Sunday, 29 December 2013
Thursday, 26 December 2013
Monday, 23 December 2013
Sunday, 22 December 2013
Friday, 20 December 2013
Sunday, 15 December 2013
Saturday, 14 December 2013
Thursday, 12 December 2013
Wednesday, 11 December 2013
Friday, 6 December 2013
Wednesday, 4 December 2013
Monday, 2 December 2013
Saturday, 30 November 2013
Friday, 29 November 2013
Thursday, 28 November 2013
Sunday, 24 November 2013
Friday, 22 November 2013
Wednesday, 20 November 2013
Wednesday, 13 November 2013
Wednesday, 6 November 2013
Sunday, 3 November 2013
Wednesday, 23 October 2013
Monday, 21 October 2013
Sunday, 20 October 2013
Saturday, 19 October 2013
Monday, 7 October 2013
Saturday, 5 October 2013
Saturday, 28 September 2013
Thursday, 26 September 2013
Tuesday, 24 September 2013
Saturday, 14 September 2013
Tuesday, 10 September 2013
Monday, 9 September 2013
Sunday, 8 September 2013
Monday, 2 September 2013
Friday, 30 August 2013
Wednesday, 28 August 2013
Tuesday, 27 August 2013
Monday, 26 August 2013
Friday, 23 August 2013
Wednesday, 21 August 2013
Tuesday, 20 August 2013
Wednesday, 14 August 2013
Tuesday, 13 August 2013
Thursday, 1 August 2013
Wednesday, 31 July 2013
Sunday, 28 July 2013
Friday, 26 July 2013
Wednesday, 17 July 2013
Tuesday, 16 July 2013
Monday, 15 July 2013
Sunday, 14 July 2013
Monday, 8 July 2013
Tuesday, 2 July 2013
Friday, 28 June 2013
Wednesday, 26 June 2013
Tuesday, 25 June 2013
Monday, 17 June 2013
Sunday, 16 June 2013
Thursday, 13 June 2013
Sunday, 9 June 2013
Friday, 7 June 2013
Thursday, 6 June 2013
Monday, 3 June 2013
Wednesday, 29 May 2013
SCAN: SNP and CNV Annotation Database
http://www.scandb.org/newinterface/about.html
SCAN is a large-scale database of genetics and genomics data associated to a web-interface and a set of methods and algorithms that can be used for mining the data in it. The database contains two categories of single nucleotide polymorphism (SNP) annotations:
Physical-based annotation where SNPs are categorized according to their position relative to genes (intronic, inter-genic, etc.) and according to linkage disequilibrium (LD) patterns (an inter-genic SNP can be annotated to a gene if it is in LD with variation in the gene).
Functional annotation where SNPs are classified according to their effects on expression levels, i.e. whether they are expression quantitative trait loci (eQTLs) for that gene.
Saturday, 25 May 2013
Friday, 24 May 2013
Wednesday, 22 May 2013
Tuesday, 21 May 2013
Monday, 20 May 2013
Sunday, 19 May 2013
Trends in Genetics - Cryptic causation of human disease: reading between the (germ) lines
http://www.cell.com/trends/genetics/abstract/S0168-9525%2804%2900336-1
Somatic mutation involvement in different diseases.
Tuesday, 14 May 2013
Sunday, 12 May 2013
Friday, 3 May 2013
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