4 results match your criteria: "Ireland Research Institute[Affiliation]"
Tyrosine phosphorylation of the E3 ubiquitin ligase TRIM21 positively regulates interaction with IRF3 and hence TRIM21 activity.
PLoS One
November 2012
Department Molecular and Cellular Therapeutics, Royal College Surgeons in Ireland Research Institute, Royal College of Surgeons in Ireland, Dublin, Ireland.
Patients suffering from Systemic Lupus Erythematous (SLE) have elevated type I interferon (IFN) levels which correlate with disease activity and severity. TRIM21, an autoantigen associated with SLE, has been identified as an ubiquitin E3 ligase that targets the transcription factor IRF3 in order to turn off and limit type I IFN production following detection of viral and bacterial infection by Toll Like Receptors (TLRs). However, how the activity of TRIM21 is regulated downstream of TLRs is unknown.
View Article and Find Full Text PDFAMP kinase-mediated activation of the BH3-only protein Bim couples energy depletion to stress-induced apoptosis.
J Cell Biol
April 2010
Department of Physiology and Medical Physics, Royal College of Surgeons in Ireland Research Institute, Dublin 2, Ireland.
Article Synopsis
- Excitotoxicity from excessive glutamate receptor activation leads to cell death (necrosis or apoptosis) due to disturbances in cellular ion gradients and rapid ATP loss.
- Transient reductions in cellular energy and activation of AMPK are crucial for triggering excitotoxic apoptosis, highlighting the need for some energy recovery for this process.
- Activation of the pro-apoptotic protein Bim is linked to AMPK activation, suggesting that AMPK and Bim together connect energy depletion with stress-induced neuron death.
Absence of SHIP-1 results in constitutive phosphorylation of tank-binding kinase 1 and enhanced TLR3-dependent IFN-beta production.
J Immunol
March 2010
Molecular and Cellular Therapeutics, Royal College of Surgeons, Ireland Research Institute, Dublin 2, Ireland.
Autoimmune diseases, such as systemic lupus erythematosus and rheumatoid arthritis, result from a loss of tolerance to self-antigens and immune-mediated injury precipitated by the overproduction of type I IFN and inflammatory cytokines. We have identified the inositol 5' phosphatase SHIP-1 as a negative regulator of TLR3-induced type I IFN production. SHIP-1-deficient macrophages display enhanced TLR-induced IFN-beta production, and overexpression of SHIP-1 negatively regulates the ability of TLR3 and its adaptor, Toll/IL-1 receptor domain-containing adaptor-inducing IFN-beta, to induce IFN-beta promoter activity, indicating that SHIP-1 negatively regulates TLR-induced IFN-beta production.
View Article and Find Full Text PDFMulticentre search for genetic susceptibility loci in sporadic epilepsy syndrome and seizure types: a case-control study.
Lancet Neurol
November 2007
Department of Clinical Neurological Sciences and Molecular and Cellular Therapeutics, Royal College of Surgeons in Ireland Research Institute, and Division of Neurology, Beaumont Hospital, Dublin, Ireland.
Background: The Epilepsy Genetics (EPIGEN) Consortium was established to undertake genetic mapping analyses with augmented statistical power to detect variants that influence the development and treatment of common forms of epilepsy.
Methods: We examined common variations across 279 prime candidate genes in 2717 case and 1118 control samples collected at four independent research centres (in the UK, Ireland, Finland, and Australia). Single nucleotide polymorphism (SNP) and combined set-association analyses were used to examine the contribution of genetic variation in the candidate genes to various forms of epilepsy.