ArticleSmall GTPases
Genetic analysis of Ras genes in epidermal development and tumorigenesis.
Article in Small GTPases. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
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Who cites it
9 citing papers in PubMed, 11 citations in OpenAlex.
- Androgen Receptor and Non-Coding RNAs' Interaction in Renal Cell Carcinoma.Non-coding RNA · 2024Review
- Cell-cell communication: new insights and clinical implications.Signal transduction and targeted therapy · 2024Review
- Small molecular inhibitors for KRAS-mutant cancers.Frontiers in immunology · 2023Review
- Loss of miR-143 and miR-145 in condyloma acuminatum promotes cellular proliferation and inhibits apoptosis by targeting NRAS.Royal Society open science · 2018Article
- Oncogenic Ras: A double-edged sword for human epidermal stem and transient amplifying cells.Small GTPases · 2016Review
- The Dishevelled Protein Family: Still Rather a Mystery After Over 20 Years of Molecular Studies.Current topics in developmental biology · 2016Review
- A New View of Ras Isoforms in Cancers.Cancer research · 2016Review
- KRAS and HRAS mutations confer resistance to MET targeting in preclinical models of MET-expressing tumor cells.Molecular oncology · 2015Article
- AJP-Cell theme on "Cell Signaling: Proteins, Pathways and Mechanisms".American journal of physiology. Cell physiology · 2015Article
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3 authors at 2 institutions in 3 countries.
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Abstract
Proliferation and differentiation of epidermal keratinocytes are tightly controlled to ensure proper development and homeostasis of the epidermis. The Ras family of small GTPases has emerged as a central node in the coordination of cell proliferation in the epidermis. Recent genetic evidence from mouse models has revealed that the intensity of Ras signaling modulates the proliferative capacity of epidermal keratinocytes. Interfering with Ras signaling either by combined elimination of the 3 Ras genes from the basal layer of the epidermis or by overexpression of dominant-negative Ras isoforms caused epidermal thinning due to hypoproliferation of keratinocytes. In contrast, overexpression of oncogenic Ras mutants in different epidermal cell layers led to hyperproliferative phenotypes including the development of papillomas and squamous cell carcinomas. Here, we discuss the value of loss- and gain-of-function studies in mouse models to assess the role of Ras signaling in the control of epidermal proliferation.
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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.