GWAS: drug-induced agranulocytosis, response to clozapine
Description:
List of positional candidate genes after correcting for multiple testing and controlling the false discovery rate from genome wide association studies (GWAS) retrieved from the NHGRI-EBI Catalog of published genome-wide association studies (http://www.ebi.ac.uk/gwas/). The disease/trait examined in this study, as reported by the authors, was Clozapine-induced agranulocytosis. The EFO term drug-induced agranulocytosis, response to clozapine was annotated to this set after curation by NHGRI-EBI. Intergenic SNPS were mapped to both the upstream and downstream gene. P-value uploaded. This gene set was generated using gwas2gs v. 0.1.8 and the GWAS Catalog v. 1.0.1.
Authors:
JI Goldstein, LF Jarskog, C Hilliard, A Alfirevic, L Duncan, D Fourches, H Huang, M Lek, BM Neale, S Ripke, K Shianna, JP Szatkiewicz, A Tropsha, EJ van den Oord, I Cascorbi, M Dettling, E Gazit, DC Goff, AL Holden, DL Kelly, AK Malhotra, J Nielsen, M Pirmohamed, D Rujescu, T Werge, DL Levy, RC Josiassen, JL Kennedy, JA Lieberman, MJ Daly, PF Sullivan
Genes that are upregulated in adult male C57BL/6J mice given acute cocaine vs. acute saline. Tissue was collected from the ventral tegmental area (VTA) of the brain. Gene expression was evaluated via RNA-seq, and differential gene expression was determined via the Bayesian-regulated t-test (BayT). Values presented are p-values. Data taken from Supplementary Table 1. Data available from GEO with accession number GSE155313."""
Authors:
Rianne R Campbell, Siwei Chen, Joy H Beardwood, Alberto J López, Lilyana V Pham, Ashley M Keiser, Jessica E Childs, Dina P Matheos, Vivek Swarup, Pierre Baldi, Marcelo A Wood
Genes that are downregulated in adult male C57BL/6J mice given chronic cocaine vs. chronic saline. Tissue was collected from the ventral tegmental area (VTA) of the brain. Gene expression was evaluated via RNA-seq, and differential gene expression was determined via the Bayesian-regulated t-test (BayT). Values presented are p-values. Data taken from Supplementary Table 1. Data available from GEO with accession number GSE155313."""
Authors:
Rianne R Campbell, Siwei Chen, Joy H Beardwood, Alberto J López, Lilyana V Pham, Ashley M Keiser, Jessica E Childs, Dina P Matheos, Vivek Swarup, Pierre Baldi, Marcelo A Wood
BayT cocaine conditioning vs saline conditioning downreg
Description:
Genes that are downregulated in adult male C57BL/6J mice given cocaine conditioning vs. saline conditioning. Tissue was collected from the ventral tegmental area (VTA) of the brain. Gene expression was evaluated via RNA-seq, and differential gene expression was determined via the Bayesian-regulated t-test (BayT). Values presented are p-values. Data taken from Supplementary Table 1. Data available from GEO with accession number GSE155313."""
Authors:
Rianne R Campbell, Siwei Chen, Joy H Beardwood, Alberto J López, Lilyana V Pham, Ashley M Keiser, Jessica E Childs, Dina P Matheos, Vivek Swarup, Pierre Baldi, Marcelo A Wood
Genes that are induced by THC in CD4 cells in C57BL/6J mice. Gene expression was evaluated via RNA-seq. Values presented are "1" for effect presence. Data taken from Supplemental Data 1.
Authors:
Xiaoming Yang, Marpe Bam, Prakash S Nagarkatti, Mitzi Nagarkatti
This gene set describes genes that are down-regulated in blood of children with COVID-19, the disease caused by SARS-CoV2, versus healthy controls using RNAseq analysis. These children did not have MIS-C. The genes were filtered for a p-value < 0.05 and a log fold-change of greater than 1.0 given in supplemental table 7. Genes were entered into GeneWeaver using the reported EnsEMBL identifiers. Values are log-fold change.
