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Myc inhibits JNK-mediated cell death in vivo.
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- Additional Information
- Source:
Publisher: Springer Country of Publication: Netherlands NLM ID: 9712129 Publication Model: Print Cited Medium: Internet ISSN: 1573-675X (Electronic) Linking ISSN: 13608185 NLM ISO Abbreviation: Apoptosis Subsets: MEDLINE
- Publication Information:
Publication: 2005- : Dordrecht, Netherlands : Springer
Original Publication: London : Rapid Science Publishers,
- Subject Terms:
- Abstract:
The proto-oncogene Myc is well known for its roles in promoting cell growth, proliferation and apoptosis. However, in this study, we found from a genetic screen that Myc inhibits, rather than promotes, cell death triggered by c-Jun N-terminal kinase (JNK) signaling in Drosophila. Firstly, expression of Drosophila Myc (dMyc) suppresses, whereas loss of dMyc enhances, ectopically activated JNK signaling-induced cell death. Secondly, dMyc impedes physiologically activated JNK pathway-mediated cell death. Thirdly, loss of dMyc triggers JNK pathway activation and JNK-dependent cell death. Finally, the mammalian cMyc gene, when expressed in Drosophila, impedes activated JNK signaling-induced cell death. Thus, besides its well-studied apoptosis promoting function, Myc also antagonizes JNK-mediated cell death in Drosophila, and this function is likely conserved from fly to human.
- Contributed Indexing:
Keywords: Cell death; Drosophila; JNK pathway; Myc
- Accession Number:
0 (DNA-Binding Proteins)
0 (Drosophila Proteins)
0 (GAL4 protein, Drosophila)
0 (MAS1 protein, human)
0 (MYC protein, human)
0 (Membrane Proteins)
0 (Myc protein, Drosophila)
0 (Protein Isoforms)
0 (Proto-Oncogene Mas)
0 (Proto-Oncogene Proteins c-myc)
0 (Recombinant Fusion Proteins)
0 (Transcription Factors)
0 (egr protein, Drosophila)
- Publication Date:
Date Created: 20170203 Date Completed: 20180306 Latest Revision: 20211204
- Publication Date:
20221213
- Accession Number:
10.1007/s10495-016-1340-4
- Accession Number:
28150056
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