Craig Stevens
Craig Stevens

Dr Craig Stevens

Associate Professor

 0131 455 2930

  C.Stevens@napier.ac.uk

  

Biography

Dr Craig Stevens BSc PhD FHEA is Associate Professor and Principal Investigator (PI) within the School of Applied Sciences at Edinburgh Napier University (ENU). Craig completed his undergraduate degree in Biochemistry at Heriot-Watt University, Edinburgh in 1999 and his PhD from the University of Glasgow in 2004 where he studied the role of E2F transcription factors in DNA damage checkpoint control within the group of Prof Nick LaThangue. In 2004, he moved to the Edinburgh Cancer Research Centre within the Institute of Genetics & Molecular Medicine (IGMM) at the University of Edinburgh for his first Postdoctoral Research position, joining the Cell Signalling Laboratory of Prof Ted Hupp where his research focused on the control of cell growth by mechanistic target of rapamycin (mTORC1) and death-associated protein kinase (DAPK) signalling pathways. Craig stayed at the IGMM for a Senior Research Fellow position, joining the Gastroenterology Laboratory of Prof Jack Satsangi to investigate the role of autophagy in the pathogenesis of Inflammatory Bowel Disease (IBD), specifically Crohn’s disease (CD). During this time Craig helped to secure funding from the Medical Research Council (MRC), Chief Scientist Office (CSO) and the National Association of Crohn’s and Colitis (NACC).

In 2012, Craig joined the School of Applied Sciences at ENU as Lecturer and PI, was appointed Research Leader in Biomedical Sciences in October 2016 and promoted to Associate Professor in August 2018. At ENU Craig's academic role focuses on both research and teaching of undergraduate and postgraduate degrees. Research in Craig’s group is currently supported by funding from Crohn's in Childhood Research Association (CICRA) and the CSO and focusses on three main areas:

1. Understanding the role of autophagy in CD.
2. Investigating the mechanism of action of drugs commonly used to treat patients with IBD.
3. The role of host defence peptides in IBD.

The potential for translational research results from Craig's strong collaborative links with ongoing IBD research at the Royal Hospital for Sick Children, Edinburgh (Dr Paul Henderson, Consultant Paediatric Gastroenterologist) and University of Oxford (Prof Jack Satsangi, Consultant Physician). Craig also has strong collaborative links at ENU with Dr Peter Barlow investigating novel peptide based therapeutics for the treatment of IBD.

School

Research Groups

Themes

Research Areas

Esteem

Advisory panels and expert committees or witness

  • Expert reviewer for the Royal College of Surgeons (RCSI), Ireland
  • Expert reviewer for Fondation Innovations en Infectiologie (Finovi), France

 

Conference Organising Activity

  • International congress of Mucosal Immunology, Washington, USA
  • European Crohn’s and Colitis Organisation (ECCO) congress, Barcelona, Spain
  • Autophagy UK meeting, London, England
  • European Molecular Biology Organisation (EMBO) Conference, Autophagy, from molecular principals to human diseases, Dubrovnik, Croatia
  • ER Stress, Autophagy & immune system, Bruges, Belgium
  • BSPGHAN annual meeting, Glasgow, Scotland
  • Autophagy UK meeting, Edinburgh, Scotland

 

Editorial Activity

  • Editorial Board of Advances in Biology

 

Grant Reviewer

  • Medical Research Council Peer Review

 

Invited Speaker

  • British Society of Gastroenterology (BSG), 1st Supraregional Meeting - Workshop: Intestinal Inflammation, Edinburgh, Scotland
  • British Society of Paediatric Gastroenterology, Hepatology and Nutrition (BSPGHAN) annual meeting, Edinburgh, Scotland
  • United European Gastroenterology Week (UEGW), Stockholm, Sweden

 

Membership of Professional Body

  • British Society for Immunology
  • Edinburgh Organoid Network
  • Edinburgh Infectious Diseases Network

 

Public/Community Engagement

  • Crohn’s in Childhood Research Association (CICRA) academic panel that meets children and families with IBD
  • STEM ambassador

 

Research Degree External Examining

  • MRes student for the University of Edinburgh

 

Reviewing

  • Journal of Crohn's and Colitis
  • Journal of Medical Microbiology
  • Inflammatory Bowel Diseases
  • Journal of Cancer
  • Toxicology Letters

 

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Date


38 results

The intermediate filament protein, vimentin, is a regulator of NOD2 activity

Journal Article
Stevens, C., Henderson, P., Nimmo, E. R., Soares, D. C., Dogan, B., Simpson, K. W., …Satsangi, J. (2013)
The intermediate filament protein, vimentin, is a regulator of NOD2 activity. Gut, 62(5), 695-707. https://doi.org/10.1136/gutjnl-2011-301775
Objective Mutations in the nucleotide-binding oligomerisation domain-containing protein 2 (NOD2) gene remain the strongest genetic determinants for Crohn's disease (CD). Havin...

TLE1 modifies the effects of NOD2 in the pathogenesis of Crohn's Disease

Journal Article
Nimmo, E. R., Stevens, C., Phillips, A. M., Smith, A., Drummond, H. E., Noble, C. L., …Satsangi, J. (2011)
TLE1 modifies the effects of NOD2 in the pathogenesis of Crohn's Disease. Gastroenterology, 141(3), 972-981.e2. https://doi.org/10.1053/j.gastro.2011.05.043
Background & Aims The mechanisms by which specific mutations in NOD2/CARD15 increase the risk for Crohn's disease (CD) are unclear. We identified proteins that interact with {...

