Posts Tagged ‘psychencode’

Spatiotemporal 16p11.2 Protein Network Implicates Cortical Late Mid-Fetal Brain Development and KCTD13-Cul3-RhoA Pathway in Psychiatric Diseases

Tuesday, November 15th, 2016

Spatiotemporal…Protein Network Implicates Cortical…Fetal Brain Development & KCTD13…RhoA Pathway in…Diseases
http://www.sciencedirect.com/science/article/pii/S0896627315000367

dyanamic PPI w brainspan data

Spatiotemporal 16p11.2 Protein Network Implicates Cortical Late Mid-Fetal Brain Development and KCTD13-Cul3-RhoA Pathway in
Psychiatric Diseases

Guan Ning Lin1, 5,
Roser Corominas1, 5,
Irma Lemmens2,
Xinping Yang3,
Jan Tavernier2,
David E. Hill3,
Marc Vidal3,
Jonathan Sebat1, 4,
Lilia M. Iakoucheva1,

http://dx.doi.org/10.1016/j.neuron.2015.01.010

R package: variancePartition

Sunday, November 13th, 2016

https://bioconductor.org/packages/release/bioc/html/variancePartition.html

new tool in psychencode meeting

miRNA atlas

Tuesday, November 1st, 2016

Distribution of #miRNA expression across human tissues
http://nar.oxfordjournals.org/content/44/8/3865 Atlas of ~1400 RNAs in at least 1 of 61 tissues; 143 in all

https://ccb-web.cs.uni-saarland.de/tissueatlas/

Human Developmental Biology Resource (HDBR)

Friday, October 21st, 2016

The MRC-Wellcome Trust Human Developmental Biology Resource (HDBR) HDBR EXPRESSION – An online resource for studying prenatal human brain development
http://www.hdbr.org/expression/

Single Cell Analysis paper

Saturday, October 8th, 2016

16 Neuronal subtypes & [inter-regional] diversity revealed by [#singlecell]-nucleus RNAseq of…the brain
http://science.sciencemag.org/content/352/6293/1586.long

Neuronal subtypes and diversity revealed by single-nucleus RNA sequencing of the human brain.
Lake BB, Ai R, Kaeser GE, Salathia NS, Yung YC, Liu R, Wildberg A, Gao D, Fung HL, Chen S, Vijayaraghavan R, Wong J, Chen A, Sheng X, Kaper F, Shen R, Ronaghi M, Fan JB, Wang W, Chun J, Zhang K.
Science. 2016 Jun 24;352(6293):1586-90. doi: 10.1126/science.aaf1204.

Integrated Systems Approach Identifies Genetic Nodes and Networks in Late-Onset Alzheimer’s Disease: Cell

Saturday, October 1st, 2016

Zhang, Bin, Chris Gaiteri, Liviu-Gabriel Bodea, Zhi Wang, Joshua McElwee, Alexei A. Podtelezhnikov, Chunsheng Zhang et al. "Integrated systems approach identifies genetic nodes and networks in late-onset Alzheimer’s disease." Cell 153, no. 3 (2013): 707-720.

Integrated systems approach identifies genetic…#networks in…Alzheimer’s http://www.Cell.com/cell/abstract/S0092-8674(13)00387-5 Determining causality from co-expression

The Brain That Couldn’t Remember – The New York Times

Saturday, August 13th, 2016

The #Brain That Couldn’t Remember
http://www.NYTimes.com/2016/08/07/magazine/the-brain-that-couldnt-remember.html Fight over the ownership of HM’s highlights issues in consent HT @FearLoathingBTX

What Dead Pigs Can’t Teach Us About ‘C.S.I.’

Sunday, July 24th, 2016

What Dead Pigs Can’t Teach Us About @CSI_CBS
http://www.nytimes.com/2016/06/14/science/forensic-science-body-farm.html Wonder what this tells us about RIN? #RNAseq

Epigenomic analysis detects aberrant super-enhancer DNA methylation in human cancer | Genome Biology | Full Text

Sunday, April 17th, 2016

two papers for journal club:

1. What are super-enhancers? Pott et al., Nature Genetics (2015) http://www.nature.com/ng/journal/v47/n1/full/ng.3167.html

2. Epigenomic analysis detects aberrant super-enhancer DNA methylation in human cancer, Heyn et al., Genome Biology (2016)
https://genomebiology.biomedcentral.com/articles/10.1186/s13059-016-0879-2

#Epigenomic analysis detects aberrant super-enhancer DNA methylation in human #cancer
https://GenomeBiology.biomedcentral.com/articles/10.1186/s13059-016-0879-2 hypo-Me of many large blocks

Runs in the Family – The New Yorker

Monday, April 11th, 2016

Runs in the Family
http://www.newyorker.com/magazine/2016/03/28/the-genetics-of-schizophrenia Overview of recent results that #SCZ is due to synaptic overpruning from excessive C4 activity

QT:{{”
A magnificently simple theory began to convulse out of the results. Perhaps C4A, like the other immunological factors that Stevens had identified in synapse pruning, marks neuronal synapses destined to be eliminated during normal brain development. During the maturation of the brain, microglia recognize these factors as tags and engulf the tagged synapses. Variations in the C4A gene cause different amounts of the C4A protein to be expressed in the human brain. The overabundance of C4A protein in some people contributes to an excessively exuberant pruning of synapses—thereby decreasing the number of synapses in the brain, which would explain the well-established fact that
schizophrenic patients tended to have fewer neuronal connections. That the symptoms of schizophrenia break loose during the second and third decades of life makes sense, in retrospect: adolescence and early adulthood are periods when synaptic pruning reaches a climax in the regions of the brain that govern planning and thinking.
“}}