Kwon sandbox: Difference between revisions

c-Myc is further along in the signal transduction pathway of the epithelial growth factor receptor (EGF receptor) which deals with the proliferation of cells.  Mutations of c-Myc have a strong correlation to cancer.  Normally c-myc is tightly regulated and c-Myc is short lived, but cancer cells express c-myc uncontrollably and are unable to degrade the c-Myc protein.  This over expression and inability to rid the protein causes it to be active much longer, thus causing it to promote the over expression of genes needed for cell proliferation causing cancer.  Over expression of c-Myc is prevalent in 80% of brest cancers, 70% colorectal cancers, 90% of gynecological cancers, 50% of hepatocellular carcinomas and is particularly prevalent Burkitt’s Lymphoma.

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 is also involved in the body's system of remembering past diseases.  T-cells help the body to remember diseases it has previously had.  C-myc controls the regulation of T-cells.  Without C-myc the T-cells would not be triggered to multiply when a disease that the body has seen before infiltrates the body again.

== References ==