Tuberous sclerosis-2 (TSC2) regulates the stability of death-associated protein kinase-1 (DAPK) through a lysosome-dependent degradation pathway

Journal Article
Hupp, T., Lin, Y., Henderson, P., Pettersson, S., Satsangi, J., Hupp, T. R., & Stevens, C. (2010)
Tuberous sclerosis-2 (TSC2) regulates the stability of death-associated protein kinase-1 (DAPK) through a lysosome-dependent degradation pathway. FEBS Journal, 278(2), 354-370. https://doi.org/10.1111/j.1742-4658.2010.07959.x
We previously identified a novel interaction between tuberous sclerosis-2 (TSC2) and death-associated protein kinase-1 (DAPK), the consequence being that DAPK catalyses the in...

Peptide Combinatorial Libraries Identify TSC2 as a Death-associated Protein Kinase (DAPK) Death Domain-binding Protein and Reveal a Stimulatory Role for DAPK in mTORC1 Signaling

Journal Article
Stevens, C., Lin, Y., Harrison, B., Burch, L., Ridgway, R. A., Sansom, O. J., & Hupp, T. R. (2009)
Peptide Combinatorial Libraries Identify TSC2 as a Death-associated Protein Kinase (DAPK) Death Domain-binding Protein and Reveal a Stimulatory Role for DAPK in mTORC1 Signaling. Journal of Biological Chemistry, 284, 334-344. https://doi.org/10.1074/jbc.M805165200
Death-associated protein kinase (DAPK) is a multidomain enzyme that plays a central role in autophagic and apoptotic signaling, although the protein-protein interactions regul...

Death‐associated protein kinase (DAPK) and signal transduction: blebbing in programmed cell death.

Journal Article
Bovellan, M., Fritzsche, M., Stevens, C., & Charras, G. (2009)
Death‐associated protein kinase (DAPK) and signal transduction: blebbing in programmed cell death. FEBS Journal, 277(1), (58-65). ISSN 1742-464X
Death-associated protein kinase (DAPK) is a stress-regulated protein kinase that mediates a range of processes, including signal-induced cell death and autophagy. Although the...

Death-associated protein kinase (DAPK) and signal transduction: additional roles beyond cell death: DAPK and signal transduction

Journal Article
Lin, Y., Hupp, T. R., & Stevens, C. (2009)
Death-associated protein kinase (DAPK) and signal transduction: additional roles beyond cell death: DAPK and signal transduction. FEBS Journal, 277(1), (48-57). ISSN 1742-464X
Death-associated protein kinase (DAPK) is a stress-regulated protein kinase that mediates a range of processes, including signal-induced cell death and autophagy. Although the...

Autophagy: from basic science to clinical application

Journal Article
Van Limbergen, J., Stevens, C., Nimmo, E. R., Wilson, D. C. & Satsangi, J. (2009)
Autophagy: from basic science to clinical application. Mucosal immunology. 2(4), 315-330. doi:10.1038/mi.2009.20. ISSN 1933-0219
Autophagy is a cellular pathway involved in protein and organelle degradation, which is likely to represent an innate adaptation to starvation. In times of nutrient deficiency...

The alternative splice variant of DAPK-1, s-DAPK-1, induces proteasome-independent DAPK-1 destabilization.

Journal Article
Lin, Y., Stevens, C., Harrison, B., Pathuri, S., Amin, E., & Hupp, T. R. (2009)
The alternative splice variant of DAPK-1, s-DAPK-1, induces proteasome-independent DAPK-1 destabilization. Molecular and Cellular Biochemistry, 328(1-2), (101-107). doi:10.1007/s11010-009-0079-4. ISSN 0300-8177
Death-associated protein kinase 1 (DAPK-1) is a Ca2+/CaM-regulated kinase involved in multiple cellular signalling pathways that trigger cell survival, apoptosis, and autophag...

ATP stimulates MDM2-mediated inhibition of the DNA-binding function of E2F1: ATP stimulated inhibition of E2F1 by MDM2

Journal Article
Stevens, C., Pettersson, S., Wawrzynow, B., Wallace, M., Ball, K., Zylicz, A., & Hupp, T. R. (2008)
ATP stimulates MDM2-mediated inhibition of the DNA-binding function of E2F1: ATP stimulated inhibition of E2F1 by MDM2. FEBS Journal, 275(19), 4875-4886. https://doi.org/10.1111/j.1742-4658.2008.06627.x
Murine double minute 2 (MDM2) protein exhibits many diverse biochemical functions on the tumour suppressor protein p53, including transcriptional suppression and E3 ubiquitin ...

An alternative transcript from the death-associated protein kinase 1 locus encoding a small protein selectively mediates membrane blebbing: Functional transcript expressed by DAPK-1 locus

Journal Article
Lin, Y., Stevens, C., Hrstka, R., Harrison, B., Fourtouna, A., Pathuri, S., …Hupp, T. (2008)
An alternative transcript from the death-associated protein kinase 1 locus encoding a small protein selectively mediates membrane blebbing: Functional transcript expressed by DAPK-1 locus. FEBS Journal, 275(10), (2574-2584). doi:10.1111/j.1742-4658.2008.06404.x. ISSN 1742-464X
Death-associated protein kinase 1 (DAPK-1) is a multidomain protein kinase with diverse roles in autophagic, apoptotic and survival pathways. Bioinformatic screens were used t...

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