Professor Neil Perkins
Prof of Gene Exp & Signalling

  • Email: neil.perkins@ncl.ac.uk
  • Telephone: +44 (0) 191 208 8866
  • Fax: +44 (0) 191 208 7424
  • Address: Institute for Cell and Molecular Biosciences (ICaMB)
    Medical School
    Newcastle University
    Catherine Cookson Building
    Framlington Place
    Newcastle upon Tyne
    NE2 4HH
    United Kingdom

Background

My PhD was completed in Graham Goodwin's laboratory at the Chester Beatty Laboratories, Institute of Cancer Research, London in 1990. This work concerned the investigation of chicken beta globin gene expression and resulted in the identification of the transcription factor that later became known as GATA1 (known as EF1 in the Goodwin lab).

From 1990 to 1996 I was a postdoctoral researcher in Gary Nabel's laboratory, at the Howard Hughes Medical Institute at the University of Michigan, where my interest in the NF-κB transcription factor family began. Much of this work concerned the ability of NF-κB to function as a regulator of human immunodeficiency virus (HIV) 1.

Previous Positions

October 1986 - March 1990: Ph.D. student in the laboratory of Dr. Graham Goodwin, Chester Beatty Laboratories, Institute of Cancer Research.

March 1990- March 1996: Postdoctoral Fellow in the laboratory of Prof. Gary J. Nabel, Howard Hughes Medical Institute, University of Michigan Medical Center, Ann Arbor, MI, USA.

March 1996 – Nov 2007: Lecturer and then Reader, Principal Investigator, University of Dundee

October 1996 - September 2005: Royal Society University Research Fellow

Nov 2007 – June 2008: Professor of Gene Expression and Signalling in the Wellcome Centre for Gene Regulation and Expression, College of Life Sciences, University of Dundee

July 2008 – March 2010: Professor of Molecular Cell Biology, Department of Cellular & Molecular Medicine, University of Bristol

April 2010 - present: Professor of Gene Expression and Signalling, Newcastle University

Regulation of cancer cell proliferation and survival by NF-κB

NF-κB is a collective name for the complexes formed by the multigene NF-κB-Rel family which function as DNA-binding proteins and transcription factors. NF-κB subunits induce the expression of a wide range of genes encoding proteins involved in inflammation, regulation of cell death, cell adhesion, proliferation and other critical cellular functions. Aberrant activation of NF-κB therefore leads to overproduction of these proteins, which can contribute to many types of human disease. In particular, NF-κB has an important role in many inflammatory diseases and cancer. Moreover, NF- κB is activated by many cancer therapies and can have an inhibitory effect on these treatments. The pathways regulating NF-κB are therefore thought to be good targets for the development of new anti-inflammatory and anti-cancer drugs.

My laboratory is interested in how NF-κB subunits are regulated by oncogenes, tumour suppressors and stimuli associated with cancer development and therapy. A theme emerging from these studies has been the importance of context for NF-κB activity and how subunits can both repress as well as activate gene targets, leading to alterations in cell fate. We have revealed the importance of post-translational modifications in controlling these activities and argued that the activity of parallel signaling pathways have a critical role in determining NF-κB dependent transcriptional output. Based on this work, together with that from other researchers, we propose that the concerted action of tumour suppressors functions to keep the oncogenic activities of NF-κB subunits in check and that loss of tumour suppressor activity during tumour development is required to unleash these anti apoptotic and pro-metastatic activities in malignant cancer cells.

We are also interested in a protein known as Smad nuclear interacting protein 1 (SNIP1). We have previously described SNIP1 as a regulator of Cyclin D1 expression. Recently we have identified a SNIP1 containing complex and demonstrated that this functions as a novel regulator of Cyclin D1 RNA stability.