Simon Wilkinson

ORCID: 0000-0003-1082-8218
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About
Contact & Profiles
Research Areas
  • Autophagy in Disease and Therapy
  • Endoplasmic Reticulum Stress and Disease
  • Cellular transport and secretion
  • Prostate Cancer Diagnosis and Treatment
  • Cancer Research and Treatments
  • Cancer-related Molecular Pathways
  • Cystic Fibrosis Research Advances
  • Immune Response and Inflammation
  • Epigenetics and DNA Methylation
  • Complementary and Alternative Medicine Studies
  • RNA Interference and Gene Delivery
  • Ubiquitin and proteasome pathways
  • Phytochemistry Medicinal Plant Applications
  • Calcium signaling and nucleotide metabolism
  • Cell death mechanisms and regulation
  • Lysosomal Storage Disorders Research
  • Cancer-related gene regulation
  • MicroRNA in disease regulation
  • Phagocytosis and Immune Regulation
  • TGF-β signaling in diseases
  • Biomedical Text Mining and Ontologies
  • Hippo pathway signaling and YAP/TAZ
  • Pancreatic function and diabetes
  • interferon and immune responses
  • Immune cells in cancer

University of Edinburgh
2012-2025

Edinburgh Cancer Research
2011-2023

Auckland University of Technology
2023

Institute of Genetics and Cancer
2012-2021

The University of Melbourne
2019

Western General Hospital
2011-2018

Cancer Research UK Scotland Institute
2006-2017

Discovery Institute
2017

Sanford Burnham Prebys Medical Discovery Institute
2013-2017

Cancer Research UK
2017

Highlights•CCPG1 is an ER stress-inducible ER-phagy cargo receptor in mammals•CCPG1 binds directly to ATG8 proteins and FIP200 via distinct peptide motifs•CCPG1 lysosomal degradation both require these interactions•CCPG1 maintains normal luminal proteostasis pancreatic acinar cells vivoSummaryMechanisms of selective autophagy the ER, known as ER-phagy, molecular delineation, particularly vivo. It unclear how events control cellular health. Here, we identify cell-cycle progression gene 1...

10.1016/j.devcel.2017.11.024 article EN cc-by Developmental Cell 2017-12-28

Highlights•BRD4 represses a program of autophagy and lysosome genes independently MiT/TFE•BRD4 de-repression promotes certain types autophagy, but not others•Nutrient deprivation de-represses BRD4 via AMPK signaling to promote cell survival•Oncoprotein BRD4-NUT is potent repressor functionSummaryAutophagy membrane-trafficking process that directs degradation cytoplasmic material in lysosomes. The cellular fidelity, while the core machinery known, mechanisms sustain are less well defined....

10.1016/j.molcel.2017.04.027 article EN cc-by Molecular Cell 2017-05-01

Cellular homoeostatic pathways such as macroautophagy (hereinafter autophagy) are regulated by basic mechanisms that conserved throughout the eukaryotic kingdom. However, it remains poorly understood how these further evolved in higher organisms. Here we describe a modification autophagy pathway vertebrates, which promotes its activity response to oxidative stress. We have identified two oxidation-sensitive cysteine residues prototypic receptor SQSTM1/p62, allow activation of pro-survival...

10.1038/s41467-017-02746-z article EN cc-by Nature Communications 2018-01-11

K-Ras dependent non-small cell lung cancer (NSCLC) cells are 'addicted' to basal autophagy that reprograms cellular metabolism in a lysosomal-sensitive manner. Here we demonstrate the xenophagy-associated kinase TBK1 drives autophagy, consistent with its known requirement K-Ras-dependent NSCLC proliferation. Furthermore, this context is characterised by sequestration of xenophagy cargo receptor Ndp52 and paralogue Tax1bp1, which here be bona fide receptor. Autophagy these receptors promotes...

