Kwon sandbox: Difference between revisions

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Proteopedia Page Contributors and Editors (what is this?)Proteopedia Page Contributors and Editors (what is this?)

Jason Kwon, Ann Taylor

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-==This is a placeholder==
+{{PBB|geneid=4609}}
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+'''Myc''' (cMyc) codes for a protein that binds to the DNA of other genes. When Myc is mutated, or overexpressed, the protein doesn't bind correctly, and often causes [[cancer]].
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-{{STRUCTURE_3cin |  PDB=3cin  |  SCENE=  }}
+When a gene like Myc is altered to cause cancer, the cancerous version of the gene is called an [[oncogene]]. The healthy version of the gene that it is derived from is called a [[proto-oncogene]].
+Myc gene encodes for a [[transcription factor]] that is believed to regulate expression of 15% of all genes <ref>Gearhart J, Pashos EE, Prasad MK, Pluripotency Redeux -- advances in stem-cell research, N Engl J Med 357(15):1469 [http://content.nejm.org/cgi/content/full/357/15/1469 Free full text]</ref> through binding on Enhancer Box sequences (E-boxes) and recruiting [[histone acetyltransferase]]s (HATs). Myc belongs to Myc family of transcription factors, which also includes [[N-Myc]] and L-Myc genes. Myc-family transcription factors contain the [[bHLH]]/LZ (basic Helix-Loop-Helix [[Leucine Zipper]]) domain.
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+A mutated version of Myc is found in many cancers which causes Myc to be persistently expressed. This leads to the unregulated expression of many genes some of which are involved in cell proliferation and results in the formation of [[cancer]]. A common [[translocation]] which involves Myc is t(8:14) is involved in the development of a lymphoma. A recent study demontrated that temporary inhibition of Myc selectively kills mouse lung cancer cells, making it a potential cancer drug target.<ref>{{cite journal
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+  | last = Soucek
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+  | first = Laura
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+  | authorlink =
+  | coauthors = Jonathan Whitfield, Carla P. Martins, Andrew J. Finch, Daniel J. Murphy, Nicole M. Sodir, Anthony N. Karnezis, Lamorna Brown Swigart, Sergio Nasi  &  Gerard I. Evan
+  | title = Modelling Myc inhibition as a cancer therapy
+  | journal = Nature
+  | volume = 455
+  | issue =
+  | pages = 679–683
+  | publisher = Nature Publishing Group
+  | location = London, UK
+  | date = [[2008-10-02]]
+  | url = http://www.nature.com/nature/journal/v455/n7213/abs/nature07260.html
+  | doi = 10.1038/nature07260
+  | id =
+  | accessdate = 2008-10-14}}</ref>
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+==Discovery==
+Myc gene was first discovered in [[Burkitt's lymphoma]] patients. In Burkitt's lymphoma, cancer cells show [[chromosomal translocation]]s, in which [[Chromosome 8]] is frequently involved. Cloning the break point of the fusion chromosomes revealed a gene that was similar to myelocytomatosis viral oncogene (v-Myc). Thus, the newfound cellular gene was named c-Myc.
-<scene name='C-Myc/Custom/2'>TextToBeDisplayed</scene>
+==Structure==
-== Introduction ==
+Myc protein belongs to Myc family of transcription factors, which also includes N-Myc and L-Myc genes. Myc family of transcription factors contain [[bHLH]]/LZ (basic Helix-Loop-Helix [[Leucine Zipper]]) domain. Myc protein, through its bHLH domain can bind to [[DNA]], while the leucine zipper domain allows the dimerisation with its partner Max, another bHLH transcription factor.
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+Myc [[mRNA]] contains an [[IRES]] (internal ribosome entry site) that allows the RNA to be translated into protein when [[5' cap]] dependent translation is inhibited; such as during viral infection.
-<scene name='C-Myc/Custom/2'>TextToBeDisplayed</scene>
+==Molecular Function==
-The c-Myc is a protonocogene, has the potential of becoming an oncogene if it under went specific mutations.  This protein has been found to be mutated in Burkitt's lymphoma cell lines.  The c-Myc protein is a transcription factor that regulates the expression of cell proliferation proteins.  This protein is normally short lived, but when it has a point mutation that causes Thr58, it has been shown to have a much longer turnover rate.
+Myc protein is a [[transcription factor]] that activates expression of a great number of genes through binding on [[consensus sequence]]s (Enhancer Box sequences (E-boxes)) and recruiting [[histone acetyltransferase]]s (HATs). It can also act as a transcriptional repressor. By binding Miz-1 transcription factor and displacing the [[EP300|p300]] [[co-activator]], it inhibits expression of Miz-1 target genes.
+Myc is activated upon various [[mitogen|mitogenic signal]]s such as [[Wnt signalling pathway|Wnt]], [[Sonic hedgehog|Shh]] and [[Epidermal growth factor|EGF]] (via the [[MAPK/ERK pathway]]).
+By modifying the expression of its target genes, Myc activation results in numerous biological effects. The first to be discovered was its capability to drive [[cell proliferation]] (upregulates cyclins, downregulates p21), but it also plays a very important role in regulating [[cell growth]] (upregulates ribosomal RNA and proteins), [[apoptosis]] (downregulates [[Bcl-2]]), differentiation and [[stem cell]] self-renewal. Myc is a very strong [[Oncogene#Proto-oncogene|proto-oncogene]] and it is very often found to be [[upregulation|upregulated]] in many types of cancers.