survival. We performed a mutational analysis of the PTP gene family in cutaneous metastatic melanoma and identified 23 phosphatase genes harboring somatic mutations. Among these, receptor-type tyrosine-protein phosphatase delta (PTPRD) was one of the most highly mutated genes, harboring 17 somatic mutations in 79 samples, a prevalence of 21.5%. Functional evaluation of six PTPRD mutations revealed enhanced anchorage-dependent and anchorage-independent growth. Interestingly, melanoma cells expressing mutant PTPRD were significantly more migratory than cells expressing wild-type PTPRD or vector alone, indicating a novel gain-of-function associated with mutant PTPRD. To understand the molecular mechanisms of PTPRD mutations, we searched for its binding partners by converting the active PTPRD enzyme into a "substrate trap" form. Using mass spectrometry and coimmunoprecipitation, we report desmoplakin, a desmosomal protein that is implicated in cell-cell adhesion, as a novel PTPRD substrate. Further analysis showed reduced phosphatase activity of mutant PTPRD against desmoplakin. Our findings identify an essential signaling cascade that is disrupted in melanoma. Moreover, because PTPRD is also mutated in glioblastomas and adenocarcinoma of the colon and lung, our data might be applicable to a large number of human cancers.
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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.