1*Highly conserved Molecule: This means the molecule has stood the test of time and has been used under that form for years, and may have become critical in basic cellular functions. In the human cell, some genes that are now "conserved" came from or were adopted from invading Virus. For such an adoption to occur, the gene must be critical and acquired without antigenicity. It is believed that ELK-1, ETS, Myb,ERG,ETV EWS, or TEL, could be an evolutive genes that are characterized with high level of co-association and remains most of all within the epigenic zone. TEL-JAK2 has been suggested in Leukemia(Lacronique et al)
while TMPRSS-ERG has been demonstrated in Prostate cancer (clark et al).
In Breast cancer, "Elk1 also interacts with BRCA1 splice variants, namely BRCA1a and BRCA1b. This interaction enhances BRCA1-mediated growth suppression in breast cancer cells. Elk1 may be a downstream target of BRCA1 in its growth control pathway. Recent literature reveals that c-fos
promoter activity is inhibited, while overexpression of BRCA1a/1b
reduces MEK-induced activation of the SRE. These results show that one
mechanism of growth and tumor suppression by BRCA1a/1b proteins acts
through repression of the expression of Elk1 downstream target genes
like Fos.[20]" wikepedia
Watson et al suggested :"
It has been over 15 years since Ets was originally identified as one of
the two genes (Ets and Myb) transduced by the avian leukemia virus, E26 (Watson et al., 1990);" again suggesting these gene that control epigenetic events may be evolutive as suggested above, and keeps attractive co-association capability that may have help them escape cellular immunity ! Their location at the epigenetic location show the points to a cellular zone of weakness. But it also could point to the importance of inhibitor of de-Acetylators in human cancer and point to why we need further efforst to understand epigenetic events. The fact is that medication targeting Retinoic Acid took over by surprise the world when it comes to treatment of Promyelocytic Leukemias, re-enforces this notion...
To know more about how gene elements described above interact further with P53, histone de-acetylators, and the Telomeres, read our blog of 1 year ago on 01/31/2013.
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I cannot pass to the next step without pointing to the fact that distant effect of Traumatic Brain injury (TBI) are not far from these region since they all depend on secondary release of Cytokines which originate from these regions!
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AND SO MUCH STILL TO TALK ABOUT!
2*young selective development:
3*JAK/STAT involvement
4*The cell wants to achieve selective terminal differentiation and criss cross with gene repair and gene of variable region
5*membranous event with coexistence of Death Receptor
6*factor BSAP expression
7*Activity at TLE4, a negatve regulator of PAX5
8*relation with Ibrutinib
9*Daxx gene
10*The intervention pf the Variable region of IG
11*role of RAG1
12*emu enhancer
13*role of AML1
14*role of TATA and the Retinoblastoma genes
15*Intervention of the Telomere
16*Acetylated P53 (see blog 01/31/2013)
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