http://www.ncbi.nlm.nih.gov/m/pubmed/21278188/?i=5&from=/23547033/related
Tuesday, 30 April 2013
Friday, 26 April 2013
Thursday, 25 April 2013
Wednesday, 24 April 2013
Using MEMo to Discover Mutual Exclusivity Modules in Cancer
Using MEMo to Discover Mutual Exclusivity Modules in Cancer.
Source
Computational Biology Center, Memorial Sloan-Kettering Cancer Center, New York, New York.
Abstract
Although individual tumors show surprisingly diverse genomic alterations, these events tend to occur in a limited number of pathways, and alterations that affect the same pathway tend to not co-occur in the same patient. While pathway analysis has been a powerful tool in cancer genomics, our knowledge of oncogenic pathway modules is incomplete. To systematically identify such modules, we have developed a novel method, Mutual Exclusivity Modules in Cancer (MEMo). The method searches and identifies modules characterized by three properties: (1) member genes are recurrently altered across a set of tumor samples; (2) member genes are known to or are likely to participate in the same biological process; and (3) alteration events within the modules are mutually exclusive. MEMo integrates multiple data types and maps genomic alterations to biological pathways. MEMo's mutual exclusivity uses a statistical model that preserves the number of alterations per gene and per sample. The MEMo software, source code and sample data sets are available for download at: http://cbio.mskcc.org/memo. Curr. Protoc. Bioinform. 41:8.17.1-8.17.12. © 2013 by John Wiley & Sons, Inc.
Tuesday, 23 April 2013
Friday, 19 April 2013
Monday, 15 April 2013
Sunday, 14 April 2013
Saturday, 13 April 2013
The FAM ( USP9X) Deubiquitylating Enzyme Localizes to Multiple Points of Protein Trafficking in Epithelia, where It Associates with E-cadherin and -catenin.
The FAM ( USP9X) Deubiquitylating Enzyme Localizes to Multiple Points of Protein Trafficking in Epithelia, where It Associates with E-cadherin and -catenin.
USP9X is substrate-specific deubiquitylating enzyme highly expressed in epithelia where it interacts with its
substrate, beta -catenin.
In vivo depletion of USP9X in preimplantation mouse embryos, by addition of siRNA, resulted in a parallel decrease in beta -catenin.
It proves USP9X to be a member of Beta-catenin related pathway.
Cancer Genome Landscapes
http://www.sciencemag.org/content/339/6127/1546
Bert volelstein discusses about the core signalling pathways in human cancers.
Differential principal component analysis of ChIP-seq
http://www.pnas.org/content/early/2013/04/05/1204398110.short
Principal component analysis of chip-seq.
How to identify cancer drivers from tumor somatic mutations?
How to identify cancer drivers from tumor somatic mutations?
http://bg.upf.edu/blog/2012/07/how-to-identify-cancer-drivers-from-tumor-somatic-mutations/
Up, Up, and Array | The Scientist Magazine(R)
http://www.the-scientist.com/?articles.view/articleNo/34779/title/Up--Up--and-Array/
Biography of Todd golub.
Inspiring article.
USP9x - Smad4 Interaction
FAM/USP9x, a deubiquitinating enzyme essential for TGFbeta signaling, controls Smad4 monoubiquitination.
Read the entire story on