Dr Benjamin Pickard

Senior Lecturer

Strathclyde Institute of Pharmacy and Biomedical Sciences

Personal statement

Ben Pickard obtained a BSc in Biochemistry from Imperial College London (1992), and a PhD from the University of Edinburgh (1996). Before coming to the University of Strathclyde, he worked at the Babraham Institute, Cambridge on factors regulating DNA methylation, and at the Molecular Medicine Centre, Edinburgh, identifying genetic risk factors for common psychiatric illnesses such as schizophrenia, bipolar disorder and major depression.

Publications

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Publications

Cobalt increases oxidation of CaMKII in left ventricular tissue and reduces fibroblast viability and proliferation in female hearts: Cameron Ruiz Miren, Callan Rachel, Sran Arshdeep, MacQuaide Niall, Pickard Ben, Currie Susan; Heart Vol 111, pp. A6 (2025); https://doi.org/10.1136/heartjnl-2025-SCF.14
A mechanism of global gene expression regulation is disrupted by multiple disease states and drug treatments: Pickard Ben; PLOS One (2025)
The amino acid composition of a protein influences its expression: Thompson Reece, Pickard Benjamin Simon; PLoS ONE Vol 19 (2024); https://doi.org/10.1371/journal.pone.0284234
Genes associated with amyloid-beta-induced inflammasome-mediated neuronal death identified using functional gene trap mutagenesis approach: Yap Jeremy Kean Yi, Pickard Benjamin Simon, Gan Sook Yee, Chan Elaine Wan Ling; International Journal of Biochemistry and Cell Biology Vol 136 (2021); https://doi.org/10.1016/j.biocel.2021.106014
The role of neuronal NLRP1 inflammasome in Alzheimer's disease : bringing neurons into the neuroinflammation game: Yap Jeremy Kean Yi, Pickard Benjamin Simon, Chan Elaine Wan Ling, Gan Sook Yee; Molecular Neurobiology Vol 56, pp. 7741-7753 (2019); https://doi.org/10.1007/s12035-019-1638-7
PEGylation of polypropylenimine dendrimers : effects on cytotoxicity, DNA condensation, gene delivery and expression in cancer cells: Somani Sukrut, Laskar Partha, Altwaijry Najla, Kewcharoenvong Paphitchaya, Irving Craig, Robb Gillian, Pickard Benjamin S, Dufès Christine; Scientific Reports Vol 8 (2018); https://doi.org/10.1038/s41598-018-27400-6

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Teaching

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Teaching

Teaching across Biomedical Sciences classes: BM110, 108, 109, 210, 214, 321, 326, 327, 422, 423, 430, 432; Pharmacy: MP422; Postgraduate: BM934, 937, 951, 942, 952, 953, 959.
Coordinator of Biomedical Sciences classes BM321, BM423; Postgraduate: BM934, 937, 952.
Personal Development Advisor
Internal/external examiner PhD theses
External examiner MSc Neuroscience, UCL, (2013-2015)

Certificates of Recognition in University of Strathclyde Student Union Teaching Excellence Awards: 2012, 2013, 2014. Winner: Most Supportive Teacher 2017.

Research

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Research Interests

The traditional view is that gene expression is largely governed by promoter activity, meaning that analysis is carried out gene-by-gene. Expressed mRNAs encode expressed proteins and, again, the prevailing view is that mRNA levels are the major influence on levels of their encoded proteins.

I have discovered an entirely new level of regulation for both mRNA and protein expression that is based on the idea that the synthesis of both types of molecules is dependent on an interaction between the supply of building blocks (nucleotides or amino acids) and the demands of the sequences of the mRNAs or proteins to be made (how extreme/costly a composition they possess). Independent studies of protein expression data, and now mRNA expression data, have shown that this interaction drives a global-level regulation of expression. This is like looking at the 'wood' instead of the 'trees', and offers a high-level readout of the cellular state.

For proteins, we have shown that growth/cell proliferation eats up the amino acid supply, particularly limiting the expression of proteins involved in connective tissue structure. For mRNA, the situation much more profound. I see global mRNA expression profiles shifted in numerous disease states such as Alzheimer's disease , schizophrenia, and autoimmune conditions. Additionally, 20% of all drugs/chemicals assessed perturb the global profile, revealing a new way to think of drug action and side-effect. It's not all pathological: the cell uses this form of regulation across the circadian day and menstrual cycle, and it apears to correlate with the extent of cellular differentiation. In fact, cells appear to use changes in nucleobase supply to shift their global expression profile as an efficent way to reprogram physiological state or to respond to adversity.

The goal of my research now is to convert these largely data-driven findings into practical applications relating to disease understanding and treatment.

Professional Activities

University of the Highlands and Islands UHI: Visiting researcher; 6/2019

More professional activities

Projects

REGULATION OF PANCREATIC BETA CELL PHYSIOLOGY BY THE S-ACYLATION ENZYME ZDHHC17: Chamberlain, Luke (Principal Investigator) Pickard, Ben (Co-investigator) Allan Cockerill, Jack (Post Grad Student); 01-Jan-2023 - 30-Jan-2026
DTP 2224 University of Strathclyde | Campbell, Iona: Chamberlain, Luke (Principal Investigator) Pickard, Ben (Co-investigator) Campbell, Iona (Research Co-investigator); 01-Jan-2022 - 01-Jan-2026
Development of a long-lifetime dye for gated-STED microscopy: Edkins, Robert (Principal Investigator) Pickard, Ben (Co-investigator); 01-Jan-2020 - 31-Jan-2021
Biomedical Vacation Scholarships: Coats, Paul (Principal Investigator) Jiang, Hui-Rong (Principal Investigator) Lawrence, Catherine (Principal Investigator) McDonald, James (Principal Investigator) Pickard, Ben (Principal Investigator); 09-Jan-2018 - 31-Jan-2018
Biomedical Vacation Scholarships / R180191-5: Pickard, Ben (Principal Investigator); 02-Jan-2018 - 17-Jan-2018
Pharmacells contribution to IAA Secondment: Carswell, Hilary (Principal Investigator) Pickard, Ben (Co-investigator) McKittrick, Craig (Research Co-investigator); 25-Jan-2016 - 31-Jan-2017