ArticleMolecular & cellular proteomics : MCP2009
A mediator of Rho-dependent invasion moonlights as a methionine salvage enzyme.
Article in Molecular & cellular proteomics : MCP, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.
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Who cites it
11 citing papers in PubMed, 14 citations in OpenAlex.
- A functional missense variant iniScience · 2026Article
- Revisiting the methionine salvage pathway and its paralogues.Microbial biotechnology · 2019Article
- Rapid proteomic analysis for solid tumors reveals LSD1 as a drug target in an end-stage cancer patient.Molecular oncology · 2018Article
- Metabolic heterogeneity of idiopathic pulmonary fibrosis: a metabolomic study.BMJ open respiratory research · 2017Article
- Epigenome variation in severe asthma.Biological research for nursing · 2015Article
- Effects of human arylamine N-acetyltransferase I knockdown in triple-negative breast cancer cell lines.Cancer medicine · 2015Article
- Structural and biochemical basis for the inhibition of cell death by APIP, a methionine salvage enzyme.Proceedings of the National Academy of Sciences of the United States of America · 2014Article
- Structure of mediator of RhoA-dependent invasion (MRDI) explains its dual function as a metabolic enzyme and a mediator of cell invasion.Biochemistry · 2013Article
- Carbon monoxide: impact on remethylation/transsulfuration metabolism and its pathophysiologic implications.Journal of molecular medicine (Berlin, Germany) · 2012Review
- Functional identification of APIP as human mtnB, a key enzyme in the methionine salvage pathway.PloS one · 2012Article
- RhoA and RhoC are both required for the ROCK II-dependent promotion of centrosome duplication.Oncogene · 2010Article
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Authors and funding
15 authors at 4 institutions in 1 country.
Funding
Abstract
RhoA controls changes in cell morphology and invasion associated with cancer phenotypes. Cell lines derived from melanoma tumors at varying stages revealed that RhoA is selectively activated in cells of metastatic origin. We describe a functional proteomics strategy to identify proteins regulated by RhoA and report a previously uncharacterized human protein, named "mediator of RhoA-dependent invasion (MRDI)," that is induced in metastatic cells by constitutive RhoA activation and promotes cell invasion. In human melanomas, MRDI localization correlated with stage, showing nuclear localization in nevi and early stage tumors and cytoplasmic localization with plasma membrane accentuation in late stage tumors. Consistent with its role in promoting cell invasion, MRDI localized to cell protrusions and leading edge membranes in cultured cells and was required for cell motility, tyrosine phosphorylation of focal adhesion kinase, and modulation of actin stress fibers. Unexpectedly MRDI had enzymatic function as an isomerase that converts the S-adenosylmethionine catabolite 5-methylribose 1-phosphate into 5-methylribulose 1-phosphate. The enzymatic function of MRDI was required for methionine salvage from S-adenosylmethionine but distinct from its function in cell invasion. Thus, mechanisms used by signal transduction pathways to control cell movement have evolved from proteins with ancient function in amino acid metabolism.
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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.