linkstream2 microblog

http://www.sciencemag.org/content/340/6133/682.1.full

Super-powered switches may decide cell fate : Nature News & Comment http://www.nature.com/news/super-powered-switches-may-decide-cell-fate-1.12794

the shattering of chromosomes, w. 7 criteriaKorbel & Campbell

http://www.ncbi.nlm.nih.gov/pubmed/23498933

Pearce, Science Mag, Sept ’12
https://www.sciencemag.org/content/337/6100/1303.summary

Pseudogenes as regulators of biological function
Essays in Biochemistry (2013) 54, 103-112

http://essays.biochemistry.org/bsessays/054/bse0540103.htm

Direct Competition between hnRNP C and U2AF65 Protects the
Transcriptome from the Exonization of Alu Elements.

Kathi Zarnack, Julian König, Mojca Tajnik, Iñigo Martincorena, Sebastian Eustermann, Isabelle Stévant, Alejandro Reyes, Simon Anders, Nicholas M Luscombe, and Jernej Ule

There are ∼650,000 Alu elements in transcribed regions of the human genome. These elements contain cryptic splice sites, so they are in constant danger of aberrant incorporation into mature transcripts. Despite posing a major threat to transcriptome integrity, little is known about the molecular mechanisms preventing their inclusion. Here, we present a mechanism for protecting the human transcriptome from the aberrant exonization of transposable elements. Quantitative iCLIP data show that the RNA-binding protein hnRNP C competes with the splicing factor U2AF65 at many genuine and cryptic splice sites. Loss of hnRNP C leads to formation of previously suppressed Alu exons, which severely disrupt transcript function. Minigene experiments explain disease-associated mutations in Alu elements that hamper hnRNP C binding. Thus, by preventing U2AF65 binding to Alu elements, hnRNP C plays a critical role as a genome-wide sentinel protecting the transcriptome. The findings have important implications for human evolution and disease.

Cell, 2013 vol. 152 (3) pp. 453-466
http://www.sciencedirect.com/science/article/pii/S0092867412015450
http://eutils.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&id=23374342&retmode=ref&cmd=prlinks

Paper uses modencode data, pre comparative paper rollout
http://www.ncbi.nlm.nih.gov/pubmed/23531767

http://cancerres.aacrjournals.org/content/73/6/1699.long
Nice use of CCLE dataset which is an improvement over NCI-60

http://ecerami.github.io/vogelstein-v-lander-round1.html
Short list of 140 drivers v an ever growing list

Science. 2013 Mar 29;339(6127):1546-58. doi: 10.1126/science.1235122. Cancer genome landscapes.
Vogelstein B, Papadopoulos N, Velculescu VE, Zhou S, Diaz LA Jr, Kinzler KW. QT:”
To date, these studies have revealed ~140 genes that, when altered by intragenic mutations, can promote or “drive” tumorigenesis. A typical tumor contains two to eight of these “driver gene” mutations; the remaining mutations are passengers that confer no selective growth advantage. Driver genes can be classified into 12 signaling pathways that regulate three core cellular processes: cell fate, cell survival, and genome maintenance.
”

Lessons from the Cancer Genome
http://www.cell.com/abstract/S0092-8674(13)00288-2
QT:”
Systematic studies of the cancer genome have exploded in recent years. These studies have revealed scores of new cancer genes, including many in processes not previously known to be causal targets in cancer. “

http://www.nature.com/nature/journal/v497/n7447/full/nature12065.html