GSBS Student Publications
Title
Transactivation of gene expression by Myc is inhibited by mutation at the phosphorylation sites Thr-58 and Ser-62
GSBS Program
Biochemistry & Molecular Pharmacology
Publication Date
1993-04-15
UMMS Affiliation
Graduate School of Biomedical Sciences; Program in Molecular Medicine
Document Type
Article
Disciplines
Life Sciences | Medicine and Health Sciences
Abstract
The product of the human c-myc protooncogene (Myc) is a sequence-specific DNA binding protein. Here, we demonstrate that the placement of the specific Myc DNA binding site CACGTG upstream of a luciferase reporter gene conferred Myc-stimulated expression that was inhibited by the overexpression of the basic-helix-loop-helix/leucine zipper protein Max. It was observed that Myc was phosphorylated in vivo within the NH2-terminal domain at Thr-58 and Ser-62. Replacement of these phosphorylation sites with Ala residues caused a marked decrease in Myc-stimulated reporter gene expression. In contrast, the replacement of Thr-58 or Ser-62 with an acidic residue (Glu) caused only a small inhibition of transactivation. Together, these data demonstrate that the NH2-terminal phosphorylation sites Thr-58 and Ser-62 are required for high levels of transactivation of gene expression by Myc.
DOI of Published Version
10.1073/pnas.90.8.3216
Source
Proc Natl Acad Sci U S A. 1993 Apr 15;90(8):3216-20.
Journal/Book/Conference Title
Proceedings of the National Academy of Sciences of the United States of America
Related Resources
PubMed ID
8386367
Repository Citation
Gupta S, Seth A, Davis RJ. (1993). Transactivation of gene expression by Myc is inhibited by mutation at the phosphorylation sites Thr-58 and Ser-62. GSBS Student Publications. https://doi.org/10.1073/pnas.90.8.3216. Retrieved from https://escholarship.umassmed.edu/gsbs_sp/460