ArticleOncogene2002
Regulation of c-myc stability by selective stress conditions and by MEKK1 requires aa 127-189 of c-myc.
Article in Oncogene, 2002. 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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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.
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Who cites it
17 citing papers in PubMed, 35 citations in OpenAlex.
- MAP3K1: A Multifunctional Kinase at the Crossroads of Cancer Progression and Tumor Suppression.Cells · 2026Review
- Alterations and Co-Occurrence of C-MYC, N-MYC, and L-MYC Expression are Related to Clinical Outcomes in Various Cancers.International journal of stem cells · 2023Article
- Article
- Fine-scale mapping of the 5q11.2 breast cancer locus reveals at least three independent risk variants regulating MAP3K1.American journal of human genetics · 2015Article
- ROCK has a crucial role in regulating prostate tumor growth through interaction with c-Myc.Oncogene · 2014Article
- The PIM-2 kinase is an essential component of the ultraviolet damage response that acts upstream to E2F-1 and ATM.The Journal of biological chemistry · 2013Article
- Network modeling of CDF treated pancreatic cancer cells reveals a novel c-myc-p73 dependent apoptotic mechanism.American journal of translational research · 2011Article
- Resistance to arginine deiminase treatment in melanoma cells is associated with induced argininosuccinate synthetase expression involving c-Myc/HIF-1alpha/Sp4.Molecular cancer therapeutics · 2009Article
- Inference of cell cycle-dependent proteolysis by laser scanning cytometry.Experimental cell research · 2009Article
- Article
- Activation of TORC1 transcriptional coactivator through MEKK1-induced phosphorylation.Molecular biology of the cell · 2008Article
- RhoB facilitates c-Myc turnover by supporting efficient nuclear accumulation of GSK-3.Oncogene · 2006Article
- The expression of proapoptosis genes is increased in bipolar disorder, but not in schizophrenia.Molecular psychiatry · 2006Article
- Negative control of the Myc protein by the stress-responsive kinase Pak2.Molecular and cellular biology · 2004Article
- Myc pathways provoking cell suicide and cancer.Oncogene · 2003Review
- Controlling transcription by destruction: the regulation of yeast Gcn4p stability.Current genetics · 2003Review
- The many lives of Myc in the pancreatic β-cell.The Journal of biological chemistryReview
Corrections and comments
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Authors and funding
3 authors at 2 institutions in 1 country.
Funding
Abstract
C-myc availability is central for its ability to serve as a regulator of cell growth and death. Here we study the regulation of c-myc protein stability and identify domains of c-myc that are important for its stabilization in response to stress kinases activated following selective stress conditions. UV-irradiation elicited an increase in c-myc protein levels, which could be attenuated by inhibitors of stress kinases but also by actinomycin D-inhibitor of transcription. Inhibition of protein synthesis results in a noticeable decrease in c-myc levels, further pointing to the short half-life of the protein. However, in combination with tumor necrosis factor-alpha (TNF-alpha), cycloheximide efficiently increases steady-state levels of c-myc, suggesting that selective stress conditions are required to increase c-myc protein stability. Expression of MEKK1, an upstream regulator of protein kinases that has been implicated in mediating the response to diverse stress conditions, also results in an efficient increase in the half-life of c-myc protein. To map c-myc domains that are responsive to stress kinases, we monitored changes in the level of c-myc deletion mutants following MEKK1 expression. Of the seven c-myc deletion mutants analysed, the domain spanning amino acids 127-189 was found to be required for MEKK1-dependent increase in c-myc stability. In all, the present study identifies a novel domain that is important for the regulation of c-myc stability by stress kinases in response to selective stress conditions.
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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.