Panayiota Stylianou

ORCID: 0000-0002-0904-6043
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About
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Research Areas
  • Interstitial Lung Diseases and Idiopathic Pulmonary Fibrosis
  • Cellular Mechanics and Interactions
  • Chronic Obstructive Pulmonary Disease (COPD) Research
  • Galectins and Cancer Biology
  • Cell Adhesion Molecules Research
  • Peptidase Inhibition and Analysis
  • Hippo pathway signaling and YAP/TAZ
  • Neonatal Respiratory Health Research
  • Microtubule and mitosis dynamics
  • Genetic and Kidney Cyst Diseases
  • CAR-T cell therapy research
  • Protist diversity and phylogeny
  • Signaling Pathways in Disease
  • Wnt/β-catenin signaling in development and cancer
  • Biomedical and Engineering Education
  • Photochromic and Fluorescence Chemistry
  • Invertebrate Immune Response Mechanisms
  • Biosimilars and Bioanalytical Methods
  • Occupational and environmental lung diseases
  • HER2/EGFR in Cancer Research
  • Pediatric health and respiratory diseases
  • Quinazolinone synthesis and applications
  • Cancer therapeutics and mechanisms
  • 3D Printing in Biomedical Research
  • Phytoestrogen effects and research

University of Leicester
2016-2025

Glenfield Hospital
2022-2025

NIHR Leicester Biomedical Research Centre
2019-2024

National Institute for Health Research
2024

University of Cyprus
2006-2016

Integrin-mediated activation of the pro-fibrotic mediator transforming growth factor-β1 (TGF-β1), plays a critical role in idiopathic pulmonary fibrosis (IPF) pathogenesis. Galectin-3 is believed to contribute pathological wound healing seen IPF, although its mechanism action not precisely defined. We hypothesised that galectin-3 potentiates TGF-β1 and/or signaling lung promote fibrogenesis. show induces human fibroblasts (HLFs) and specifically extracellular promotes...

10.1016/j.jbc.2024.107300 article EN cc-by Journal of Biological Chemistry 2024-04-18

Antibodies are one of the most important reagents used in biomedical and fundamental research, to identify, quantify proteins, contribute knowledge disease mechanisms, validate drug targets. Yet many antibodies research do not recognize their intended target, or additional molecules, compromising integrity findings leading waste resources, lack reproducibility, failure projects, delays development. Researchers frequently use without confirming that they perform as application interest. Here...

10.1080/19420862.2024.2323706 article EN cc-by mAbs 2024-03-06

FAK is a non-receptor tyrosine kinase involved in wide variety of biological processes and crucial for embryonic development. In this manuscript, we report the generation new dominant negative (FF), composed C terminus (FRNK) FERM domain protein. FF, unlike FRNK FERM, mimics localization active embryo, demonstrating that both domains are necessary to target its complexes vivo. We show has role recruitment on focal adhesions controls dynamics protein these complexes. Expression FF blocks...

10.1242/dev.096073 article EN Development 2013-09-19

The epidermal growth factor receptor (EGFR) is a key target in anticancer research, whose aberrant function malignancies has been linked to severe irregularities critical cellular processes, including cell cycle progression, proliferation, differentiation, and survival. EGFR mutant variants, either transmembrane or translocated the mitochondria and/or nucleus, often exhibit resistance inhibitors. ability noninvasively image quantify provides novel approaches detection, monitoring, treatment...

10.1021/acs.molpharmaceut.9b00608 article EN Molecular Pharmaceutics 2019-09-11

Background The Focal Adhesion Kinase is a well studied tyrosine kinase involved in wide number of cellular processes including cell adhesion and migration. It has also been shown to play important roles during embryonic development targeted disruption the FAK gene mice results lethality by day 8.5. Principal Findings Here we examined pattern phosphorylation Xenopus found that phosphorylated on all major residues from early blastula stages before any morphogenetic movements take place. We go...

