Kwon sandbox: Difference between revisions

From Proteopedia
Jump to navigationJump to search
← Older editNewer edit →
Line 10: Line 10:
cMyc  is a protein that binds to DNA and regulates transcription, a transcription factor.  Bishop and collegues discovered viruses that induced chicken sarcomas.  They studied the virus and identified an oncogene that would cause uncontrolled cellular proliferation.  The viral oncogene that caused the sarcomas was identified as v-myc.  Later on the homologous gene in chickens was discovered, and called c-myc.  These findings provided evidence that activated cMyc proteins were significant in cellular growth regulation.
cMyc  is a protein that binds to DNA and regulates transcription, a transcription factor.  Bishop and collegues discovered viruses that induced chicken sarcomas.  They studied the virus and identified an oncogene that would cause uncontrolled cellular proliferation.  The viral oncogene that caused the sarcomas was identified as v-myc.  Later on the homologous gene in chickens was discovered, and called c-myc.  These findings provided evidence that activated cMyc proteins were significant in cellular growth regulation.


==Research in Structure and Function==
==Role in Cancer==
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.
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.
 


==General Functions of C-myc==  
==General Functions of C-myc==  
Retrieved from "https://proteopedia.org/Kwon_sandbox"