John Quinn

Professor in Molecular and Clinical Pharmacology

Biography

We have an integrated research program to improve our understanding of the aetiology and pathophysiology of multifactorial CNS disorders to improve diagnosis, prognosis, and therapy utilizing the latest development in genomic analysis. We aim to understand how nature and nurture combine to shape the individual and our well being and how the environment; psychological, physiological, chemical, pathogen and age alter that balance resulting in clinical symptoms.

There is an increasing awareness that in many diseases that the non-coding DNA that houses the genes themselves are important in health and disease and for the latter their progression and severity. These genomic structures determine how, where and when genes are expressed. Alterations in that regulation lead to disease. In that regard the polymorphic variation in the non-coding DNA is important in both predicting predisposition to a disease or response to drug or other environment challenge. We aim to focus on the mechanisms of this gene regulation in health and disease; this will include miRNA, epigenetic and transcriptome functional studies overlaid on the polymorphic variation observed.

Our group’s main focus will be genetic response to distinct environmental challenges and their impact on the progression and severity of disease. There are active collaborations in 1) Psychiatry with the Institute of Psychiatry in London, where Quinn is an associate member of the MRC Social Genetic & Developmental Psychiatry (SGDP) group; 2) Ageing with the University of Manchester DNA bank for cognitive genetic studies 3) Pain with the Walton Centre in Liverpool; 4) Motor Neurone Disease with KCl and Sheffield; 5) Parkinson's Disease with NIH in Bethesda (US) and University of Tartu, Estonia.

Personal Distinctions

  • External Examiner for the University of Cork for Genetics (University of Cork 2015)
  • External Examiner Genetics Course University of Aberdeen (University of Aberdeen 2010

Publications since 2017

Gianfrancesco, O., Warburton, A., Collier, D. A., Bubb, V. J. and Quinn, J. P. (2017) Novel brain expressed RNA identified at the MIR137 schizophrenia-associated locus. Schizophr Res 184, 109-115 

Gianfrancesco, O., Bubb, V. J. and Quinn, J. P. (2017) SVA retrotransposons as potential modulators of neuropeptide gene expression. Neuropeptides. Neuropeptides. 64, 3-7140.  

Gianfrancesco, O., Griffiths, D., Myers, P., Collier, D. A., Bubb, V. J. and Quinn, J. P. (2016) Identification and Potential Regulatory Properties of Evolutionary Conserved Regions (ECRs) at the Schizophrenia-Associated MIR137 Locus. J Mol Neurosci. 60, 239-247 

Bu, F., Wang, Y., Jiang, L., Ma, D., Quinn, J. P. and Wang, M. (2017) Sarcoma family kinase activity is required for cortical spreading depression. Cephalalgia,  38; 1748-1758 

Warburton, A., Vasieva, O., Quinn, P., Stewart, J. P. and Quinn, J. P. (2018) Statistical analysis of human microarray data shows that dietary intervention with n-3 fatty acids, flavonoids and resveratrol enriches for immune response and disease pathways. Br J Nutr, 119, 239-249 

Billingsley KJ, Manca M, Gianfrancesco O, Collier DA, Sharp H, Bubb VJ, et al. (2018): Regulatory characterisation of the schizophrenia-associated CACNA1C proximal promoter and the potential role for the transcription factor EZH2 in schizophrenia aetiology. Schizophr Res. 199, 168-175. 

Manca, M., Pessoa, V., Lopez, A. I. et al. (2018a) The Regulation of Monoamine Oxidase A Gene Expression by Distinct Variable Number Tandem Repeats. J Mol Neurosci, 64, 459-470. 

Manca, M., Pessoa, V., Myers, P., Pickles, A., Hill, J., Sharp, H., Murgatroyd, C., Bubb, V. J. and Quinn, J. P. (2018) Distinct chromatin structures at the monoamine oxidase-A (MAOA) promoter correlate with allele specific expression in SH-SY5Y cells. Genes Brain Behav, e12483. 

