ArticleProceedings of the National Academy of Sciences of the United States of America1999
MEKK1 suppresses oxidative stress-induced apoptosis of embryonic stem cell-derived cardiac myocytes.
Article in Proceedings of the National Academy of Sciences of the United States of America, 1999. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 36 papers.
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Who cites it
36 citing papers in PubMed, 136 citations in OpenAlex.
- A novel variant in theMolecular medicine reports · 2025Article
- MAP3K1 mutations confer tumor immune heterogeneity in hormone receptor-positive HER2-negative breast cancer.The Journal of clinical investigation · 2024Article
- MAP3K1 expression is associated with progression and poor prognosis of hormone receptor-positive, HER2-negative early-stage breast cancer.Cellular oncology (Dordrecht, Netherlands) · 2023Article
- Site-specific decreases in DNA methylation in replicating cells following exposure to oxidative stress.Human molecular genetics · 2023Article
- Coordination of MAPK and p53 dynamics in the cellular responses to DNA damage and oxidative stress.Molecular systems biology · 2022Article
- Silencing MAP3K1 expression inhibits the proliferation of goat hair follicle stem cells.In vitro cellular & developmental biology. Animal · 2021Article
- Sexual dimorphism in oxidant-induced adaptive homeostasis in multiple wild-type D. melanogaster strains.Archives of biochemistry and biophysics · 2017Article
- A RING to rule them all? Insights into the Map3k1 PHD motif provide a new mechanistic understanding into the diverse roles of Map3k1.Cell death and differentiation · 2015Review
- The MEKK1 PHD ubiquitinates TAB1 to activate MAPKs in response to cytokines.The EMBO journal · 2014Article
- Bornyl caffeate induces apoptosis in human breast cancer MCF-7 cells via the ROS- and JNK-mediated pathways.Acta pharmacologica Sinica · 2014Article
- MAP3K1: Genomic Alterations in Cancer and Function in Promoting Cell Survival or Apoptosis.Genes & cancer · 2013Article
- Sodium tanshinone IIA silate inhibits oxygen-glucose deprivation/recovery-induced cardiomyocyte apoptosis via suppression of the NF-κB/TNF-α pathway.British journal of pharmacology · 2013Article
- Article
- N-acetylglucosamine conjugated to nanoparticles enhances myocyte uptake and improves delivery of a small molecule p38 inhibitor for post-infarct healing.Journal of cardiovascular translational research · 2011Article
- Mitogen-activated protein kinase signaling in the heart: angels versus demons in a heart-breaking tale.Physiological reviews · 2010Review
- RAGE modulates hypoxia/reoxygenation injury in adult murine cardiomyocytes via JNK and GSK-3beta signaling pathways.PloS one · 2010Article
- Sustained release of a p38 inhibitor from non-inflammatory microspheres inhibits cardiac dysfunction.Nature materials · 2008Article
- Article
- Cartilage oligometric matrix protein-angiopoietin-1 promotes revascularization through increased survivin expression in dermal endothelial cells of skin grafts in mice.The American journal of pathology · 2007Article
- Roles of the Raf/MEK/ERK pathway in cell growth, malignant transformation and drug resistance.Biochimica et biophysica acta · 2007Review
Corrections and comments
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Authors and funding
6 authors at 3 institutions in 1 country.
Funding
Abstract
A combination of in vitro embryonic stem (ES) cell differentiation and targeted gene disruption has defined complex regulatory events underlying oxidative stress-induced cardiac apoptosis, a model of postischemic reperfusion injury of myocardium. ES cell-derived cardiac myocytes (ESCM) having targeted disruption of the MEKK1 gene were extremely sensitive, relative to wild-type ESCM, to hydrogen peroxide-induced apoptosis. In response to oxidative stress, MEKK1-/- ESCM failed to activate c-Jun kinase (JNK) but did activate p38 kinase similar to that observed in wild-type ESCM. The increased apoptosis was mediated through enhanced tumor necrosis factor alpha production, a response that was positively and negatively regulated by p38 and the MEKK1-JNK pathway, respectively. Thus, MEKK1 functions in the survival of cardiac myocytes by inhibiting the production of a proapoptotic cytokine. MEKK1 regulation of the JNK pathway is a critical response for the protection against oxidative stress-induced apoptosis in cardiac myocytes.
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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.