Pearce, Science Mag, Sept ’12
https://www.sciencemag.org/content/337/6100/1303.summary
Archive for the 'SciLit' Category
3d printers that can almost replicate themselves! Building… with Free, Open-Source Hardware
May 11, 2013Pseudogenes as regulators of biological function, Essays in Biochemistry
May 10, 2013Pseudogenes as regulators of biological function
Essays in Biochemistry (2013) 54, 103-112
Direct Competition between hnRNP C and U2AF65 Protects the Transcriptome from the Exonization of Alu Elements.
May 6, 2013Direct 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
Integrative analysis of C. elegans modENCODE ChIP… Genome Res. 2013 – PubMed – NCBI
May 6, 2013Paper uses modencode data, pre comparative paper rollout
http://www.ncbi.nlm.nih.gov/pubmed/23531767
Collections of Simultaneously Altered Genes as Biomarkers of Cancer Cell Drug Response
May 6, 2013http://cancerres.aacrjournals.org/content/73/6/1699.long
Nice use of CCLE dataset which is an improvement over NCI-60
Vogelstein v. Lander, Round 1
May 6, 2013http://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.
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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. “
Non-invasive analysis of acquired resistance to cancer therapy by sequencing of plasma DNA
May 4, 2013Crinkly Curves » American Scientist
April 29, 2013An Introduction to Social Media for Scientist – might be a fun read
April 28, 2013An Introduction to Social Media for Scientists
http://www.plosbiology.org/article/info%3Adoi%2F10.1371%2Fjournal.pbio.1001535 “Online social media tools can be some of the most rewarding and informative resources for scientists—IF you know how to use them.”
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