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C-Myc is a [http://en.wikipedia.org/wiki/Transcription_factor transcription factor] involved in the [http://en.wikipedia.org/wiki/Cell_cycle cell cycle] specifically with the stimulation of cell proliferation but is also involved in the regulation of [http://en.wikipedia.org/wiki/Apoptosis apoptosis], [http://en.wikipedia.org/wiki/Cell_differentiation cell differentiation], cell competition, and [http://en.wikipedia.org/wiki/Senescence senescence] <ref>PMID:22510570</ref>. C-Myc is a [http://en.wikipedia.org/wiki/DNA-binding_protein DNA binding protein] and functions primarily by inducing transcription through the formation of [http://en.wikipedia.org/wiki/Protein_dimer heterodimers] primarily with [http://en.wikipedia.org/wiki/MAX_(gene) Max proteins]. C-Myc's interactions are not limited to only Max protiens as it has been shown to interact with [http://en.wikipedia.org/wiki/BRCA1 BRCA1]<ref>PMID:9788437</ref>, [http://en.wikipedia.org/wiki/Mapk1 MAPK1]<ref>PMID: 7957875</ref>, [http://en.wikipedia.org/wiki/P73 p73]<ref>PMID:11844794</ref>, and many more. C-Myc is also a [http://en.wikipedia.org/wiki/Oncogene 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.  

The c-myc protein contains two specific regions that characterize them as transcription factors: a carboxy-terminal basix helix-loop-helix leucine zipper (bHLH-LZ) motif and an amino terminal transactivation domain<ref name="mot">PMID:8193530</ref>. The N-terminal domain functions in the activation of transcription, and the C-terminal, which contains the bHLH-LZ functions in in promoting the interaction between of c-myc and max.  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 <ref name="mot">PMID:8193530</ref>. C-myc by itself contains 3 alpha helices and 74residues. Since c-myc is essentially inactive when it homodimerizes  and has a very short half life, typically 20 to 30 minutes, it heterodimerizes with max to perform its biological functions.  

<Structure load='1NKP' size='500' frame='true' align='right' caption='Insert caption here' scene='c-Myc and Max heterodimer binding to DNA'/>

In order to find more about the transciptional and biological activity of c-myc more about it's structure and heterodimerization had to be known. The two main techinques used to identify the bHLH-LZ domains of c-myc were [http://en.wikipedia.org/wiki/Circular_dichroism Circular Dichromism] and [http://en.wikipedia.org/wiki/NMR Nuclear Magnetic Resonance(NMR)].

Most of the biological functions that c-myc performs involves herterodimerization with Max. C-Myc primary function is activating the transcription of genes involved in cell proliferation, growth, and metabolism by binding to the DNA sequence CAGTG, also known as the Enhancer box, when it has dimerized with Max. Many studies have shown that without dimerizing to Max, c-Myc would not be able to bind to DNA, which makes thier interaction important to cellular function<ref>PMID:1501888</ref><ref>PMID:7577944</ref>. When c-Myc/Max form a herterodimer and bind DNA transcription becomes activated. When Myc-Max are bound this allows for proteins involved in transcription to bind like, TBP, TBIIE, TRRAP, etc. In a normal cell c-myc is very regulated and expresses little c-myc when the cell is resting. When cells becomes stimulated by growth factors c-myc is drastically increased. Over expression of c-myc in a normal cells results in apoptosis so that the organism is protected from abnormal cell growth. In abnormal cell when the c-myc gene is over expressed leads to cancer.  

The over expression of c-myc is one of the most common findings in human cancer, however it is still unclear how it acts to promote abnormal cell growth. Studies have shown that the greater amounts of c-myc present the higher your chances are for having cancer. Researchers have been looking into the binding of c-myc with max to see if that would deregulate is expression, taking the c-myc protein out of the organism all together, and mutating certain regions where c-myc binds DNA to try and understand why it effects proliferation eventually causing cancer. One of the most common forms of cancer that c-myc is involved in is [http://en.wikipedia.org/wiki/Burkitt's_lymphoma Burkitts's lymphoma]. In this cancer, c-myc proto-oncogene is moved from its normal position on chromosome 8 by recipricol translocation to an enhancer region close to chromosome 14, the gene that is capable of making antibodies. Since antibodies are frequently used in the body to maintain a good immune system, it is frequently transcribed. So c-myc ends up becoming uncontrolably transcribed when it is translocated to this region.