10.1371/journal.pone.0050672 article EN cc-by PLoS ONE 2012-11-29

Whole-cell models that explicitly represent all cellular components at the molecular level have potential to predict phenotype from genotype. However, even for simple bacteria, whole-cell will contain thousands of parameters, many which are poorly characterized or unknown. New algorithms needed estimate these parameters and enable researchers build increasingly comprehensive models. We organized Dialogue Reverse Engineering Assessments Methods (DREAM) 8 Whole-Cell Parameter Estimation...

10.1371/journal.pcbi.1004096 article EN cc-by PLoS Computational Biology 2015-05-28

Birt-Hogg-Dubé (BHD) syndrome is a rare autosomal dominant condition caused by mutations in the FLCN gene and characterized benign hair follicle tumors, pneumothorax, renal cancer. Folliculin (FLCN), protein product of gene, poorly tumor suppressor protein, currently linked to multiple cellular pathways. Autophagy maintains homeostasis removing damaged organelles macromolecules. Although autophagy kinase ULK1 drives autophagy, underlying mechanisms are still being unraveled few substrates...

10.4161/auto.29640 article EN Autophagy 2014-07-22

Mechanistic target of rapamycin complex 1 (MTORC1) and polo like kinase (PLK1) are major drivers cancer cell growth proliferation, inhibitors both protein kinases currently being investigated in clinical studies. To date, MTORC1's PLK1's functions mostly studied separately, reports on their mutual crosstalk scarce. Here, we identify PLK1 as a physical MTORC1 interactor human cells. inhibition enhances activity under nutrient sufficiency starved cells, directly phosphorylates the component...

10.1080/15548627.2016.1263781 article EN cc-by Autophagy 2017-01-19

No AccessJournal of UrologyCLINICAL UROLOGY: Original Articles1 Dec 2002Attitudes and Use Complementary Medicine in Men with Prostate Cancer SIMON WILKINSON, LEONARD G. GOMELLA, JOSEPH A. SMITH, MICHAEL K. BRAWER, NANCY DAWSON, ZEV WAJSMAN, LANTING DAI, GERALD W. CHODAK WILKINSONSIMON WILKINSON , GOMELLALEONARD GOMELLA SMITHJOSEPH SMITH BRAWERMICHAEL BRAWER DAWSONNANCY DAWSON WAJSMANZEV WAJSMAN DAILANTING DAI CHODAKGERALD View All Author...

10.1016/s0022-5347(05)64178-x article EN The Journal of Urology 2002-12-01

We purified the oncoprotein SnoN and found that it functions as a corepressor of tumor suppressor p53 in regulation hepatic alpha-fetoprotein (AFP) marker gene. promotes histone deacetylase interaction at an overlapping Smad binding, regulatory element (SBE/p53RE) AFP. Comparison wild-type p53-null mouse liver tissue by using chromatin immunoprecipitation (ChIP) reveals absence protein correlates with disappearance SBE/p53RE loss AFP developmental repression. Treatment AFP-expressing...

10.1128/mcb.25.3.1200-1212.2005 article EN Molecular and Cellular Biology 2005-01-18

The selective regulation of macroautophagy remains poorly defined. Here we report that PDGFR signaling is an essential promoter hypoxia-induced macroautophagy. Hypoxia-induced in tumor cells also HIF1α-dependent, with HIF1α integrating signals from PDGFRs and oxygen tension. Inhibition reduces half-life, despite buffering steady-state protein levels by a compensatory increase mRNA. This markedly changes pool dynamics, consequently the transcriptome. As autocrine growth factor hallmark many...

10.1101/gad.521709 article EN Genes & Development 2009-06-01

Autophagy is a membrane-trafficking process that serves to deliver cytoplasmic proteins and organelles the lysosome for degradation. The genetically defined many of factors involved are conserved from yeast man. Recently, number new autophagy regulators have been defined, including Damage-Regulated Modulator (DRAM), which lysosomal protein links tumor suppressor, p53. We describe here analysis DRAM-related reveals evolutionary conservation divergence DRAM's role in autophagy. report humans 5...

10.4161/cc.8.14.9050 article EN Cell Cycle 2009-07-15
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