BEGIN:VCALENDAR
VERSION:2.0
PRODID:-//Center for RNA Biomedicine - ECPv6.15.20//NONSGML v1.0//EN
CALSCALE:GREGORIAN
METHOD:PUBLISH
X-ORIGINAL-URL:https://rna.umich.edu
X-WR-CALDESC:Events for Center for RNA Biomedicine
REFRESH-INTERVAL;VALUE=DURATION:PT1H
X-Robots-Tag:noindex
X-PUBLISHED-TTL:PT1H
BEGIN:VTIMEZONE
TZID:America/Detroit
BEGIN:DAYLIGHT
TZOFFSETFROM:-0500
TZOFFSETTO:-0400
TZNAME:EDT
DTSTART:20220313T070000
END:DAYLIGHT
BEGIN:STANDARD
TZOFFSETFROM:-0400
TZOFFSETTO:-0500
TZNAME:EST
DTSTART:20221106T060000
END:STANDARD
BEGIN:DAYLIGHT
TZOFFSETFROM:-0500
TZOFFSETTO:-0400
TZNAME:EDT
DTSTART:20230312T070000
END:DAYLIGHT
BEGIN:STANDARD
TZOFFSETFROM:-0400
TZOFFSETTO:-0500
TZNAME:EST
DTSTART:20231105T060000
END:STANDARD
BEGIN:DAYLIGHT
TZOFFSETFROM:-0500
TZOFFSETTO:-0400
TZNAME:EDT
DTSTART:20240310T070000
END:DAYLIGHT
BEGIN:STANDARD
TZOFFSETFROM:-0400
TZOFFSETTO:-0500
TZNAME:EST
DTSTART:20241103T060000
END:STANDARD
END:VTIMEZONE
BEGIN:VEVENT
DTSTART;TZID=America/Detroit:20230109T160000
DTEND;TZID=America/Detroit:20230109T170000
DTSTAMP:20260512T030753
CREATED:20220902T192057Z
LAST-MODIFIED:20230109T135614Z
UID:10565-1673280000-1673283600@rna.umich.edu
SUMMARY:RNA Innovation Seminar: Karen Mohlke\, UNC
DESCRIPTION:“Genetic Variant Effects on Adipose Gene Expression and Their Role in Cardiometabolic Traits.”\nKaren Mohlke\, Ph.D.\nProfessor and Associate Chair for Research\nOliver Smithies Investigator\nDepartment of Genetics\, University of North Carolina\nIn-person: BSRB\, ABC seminar rooms / hybrid link \nAbstract: Noncoding genetic variants can affect common diseases and related quantitative traits. Variants may affect the expression levels of transcripts and alternatively-spliced isoforms\, dependent on cell context. I will describe genetic variants associated with adipose tissue gene expression level in >2\,200 people and their putative roles in cardiometabolic disease traits. Similarly\, I will implicate variants associated with splice junction usage in disease risk. Finally\, based on chromatin accessibility during adipocyte differentiation\, I will show genetic regulatory effects that depend on cell context. Together\, these studies help identify regulatory mechanisms for common diseases.\nKeywords: Transcriptome\, expression quantitative trait loci (eQTL)\, splice QTL (sQTL)\, genome-wide association study (GWAS)\, chromatin accessibility\, epigenome\, adipose tissue\, adipocyte.
URL:https://rna.umich.edu/events/karen-mohlke/
LOCATION:MI
END:VEVENT
BEGIN:VEVENT
DTSTART;TZID=America/Detroit:20230130T160000
DTEND;TZID=America/Detroit:20230130T170000
DTSTAMP:20260512T030753
CREATED:20221102T121834Z
LAST-MODIFIED:20230110T144621Z
UID:10666-1675094400-1675098000@rna.umich.edu
SUMMARY:RNA Innovation Seminar: Carlos Cruchaga\,  Washington University in St Louis
DESCRIPTION:“Role of Circular RNA in Alzheimer’s Disease”\nCarlos Cruchaga\, Ph.D.\nDirector\, NeuroGenomics and Informatics Center\nWashington University in St Louis\nIn-person: BSRB\, ABC seminar rooms / hybrid link \nShort Bio: Dr. Cruchaga is a human genomicist with expertise in multiomics\, informatics\, and neurodegeneration. He completed his PhD in Biochemistry & Molecular Biology in 2005 at the University of Navarra in Spain. During his first postdoc with Dr. Pastor he conducted statistical human genetics studies focused on Alzheimer’s disease (AD) and Parkinson’s disease (PD). He then moved to Dr. Goate’s Lab to complete his training in quantitative human genomics. Dr Cruchaga established his laboratory at Washington University in  2011 to study the genetic architecture of neurodegenerative diseases. His interests are focused on using human genomic and other -omis data (proteomics\, metabolomics\, & lipidomics) to identify and understand the biological processes that lead to AD\, PD\, frontotemporal dementia\, and other neurodegenerative processes. He is the founding director of the NeuroGenomics and Informatics Center at Washington University. \nAbstract: Circular RNAs (circRNAs) are a class of RNAs highly expressed in the nervous system and enriched in synaptoneurosomes. In Alzheimer Disease\, synapse lost is one of the events implicated on disease. circRNA are form by back-splicing (head-to-tail splicing)\, and where first described in eukaryotic cells and other studies suggested that synapse could be enriched for circRNA. Based on we hypothesized that specific circRNA would be differentially expressed in AD cases compared to controls and that those effects could be detected early in the disease. We optimized and validated a novel analyses pipeline for circular RNAs (circRNA). We performed a three-stage study design to robustly identify circRNA associated with AD and AD-related phenotypes. Additional analyses were performed to demonstrate that the expression of circRNA were independent of the lineal form as well as the cell proportion that can confound results. Co-expression analyses of all the circRNA together with the lineal forms and found that circRNA\, including those that were differentially expressed in Alzheimer disease compared to controls co-expressed with known causal Alzheimer genes\, such as APP and PSEN1\, indicating that some circRNA are also part of the causal pathway. We also demonstrated that cirRNAs brain expression explained more about Alzheimer clinical manifestations that the number of APOε4 alleles\, suggesting that could be used as a potential biomarker for Alzheimer disease. In summary\, we demonstrated for the first time that brain circular RNAs (circRNA) are part of the pathogenic events that lead to Alzheimer’s disease
URL:https://rna.umich.edu/events/carlos-cruchaga/
LOCATION:MI
END:VEVENT
END:VCALENDAR