Irina Vlasova-St. Louis

Dr. Irina Vlasova-St. Louis

Rare Diseases, Vinnana Genetics LLC, Sheridan, Wyoming, USA
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Research Focus & Metrics

Academic Career Length

23Years (2004-Present)

(Calculated once Scilit publication data is synced: current year − year of first publication + 1)

Representative Publications

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17 April 2007 in Proceedings of the National Academy of Sciences
Verified
Journal Article
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RGRobert R. Graham
Robert R. Graham
CKChieko Kyogoku
Chieko Kyogoku
SSSnaevar Sigurdsson
Snaevar Sigurdsson
Irina Vlasova-St. LouisIrina Vlasova-St. Louis
Irina Vlasova-St. Louis
LDLeela R. L. Davies
Leela R. L. Davies
DADavid Altshuler
David Altshuler
Systematic genome-wide studies to map genomic regions associated with human diseases are becoming more practical. Increasingly, efforts will be focused on the identification of the specific functional variants responsible for the disease. The challenges of identifying causal variants include the need for complete ascertainment of genetic variants and the need to consider the possibility of multiple causal alleles. We recently reported that risk of systemic lupus erythematosus (SLE) is strongly associated with a common SNP in IFN regulatory factor 5 ( IRF5 ), and that this variant altered spicing in a way that might provide a functional explanation for the reproducible association to SLE risk. Here, by resequencing and genotyping in patients with SLE, we find evidence for three functional alleles of IRF5 : the previously described exon 1B splice site variant, a 30-bp in-frame insertion/deletion variant of exon 6 that alters a proline-, glutamic acid-, serine- and threonine-rich domain region, and a variant in a conserved polyA+ signal sequence that alters the length of the 3′ UTR and stability of IRF5 mRNAs. Haplotypes of these three variants define at least three distinct levels of risk to SLE. Understanding how combinations of variants influence IRF5 function may offer etiological and therapeutic insights in SLE; more generally, IRF5 and SLE illustrates how multiple common variants of the same gene can together influence risk of common disease.

1 February 2008 in Molecular Cell
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Journal Article
Closed access
Irina Vlasova-St. LouisIrina Vlasova-St. Louis
Irina Vlasova-St. Louis
NTNuzha M. Tahoe
Nuzha M. Tahoe
DFDanhua Fan
Danhua Fan
OLOla Larsson
Ola Larsson
BRBernd Rattenbacher
Bernd Rattenbacher
PBPaul Bohjanen
Paul Bohjanen

1 April 2009 in Journal of Biological Chemistry
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Journal Article
Open access
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RORachel L. Ogilvie
Rachel L. Ogilvie
JSJulius R. SternJohn
Julius R. SternJohn
BRBernd Rattenbacher
Bernd Rattenbacher
Irina Vlasova-St. LouisIrina Vlasova-St. Louis
Irina Vlasova-St. Louis
DWDarlisha A. Williams
Darlisha A. Williams
PBPaul Bohjanen
Paul Bohjanen
Tristetraprolin (TTP) regulates expression at the level of mRNA decay of several cytokines, including the T cell-specific cytokine, interleukin-2. We performed experiments to determine whether another T cell-specific cytokine, interferon-γ (IFN-γ), is also regulated by TTP and found that T cell receptor-activated T cells from TTP knock-out mice overproduced IFN-γ mRNA and protein compared with activated T cells from wild-type mice. The half-life of IFN-γ mRNA was 23 min in anti-CD3-stimulated T cells from wild-type mice, whereas it was 51 min in anti-CD3-stimulated T cells from TTP knock-out mice, suggesting that the overexpression of IFN-γ mRNA in TTP knock-out mice was due to stabilization of IFN-γ mRNA. Insertion of a 70-nucleotide AU-rich sequence from the murine IFN-γ 3′-untranslated region, which contained a high affinity binding site for TTP, into the 3′-untranslated region of a β-globin reporter transcript conferred TTP-dependent destabilization on the β-globin transcript. Together these results suggest that TTP binds to a functional AU-rich element in the 3′-untranslated region of IFN-γ mRNA and mediates rapid degradation of the IFN-γ transcript. Thus, TTP plays an important role in turning off IFN-γ expression at the appropriate time during an immune response.

1 August 2011 in Current Opinion in Genetics & Development
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Journal Article
Closed access
Irina Vlasova-St. LouisIrina Vlasova-St. Louis
Irina Vlasova-St. Louis
PBPaul Bohjanen
Paul Bohjanen

1 June 2013 in Biochimica et Biophysica Acta (BBA) - Gene Regulatory Mechanisms
Verified
Journal Article
Closed access
Irina Vlasova-St. LouisIrina Vlasova-St. Louis
Irina Vlasova-St. Louis
ADAlexa M. Dickson
Alexa M. Dickson
PBPaul Bohjanen
Paul Bohjanen
CWCarol J. Wilusz
Carol J. Wilusz

1 January 2012 in Journal of Biological Chemistry
Verified
Journal Article
Open access
DBDaniel Beisang
Daniel Beisang
BRBernd Rattenbacher
Bernd Rattenbacher
Irina Vlasova-St. LouisIrina Vlasova-St. Louis
Irina Vlasova-St. Louis
PBPaul Bohjanen
Paul Bohjanen
The RNA-binding protein, CUG-binding protein 1 (CUGBP1), regulates gene expression at the levels of alternative splicing, mRNA degradation, and translation. We used RNA immunoprecipitation followed by microarray analysis to identify the cytoplasmic mRNA targets of CUGBP1 in resting and activated primary human T cells and found that CUGBP1 targets were highly enriched for the presence of GU-rich elements (GREs) in their 3'-untranslated regions. The number of CUGBP1 target transcripts decreased dramatically following T cell activation as a result of activation-dependent phosphorylation of CUGBP1 and decreased ability of CUGBP1 to bind to GRE-containing RNA. A large percentage of CUGBP1 target transcripts exhibited rapid and transient up-regulation, and a smaller percentage exhibited transient down-regulation following T cell activation. Many of the transiently up-regulated CUGBP1 target transcripts encode important regulatory proteins necessary for transition from a quiescent state to a state of cellular activation and proliferation. Overall, our results show that CUGBP1 binding to certain GRE-containing target transcripts decreased following T cell activation through activation-dependent phosphorylation of CUGBP1.