User:Hillary Sigale/Sandbox 1
From Proteopedia
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Revision as of 13:25, 11 September 2009
The c-myc protein cannot homodimerize without the protein Max. Max can sometimes heterodimerize with Mad family proteins. The Mad-Max, Mad3-Max, Mad4-Max, and Mnt-Max heterodimers are antagonist of c-myc. The myc-max connection is unstable which allows for high populations of dissociated monomers and it impedes reassortment dictated by the level of expression of c-myc, mad, and mxi1 genes and transduction of cell growth and differentiation signals. For oncogenic activity to occur c-myc must bind with the Max protein. All max proteins will bind to the same DNA sequence.
General Functions of C-myc
C-myc is used in cell cycle entry, proliferation, and differentiation. C-myc also helps to bind DNA which activates transcription. The c-myc lives a very short life. It is controlled by the level and temporal pattern of expression of their corresponding gene. Without C-myc an organism is unable to survive since there is nothing allowing cells to differentiate or proliferate. The organisms cannot survive after the pre-T-cell receptor proliferation is unable to be completed.
C-myc's Role in Cancer
C-myc's proliferation is induced by enhancers that help to increase immunoglobin genes functions. It has been seen that the greater amount of C-myc present the higher the cnances that cancer is also present. Cancer is often able to grow best in people with bad immune systems. Since the immune system is weak the T-cells and B-cells pass over the cancer without noticing that anything is wrong. This combined with the fact that these enhancers cause C-myc to rapidly produce cells is causing cancer in a body that cannot fight it off. The newly formed cells continue to grow on eachother. This causes a tumor that is cancerous that is unnoticed. The most common form of cancer that c-myc plays a role in is Burkitt's Lymphoma.