Authors:
Noam D Beckmann, Phillip H Comella, Esther Cheng, Lauren Lepow, Aviva G Beckmann, Scott R Tyler, Konstantinos Mouskas, Nicole W Simons, Gabriel E Hoffman, Nancy J Francoeur, Diane Marie Del Valle, Gurpawan Kang, Anh Do, Emily Moya, Lillian Wilkins, Jessica Le Berichel, Christie Chang, Robert Marvin, Sharlene Calorossi, Alona Lansky, Laura Walker, Nancy Yi, Alex Yu, Jonathan Chung, Matthew Hartnett, Melody Eaton, Sandra Hatem, Hajra Jamal, Alara Akyatan, Alexandra Tabachnikova, Lora E Liharska, Liam Cotter, Brian Fennessy, Akhil Vaid, Guillermo Barturen, Hardik Shah, Ying-Chih Wang, Shwetha Hara Sridhar, Juan Soto, Swaroop Bose, Kent Madrid, Ethan Ellis, Elyze Merzier, Konstantinos Vlachos, Nataly Fishman, Manying Tin, Melissa Smith, Hui Xie, Manishkumar Patel, Kai Nie, Kimberly Argueta, Jocelyn Harris, Neha Karekar, Craig Batchelor, Jose Lacunza, Mahlet Yishak, Kevin Tuballes, Ieisha Scott, Arvind Kumar, Suraj Jaladanki, Charuta Agashe, Ryan Thompson, Evan Clark, Bojan Losic, Lauren Peters, , Panagiotis Roussos, Jun Zhu, Wenhui Wang, Andrew Kasarskis, Benjamin S Glicksberg, Girish Nadkarni, Dusan Bogunovic, Cordelia Elaiho, Sandeep Gangadharan, George Ofori-Amanfo, Kasey Alesso-Carra, Kenan Onel, Karen M Wilson, Carmen Argmann, Supinda Bunyavanich, Marta E Alarcón-Riquelme, Thomas U Marron, Adeeb Rahman, Seunghee Kim-Schulze, Sacha Gnjatic, Bruce D Gelb, Miriam Merad, Robert Sebra, Eric E Schadt, Alexander W Charney
Chronic alcohol abuse alters the molecular structure and function of brain cells. Recent work suggests adaptations made by glial cells, such as astrocytes and microglia, regulate physiological and behavioral changes associated with addiction. Defining how alcohol dependence alters the transcriptome of different cell types is critical for developing the mechanistic hypotheses necessary for a nuanced understanding of cellular signaling in the alcohol-dependent brain. We performed RnA-sequencing on total homogenate and glial cell populations isolated from mouse prefrontal cortex (pfc) following chronic intermittent ethanol vapor exposure (cie). compared with total homogenate, we observed unique and robust gene expression changes in astrocytes and microglia in response to cie. Gene co-expression network analysis revealed biological pathways and hub genes associated with cie in astrocytes and microglia that may regulate alcohol-dependent phenotypes. Astrocyte identity and synaptic calcium signaling genes were enriched in alcohol-associated astrocyte networks, while tGf-β signaling and inflammatory response genes were disrupted by CIE treatment in microglia gene networks. Genes related to innate immune signaling, specifically interferon pathways, were consistently up-regulated across cie-exposed astrocytes, microglia, and total homogenate pfc tissue. This study illuminates the cell-specific effects of chronic alcohol exposure and provides novel molecular targets for studying alcohol dependence.
Authors:
Emma K Erickson, Yuri A Blednov, R Adron Harris, R Dayne Mayfield
The current study used two inbred mouse strains, C57BL/6 J and A/J, to investigate the genetics of behavioral responses to fentanyl. Mice were tested for conditioned place preference and fentanyl-induced locomotor activity. C57BL/6J mice formed a conditioned place preference to fentanyl injections and fentanyl increased their activity. Neither effect was noted in A/J mice. We conducted RNA-sequencing on the nucleus accumbens of mice used for fentanyl-induced locomotor activity. Surprisingly, we noted few differentially expressed genes using treatment as the main factor. However many genes differed between strains.
Authors:
Samuel J Harp, Mariangela Martini, Will Rosenow, Larry D Mesner, Hugh Johnson, Charles R Farber, Emilie F Rissman
Data from GEO GSE194368 and analyzed using GEO2R, only top gene shown. Authors identified transcriptional adaptations of GR signaling in the amygdala of humans with OUD. Thus, GRs, their coregulators and downstream systems may represent viable therapeutic targets to treat the “stress side” of OUD.
Authors:
Stephanie A Carmack, Janaina C M Vendruscolo, M Adrienne McGinn, Jorge Miranda-Barrientos, Vez Repunte-Canonigo, Gabriel D Bosse, Daniele Mercatelli, Federico M Giorgi, Yu Fu, Anthony J Hinrich, Francine M Jodelka, Karen Ling, Robert O Messing, Randall T Peterson, Frank Rigo, Scott Edwards, Pietro P Sanna, Marisela Morales, Michelle L Hastings, George F Koob, Leandro F Vendruscolo
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