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C-Myc

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Introduction

C-Myc is a transcription factor involved in the cell cycle specifically with the stimulation of cell proliferation but is also involved in the regulation of apoptosis, cell differentiation, cell competition, and senescence [1]. C-Myc is a DNA binding protein and functions primarily by inducing transcription through the formation of heterodimers primarily with Max proteins. C-Myc's interactions are not limited to only Max protiens as it has been shown to interact with BRCA1[2], MAPK1[3], p73[4], and many more. C-Myc is also a protooncogene, and when normally expressed is strictly regulated by signals within the cell cycle, so that when a cell is resting its c-myc expression is little while when growing it expresses high levels of c-myc. When normal cells overexpression of c-myc activates a protection pathway and the abnormal cells are thus eliminated from the host organism through apoptosis, thus protecting the organism.

Structure

The c-myc protein contains two specific regions that characterize them as transcription factors: a carboxy-terminal basix helix-loop-helix leucine zipper motif and an amino terminal transactivation domain[5]. Immediatley following the basic region within the c-myc protein is the helix -loop-helix motif which has been shown to interact with DNA through binding [6]. The c-myc gene is essientially found on human chromosome 8q24 and contains three exons.


Mechanism

Most of the biological functions that c-myc performs involves herterodimerization with Max.


Medical Uses and Therapeutic Opportunities

References

  1. ↑ Uribesalgo I, Benitah SA, Di Croce L. From oncogene to tumor suppressor: The dual role of Myc in leukemia. Cell Cycle. 2012 May 1;11(9). PMID:22510570
  2. ↑ Wang Q, Zhang H, Kajino K, Greene MI. BRCA1 binds c-Myc and inhibits its transcriptional and transforming activity in cells. Oncogene. 1998 Oct 15;17(15):1939-48. PMID:9788437 doi:10.1038/sj.onc.1202403
  3. ↑ Gupta S, Davis RJ. MAP kinase binds to the NH2-terminal activation domain of c-Myc. FEBS Lett. 1994 Oct 24;353(3):281-5. PMID:7957875
  4. ↑ Watanabe K, Ozaki T, Nakagawa T, Miyazaki K, Takahashi M, Hosoda M, Hayashi S, Todo S, Nakagawara A. Physical interaction of p73 with c-Myc and MM1, a c-Myc-binding protein, and modulation of the p73 function. J Biol Chem. 2002 Apr 26;277(17):15113-23. Epub 2002 Feb 13. PMID:11844794 doi:10.1074/jbc.M111281200
  5. ↑ Amati B, Land H. Myc-Max-Mad: a transcription factor network controlling cell cycle progression, differentiation and death. Curr Opin Genet Dev. 1994 Feb;4(1):102-8. PMID:8193530
  6. ↑ Amati B, Land H. Myc-Max-Mad: a transcription factor network controlling cell cycle progression, differentiation and death. Curr Opin Genet Dev. 1994 Feb;4(1):102-8. PMID:8193530
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