Tim is the Director of the Centre for Atherothrombosis and Metabolic Disease.
Tim obtained an Honours degree in Biochemistry at the University of Manchester and a PhD in Molecular Pharmacology at the University of Glasgow. He carried out postdoctoral training as an American Heart Association Research Fellow in the Cardiology Division at Duke University Medical Centre, North Carolina, USA.
He returned to the UK in 1997 as Lecturer in Biochemistry at the University of Glasgow and developed an externally funded research programme focusing on cardiovascular cell signalling and disease.
From 2015 he was Professor of Pharmacology and Head of Pharmacology and Experimental Therapeutics at the School of Pharmacy and Medical Sciences at the University of Bradford before being recruited to a Chair in Cardiovascular Biology at Hull York Medical School in 2018.
Professor Palmer’s interests are identifying the molecular mechanisms responsible for cardiovascular disease. Localised inflammation of branch points within large blood vessels is a pivotal event in the development of atherosclerotic plaque responsible for hear attack and stroke. Inflammation is driven by long-term exposure to chemical signals termed "cytokines" which trigger multiple pathways that ultimately lead to the defective vascular cell function responsible for cardiovascular disease. These processes are also responsible for the failure of bypass and stenting procedures used for acute treatment of patients who have suffered a heart attack.
- Inhibition of pro-inflammatory JAK-STAT signalling by AMP-activated protein kinase
- Manipulation of suppressor of cytokine signalling 3 (SOCS3) stability and function to inhibit vascular inflammation and re-modelling
- Exploiting novel protein-protein interactions as targets for new anti-inflammatory JAK-STAT signalling inhibitors
A full publication list is available to view on Google Scholar.
Williams JJL, Alotaiq N, Mullen W, Burchmore R, Liu L, Baillie GS, Schaper F, Pilch PF, Palmer TM. Interaction of suppressor of cytokine signalling 3 with cavin-1 links SOCS3 function and cavin-1 stability. Nat Commun. 2018 Jan 12;9(1):168. doi: 10.1038/s41467-017-02585-y.
Mancini SJ, White AD, Bijland S, Rutherford C, Graham D, Richter EA, Viollet B, Touyz RM, Palmer TM, Salt IP. Activation of AMP-activated protein kinase rapidly suppresses multiple pro-inflammatory pathways in adipocytes including IL-1 receptor-associated kinase-4 phosphorylation. Mol Cell Endocrinol. 2017 Jan 15;440:44-56. doi: 10.1016/j.mce.2016.11.010.
Rutherford C, Speirs C, Williams JJ, Ewart MA, Mancini SJ, Hawley SA, Delles C, Viollet B, Costa-Pereira AP, Baillie GS, Salt IP, Palmer TM. Phosphorylation of Janus kinase 1 (JAK1) by AMP-activated protein kinase (AMPK) links energy sensing to anti-inflammatory signaling. Sci Signal. 2016 Nov 8;9(453):ra109.
Rutherford C, Childs S, Ohotski J, McGlynn L, Riddick M, MacFarlane S, Tasker D, Pyne S, Pyne NJ, Edwards J, Palmer TM. Regulation of cell survival by sphingosine-1-phosphate receptor S1P1 via reciprocal ERK-dependent suppression of Bim and PI-3-kinase/protein kinase C-mediated upregulation of Mcl-1. Cell Death Dis. 2013 Nov 21;4:e927. doi: 10.1038/cddis.2013.455.
Cannavo A, Rengo G, Liccardo D, Pagano G, Zincarelli C, De Angelis MC, Puglia R, Di Pietro E, Rabinowitz JE, Barone MV, Cirillo P, Trimarco B, Palmer TM, Ferrara N, Koch WJ, Leosco D, Rapacciuolo A. β1-adrenergic receptor and sphingosine-1-phosphate receptor 1 (S1PR1) reciprocal downregulation influences cardiac hypertrophic response and progression to heart failure: protective role of S1PR1 cardiac gene therapy. Circulation. 2013 Oct 8;128(15):1612-22. doi: 10.1161/CIRCULATIONAHA.113.002659.
Long JS, Crighton D, O'Prey J, Mackay G, Zheng L, Palmer TM, Gottlieb E, Ryan KM. Extracellular adenosine sensing-a metabolic cell death priming mechanism downstream of p53. Mol Cell. 2013 May 9;50(3):394-406. doi: 10.1016/j.molcel.2013.03.016.
1996-1997; American Heart Association Basic Science Research Fellowship