10.1371/journal.pone.0042577 article EN cc-by PLoS ONE 2012-08-06

Abstract Chronic obstructive pulmonary disease (COPD) constitutes a major cause of morbidity and mortality. Genome wide association studies have shown significant associations between airflow obstruction or COPD with non-synonymous SNP in the TNS1 gene, which encodes tensin1. However, expression, cellular distribution function tensin1 human airway tissue cells are unknown. We therefore examined these characteristics from controls people asthma. Airway was immunostained for Tensin1 expression...

10.1038/s41598-019-55405-2 article EN cc-by Scientific Reports 2019-12-12

<h3>Background and Aims</h3> Idiopathic pulmonary fibrosis (IPF) is a chronic interstitial lung disease with unknown aetiology. Variant rs115982800 was identified in GWAS of decline forced vital capacity individuals IPF. PKN2 as the nearest gene. We aim to investigate role TGFβ1-dependent pro-fibrotic processes human myofibroblasts (HLMFs). <h3>Methods</h3> The genotype-tissue expression (GTEx) project IPF cell atlas were used gene bulk tissue, at cellular level single-cell RNA-sequencing...

10.1136/thorax-2024-btsabstracts.162 article EN 2024-11-01

<h3>Introduction and Aim</h3> Novel treatments for idiopathic pulmonary fibrosis (IPF) are required urgently. TGFβ1 is a central pro-fibrotic mediator in IPF. A better understanding of the molecular pathways activated by human lung tissue may facilitate development novel more effective anti-fibrotic medications. Our aim was to examine protein changes exposed TGFβ1. In current study we have used proteomic analysis test hypothesis that <i>TGFβ1 exerts effects on parenchyma this viable model...

10.1136/thorax-2024-btsabstracts.78 article EN 2024-11-01

Abstract Integrin-mediated activation of the pro-fibrotic mediator transforming growth factor-β1 (TGF-β1), plays a critical role in idiopathic pulmonary fibrosis (IPF) pathogenesis. Galectin-3 is believed to contribute pathological wound healing seen IPF individuals, although its mechanism action not precisely defined. We hypothesised that galectin-3 potentiates TGF-β1 and/or signaling lung promote fibrogenesis. show induces human fibroblasts (HLFs) and specifically extracellular promotes...

10.1101/2023.10.11.561855 preprint EN cc-by-nc-nd bioRxiv (Cold Spring Harbor Laboratory) 2023-10-11

Abstract Progressive fibrosing interstitial lung diseases (PFILDs) cause substantial morbidity and mortality. Antifibrotic agents slow progression, but most of the clinical need remains unmet. The archetypal PFILD is idiopathic pulmonary fibrosis (IPF). Chronic progression driven by transforming growth factor (TGF-)β1 signalling. It punctuated inflammatory flares known as acute exacerbations (AE-IPF), which are associated with accelerated decline high We hypothesized that injury responses...

10.1101/2022.08.12.503154 preprint EN bioRxiv (Cold Spring Harbor Laboratory) 2022-08-15

<h3>Background</h3> Galectin-3 critically mediates experimental fibrosis, potentiating pro-fibrotic effects of transforming growth factor (TGF)-β1, and is highly expressed in idiopathic pulmonary fibrosis (IPF). Therefore, a galectin-3 small molecule glycomimetic antagonist Phase 2B trials. may mediate pathogenesis alveolar epithelial cells (AECs) myofibroblasts by nucleating macromolecular complex assembly on the cell surface. We term this 'gal-3-fibrosome'. In addition to galectin-3,...

10.1136/thorax-2019-btsabstracts2019.95 article EN 2019-11-12

<b>Background</b> Chronic obstructive pulmonary disease (COPD) constitutes a major cause of morbidity and mortality. A recent genome wide association study (GWAS) showed significant the TNS1 gene (which encodes tensin1) with COPD. non-synonymous single nucleotide polymorphism (SNP) (W1197R) in is associated airflow obstruction GWAS. <b>Aim</b> To examine mRNA, protein expression prevalence W1197R tensin1 structural cells from healthy subjects patients <b>Methods Materials</b> Lung resections...

10.1183/13993003.congress-2016.pa4650 article EN 03.02 - Airway cell biology and immunopathology 2016-09-01
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