ArticlePloS one2011
MEK2 is sufficient but not necessary for proliferation and anchorage-independent growth of SK-MEL-28 melanoma cells.
Article in PloS one, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 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
17 citing papers in PubMed, 25 citations in OpenAlex.
- ERK pathway reactivation prevents anthrax toxin lethality in mice.Nature microbiology · 2025Article
- ATP depletion in anthrax edema toxin pathogenesis.PLoS pathogens · 2025Article
- Article
- Caspase 3-specific cleavage of MEK1 suppresses ERK signaling and sensitizes cells to stress-induced apoptosis.FEBS open bio · 2023Article
- Investigating a Library of Flavonoids as Potential Inhibitors of a Cancer Therapeutic Target MEK2 Using in Silico Methods.International journal of molecular sciences · 2023Article
- The subversion of toll-like receptor signaling by bacterial and viral proteases during the development of infectious diseases.Molecular aspects of medicine · 2022Review
- Context-Dependent Immunomodulatory Effects of MEK Inhibition Are Enhanced with T-cell Agonist Therapy.Cancer immunology research · 2021Article
- Identification of the transcription factor Miz1 as an essential regulator of diphthamide biosynthesis using a CRISPR-mediated genome-wide screen.PLoS genetics · 2020Article
- Overcoming Resistance to Targeted Anticancer Therapies through Small-Molecule-Mediated MEK Degradation.Cell chemical biology · 2018Article
- Anthrax lethal toxin rapidly reduces c-Jun levels by inhibiting c-Jun gene transcription and promoting c-Jun protein degradation.The Journal of biological chemistry · 2017Article
- Identification of a Substrate-selective Exosite within the Metalloproteinase Anthrax Lethal Factor.The Journal of biological chemistry · 2017Article
- Mitogen-activated Protein Kinase Kinase Activity Maintains Acinar-to-Ductal Metaplasia and Is Required for Organ Regeneration in Pancreatitis.Cellular and molecular gastroenterology and hepatology · 2017Article
- Activation of MEK2 is sufficient to induce skin papilloma formation in transgenic zebrafish.Journal of biomedical science · 2015Article
- Combined inhibition of MEK and mTOR has a synergic effect on angiosarcoma tumorgrafts.International journal of oncology · 2015Article
- Establishment and characterization of a receptor-negative, hormone-nonresponsive breast cancer cell line from an Iraqi patient.Breast cancer (Dove Medical Press) · 2015Article
- Anthrax lethal and edema toxins in anthrax pathogenesis.Trends in microbiology · 2014Review
- MEK genomics in development and disease.Briefings in functional genomics · 2012Review
Corrections and comments
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Authors and funding
7 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Mitogen-activated protein kinase kinases (MKK or MEK) 1 and 2 are usually treated as redundant kinases. However, in assessing their relative contribution towards ERK-mediated biologic response investigators have relied on tests of necessity, not sufficiency. In response we developed a novel experimental model using lethal toxin (LeTx), an anthrax toxin-derived pan-MKK protease, and genetically engineered protease resistant MKK mutants (MKKcr) to test the sufficiency of MEK signaling in melanoma SK-MEL-28 cells. Surprisingly, ERK activity persisted in LeTx-treated cells expressing MEK2cr but not MEK1cr. Microarray analysis revealed non-overlapping downstream transcriptional targets of MEK1 and MEK2, and indicated a substantial rescue effect of MEK2cr on proliferation pathways. Furthermore, LeTx efficiently inhibited the cell proliferation and anchorage-independent growth of SK-MEL-28 cells expressing MKK1cr but not MEK2cr. These results indicate in SK-MEL-28 cells MEK1 and MEK2 signaling pathways are not redundant and interchangeable for cell proliferation. We conclude that in the absence of other MKK, MEK2 is sufficient for SK-MEL-28 cell proliferation. MEK1 conditionally compensates for loss of MEK2 only in the presence of other MKK.
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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.