Thursday, November 7, 2013

A WILD GENE! THE EP 300

Every time we talk about a "wild gene", we get a reaction from our readers.  This is a good sign.  Basically, what we call wild gene is one full of interactions.  We talked about adapter genes which basically direct in one or the other direction of global Metabolism, but we also make sure that readers understand that these adapters can allow a gene to acquire proliferative potential by hooking it to another gene that routinely drives proliferation (such as the gene that pushes Antibody formation).  By all definitions, EP300 is a wild gene.

Another power to this gene is the fact that it leads to Malformation when it is missing:
"Rubinstein-Taybi syndrome.", THROUGH THE MAML1 GENE, THIS GENE IS IN COMPLICITY WITH THE NOTCH1.  And you know how we hold dearly the Notch as an important gene/pathway...

EP300 is involved in all major cancers including Acute Leukemia.  You remember that Acute AML cells have not fully completed differentiation.  EP300 is the master of differentiation and of course will be mutated or altered in bad AML.  So, in a way, it is prognostic!

" Somatic mutations in the EP300 gene have been found in a small number of solid tumors, including cancers of the colon and rectum, stomach, breast, and pancreas. Studies suggest that EP300 mutations may also play a role in the development of some prostate cancers, and could help predict whether these tumors will increase in size or spread to other parts of the body. In cancer cells, EP300 mutations prevent the gene from producing any functional protein. Without p300, cells cannot effectively restrain growth and division, which can allow cancerous tumors to form."

HOW MANY GENES INTERACT WITH EP300? YOU BE THE JUDGE!

"Interactions"

EP300 has been shown to interact with Mothers against decapentaplegic homolog 7,[6] MAF,[7] TSG101,[8] Peroxisome proliferator-activated receptor alpha,[9][10] NPAS2,[11] PAX6,[12] DDX5,[13] MYBL2,[14] Mothers against decapentaplegic homolog 1,[15][16] Mothers against decapentaplegic homolog 2,[17][18] Lymphoid enhancer-binding factor 1,[19] SNIP1,[20] TRERF1,[21] STAT3,[16] EID1,[22][23] RAR-related orphan receptor alpha,[24] ELK1,[25] HIF1A,[26][27] ING5,[28] Peroxisome proliferator-activated receptor gamma,[29][30] SS18,[31] TCF3,[32] Zif268,[33] Estrogen receptor alpha,[29][34][35] GPS2,[36] MyoD,[24][37] YY1,[38][39] ING4,[28] PROX1,[7] CITED1,[40] HNF1A,[41] MEF2C,[37] MEF2D,[42][43] MAML1,[44][45] Twist transcription factor,[46] PTMA,[47] IRF2,[48] DTX1,[49] Flap structure-specific endonuclease 1,[50] Myocyte-specific enhancer factor 2A,[51] CDX2,[12] BRCA1,[34][52] HNRPU,[53] STAT6,[54] CITED2,[55][56][57][58] RELA,[59][60] TGS1,[61] CEBPB,[62] Mdm2,[63] NCOA6,[64] NFATC2,[65] Thyroid hormone receptor alpha,[51] BCL3,[66] TFAP2A,[56] PCNA,[67] P53[68][63][69][70][71] and TAL1.[72]wikipedia"

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