Gianfrancesco, O, Bubb, V.J., Quinn, J.P. (2019). Treating the ‘E’ in ‘G x E’: Trauma-informed approaches and psychological therapy interventions in psychosis. Front Psychiatry doi: 10.3389/fpsyt.2019.00009 

Billingsley KJ, Barbosa IA, Bandres-Ciga S, Quinn JP, Bubb VJ, Deshpande C, et al. (2019): Mitochondria function associated genes contribute to Parkinson's Disease risk and later age at onset. NPJ Parkinsons Dis. 5:8. 

Billingsley KJ, Lattekivi F, Planken A, Reimann E, Kurvits L, Kadastik-Eerme L, et al. (2019): Analysis of repetitive element expression in the blood and skin of patients with Parkinson's disease identifies differential expression of satellite elements. Sci Rep. 9:4369. 

Gianfrancesco,O, Geary, B , Savage, AL, Billingsley, KJ , Bubb VJ , John P Quinn. (2019)  The role of SINE-VNTR-Alu (SVA) retrotransposons in shaping the human genome.  International Journal of Molecular Sciences 20(23), 5977 

Bu F, Nie L, Quinn JP, Wang M. Sarcoma Family Kinase-Dependent Pannexin-1 Activation after Cortical Spreading Depression is Mediated by NR2A-Containing Receptors. Int J Mol Sci 2020; 21(4). 

Hall A, Quinn JP, Billingsley KJ. Letter to the editor regarding "TGM6 variants in Parkinson's disease: clinical findings and functional evidence". J Integr Neurosci 2020; 19(4): 735-7. 

Hall A, Moore AK, Hernandez DG, et al. A SINE-VNTR-Alu in the LRIG2 Promoter Is Associated with Gene Expression at the Locus. Int J Mol Sci 2020; 21(22). 

Hall A, Bandres-Ciga S, Diez-Fairen M, Quinn JP, Billingsley KJ. Genetic Risk Profiling in Parkinson's Disease and Utilizing Genetics to Gain Insight into Disease-Related Biological Pathways. Int J Mol Sci 2020; 21(19). 

Price, E., Gianfrancesco, O., Harrison, P.T., Frank, B., Bubb, V.J. and Quinn, J.P. (2021) CRISPR Deletion of a SVA Retrotransposon Demonstrates Function as a cis-Regulatory Element at the TRPV1/TRPV3 Intergenic Region. Int J Mol Sci, 22. 

Marshall, J.N., Lopez, A.I., Pfaff, A.L., Koks, S., Quinn, J.P. and Bubb, V.J. (2021) Variable number tandem repeats - Their emerging role in sickness and health. Exp Biol Med (Maywood), 246, 1368-1376. 

Nie, L., Jiang, L., Quinn, J.P., Grubb, B.D. and Wang, M. (2021) TRPA1-Mediated Src Family Kinases Activity Facilitates Cortical Spreading Depression Susceptibility and Trigeminovascular System Sensitization. Int J Mol Sci, 22. 

Nie, L., Ma, D., Quinn, J.P. and Wang, M. (2021) Src family kinases activity is required for transmitting purinergic P2X7 receptor signaling in cortical spreading depression and neuroinflammation. J Headache Pain, 22, 146. 

Frohlich, A.; Pfaff, A. L.; Bubb, V. J.; Koks, S.; Quinn, J. P., Characterisation of the Function of a SINE-VNTR-Alu Retrotransposon to Modulate Isoform Expression at the MAPT Locus. Front Mol Neurosci 2022, 15.  

Lingdi Nie, Kai Sun, Ziyang Gong, Haoyang Li, John P. Quinn, Minyan Wang.   Family Kinases Facilitate the Crosstalk between CGRP and Cytokines in Sensitizing Trigeminal Ganglion via Transmitting CGRP Receptor/PKA Pathway..  Cells (MDPI) in press 

Marshall JNG, Fröhlich A, Li L, Pfaff AL, Middlehurst B, Spargo TP, Iacoangeli A, Lang B, Al-Chalabi A, Koks S, Bubb VJ, Quinn JP.  A polymorphic transcriptional regulatory domain in the amyotrophic lateral sclerosis risk gene CFAP410 correlates with differential isoform expression. Front Mol Neurosci. 2022 Sep 5;15:954928.