C-myc, gene expression

Naftilan, A. J., Pratt, R. E., and Dzau, V. J. 1989. Induction of platelet-derived growth factor A-chain and c-myc gene expressions by angiotensin II in cultured rat vascular smooth muscle cells. J Clin Invest 83 1419-1424. 

The c-myc gene, identified originally as the cellular homolog of the transforming determinant carried by avian myelocytomatosis virus, is altered in association with a broad spectrum of neoplasms. Consistent with the observation that altered c-myc is associated with tumors of diverse origin, it has been observed that normal c-myc is expressed in a variety of tissues. Thus, c-myc appears to encode a function associated with a ubiquitous metabolic pathway. 

Iba T, Kigawa J, Kanamori Y, et al. Expression of the c-myc gene as a predictor of chemotherapy response and a prognostic factor in patients with ovarian cancer. Cancer Sci 2004 95(5) 418-423. 

The c-myc gene is the proto-oncogene of avian myelocytoma virus. It binds to DNA and is involved in transcription regulation. The gene product, p62, is located in the nucleus of transformed cells, and levels of c-myc correlate with the rate of cell division. The c-myc protein is essential for DNA replication and enhances mRNA transcription. Activation of the c-myc gene is associated with B- and T-ceH lymphoma, sarcomas, and endotheliomas. In leukemias and lymphomas, increased c-myc expression may be due to amplification or chromosomal translocation of the gene. In acute T-celi leukemias, there is an (8 14) (q24 qll) translocation that... 

The process of lymphocyte activation can be investigated by determining whether or not a particular parameter of activation is prevented by inhibitors of ADPRT. Events that are not inhibited either occur before ADPRT is required or are independent of it. Such changes are the binding of mitogen to the cell surface, the early increase in phosphatidylinositol turnover in the plasma membrane [4], and the early increase in membrane chemiluminescence. Events that are inhibited presumably occur after ADPRT is required. These include the rejoining of DNA breaks (see below), subsequent protein and DNA synthesis [3, 4] and the increased expression of the c-myc gene [11] (Fig. 2). The later response of activated blasts to IL-2 does not appear to involve ADPRT [17]. 

Immediate early genes, e.g., c-fos, c-jun, and c-myc, are the first genes whose expression is induced in cells after a growth stimulus. They encode transcription factors and induce the expression of other growth-related genes. 

G-CSF expression is controlled at both the transcriptional and posttranscrip-tional levels. A sequence of 300 nucleotides upstream of the initiation codon is conserved in both the murine and human genes, and this appears to contain three regulatory sites. G-CSF (and some other cytokine genes) may be constitutively transcribed by cells such as blood monocytes, fibroblasts and endothelial cells, but the mRNA may be short-lived (fi/2 < 15 min). The mRNA contains poly-AUUUA sequences in the untranslated region, and this motif is usually associated with mRNA instability. Indeed, such regions have also been identified in mRNA for GM-CSF, IL-1, IL-6, interferons, TNF, some growth factors, c-jun, c-fos, c-myc and c-myb. Upon the addi-... 

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