Ciara M. Walsh

ORCID: 0000-0002-7873-5627
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About
Contact & Profiles
Research Areas
  • Ion Channels and Receptors
  • Ion channel regulation and function
  • Alzheimer's disease research and treatments
  • Prion Diseases and Protein Misfolding
  • Respiratory and Cough-Related Research
  • Signaling Pathways in Disease
  • Phytochemicals and Antioxidant Activities
  • Cellular transport and secretion
  • 14-3-3 protein interactions
  • Neuroscience and Neuropharmacology Research
  • Ubiquitin and proteasome pathways
  • Biochemical Analysis and Sensing Techniques
  • RNA Research and Splicing
  • Retinal Development and Disorders
  • Neurobiology and Insect Physiology Research
  • Connexins and lens biology
  • Toxin Mechanisms and Immunotoxins
  • Mitochondrial Function and Pathology

University College Dublin
2024

University of Liverpool
2008-2010

Royal College of Surgeons in Ireland
2006-2010

Ca2+ entry through store-operated channels involves the interaction at ER-PM (endoplasmic reticulum-plasma membrane) junctions of STIM (stromal molecule) and Orai. proteins are sensors luminal ER concentration and, following depletion Ca2+, they oligomerize translocate to where form puncta. Direct binding Orai activates their channel function. It has been suggested that an additional C-terminal polybasic domain STIM1 with PM phosphoinositides could contribute puncta formation prior In...

10.1042/bj20090884 article EN cc-by-nc Biochemical Journal 2009-10-21

Amyloidogenic processing of the amyloid precursor protein (APP) results in generation beta-amyloid, main constituent Alzheimer plaques, and APP intracellular domain (AICD). Recently, it has been demonstrated that AICD transactivation potential; however, targets AICD-dependent gene regulation hence physiological role remain largely unknown. We analyzed transcriptome changes during by using a human neural cell culture system inducible for expression AICD, its coactivator FE65, or combination...

10.1091/mbc.e06-04-0283 article EN Molecular Biology of the Cell 2006-11-09

SOCCs (store-operated Ca(2+) channels) are highly selective ion channels that activated upon release of from intracellular stores to regulate a multitude diverse cellular functions. It was reported previously Golli-BG21, member the MBP (myelin basic protein) family proteins, regulates SOCE entry) in T-cells and oligodendrocyte precursor cells, but underlying mechanism for this regulation is unknown. In present study we have discovered Golli can directly interact with ER (endoplasmic...

10.1042/bj20100650 article EN cc-by-nc Biochemical Journal 2010-07-15

Depletion of the endoplasmic reticulum (ER) calcium store triggers translocation stromal interacting molecule one (STIM1) to sub-plasmalemmal region and formation puncta-structures in which STIM1 interacts activates channels. ATP depletion induced puncta PANC1, RAMA37, HeLa cells. The sequence events triggered by inhibition production included a rapid decline ATP, phosphatidylinositol 4,5-bisphosphate (PI(4,5)P(2)) slow leak from ER followed puncta. were co-localized with clusters ORAI1...

10.1007/s00424-008-0529-y article EN cc-by-nc Pflügers Archiv - European Journal of Physiology 2008-06-09

The amyloid precursor protein (APP) is critically involved in the pathogenesis of Alzheimer's disease, and strongly up-regulated response to traumatic, metabolic, or toxic insults nervous system. processing APP by gamma/epsilon-secretase activity results generation intracellular domain (AICD). Previously, we have shown that AICD induces expression genes (transgelin, alpha2-actin) with functional roles actin organization dynamics demonstrated induction its co-activator Fe65 (AICD/Fe65)...

10.1111/j.1471-4159.2010.06615.x article EN Journal of Neurochemistry 2010-01-22

Abstract Inherited retinal diseases (IRDs) are a rare group of eye disorders characterized by progressive dysfunction and degeneration cells. In this study, we the raifteirí (raf) zebrafish, novel model inherited blindness, identified through an unbiased ENU mutagenesis screen. A mutation in largest subunit endoplasmic reticulum membrane protein complex, emc1 was subsequently as causative raf mutation. We sought to elucidate cellular molecular phenotypes −/− knockout explore association with...

10.1096/fj.202401977r article EN cc-by The FASEB Journal 2024-10-03
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