Dr Michael Fricker

Research Associate

School of Biomedical Sciences and Pharmacy

Career Summary

Biography

I am a post-doctoral researcher based at the HMRI. My work focuses on regulation of cell death and inflammation. I completed my PhD in cellular neuroscience at the University of Cambridge, UK, in 2008 and have subsequently held post-doctoral positions at the Beatson Institute for Cancer Research, Glasgow, UK and at the University of Cambridge. I joined Professor Phil Hansbro's group at the University of Newcastle in 2012, and am currently examining the role of cell death and inflammation in pulmonary disease.

Research Expertise
Research expertise in: Molecular analysis of cell death pathways including apoptosis, necrosis, necroptosis, phagoptosis, phagocytosis. Mechanisms of neurodegeneration and neuroprotection. Modelling Chronic Obstructive Pulmonary Disease (COPD) Mast cells and their role in disease. Study of muscle and fat wastage in chronic inflammatory diseases.

Teaching Expertise
Teaching expertise: Extensive experience in leading small group tutorials covering a broad range of basic biochemical and genetic topics and their relation to disease. Extensive experience assisting and leading laboratory based undergraduate practical classes and facilitating results analysis and discussion in large and small teaching groups. Extensive experience in day-to-day and overall project supervision of laboratory based masters and PhD students. 


Qualifications

  • PhD, University of Cambridge - UK

Keywords

  • Apoptosis
  • Biochemistry
  • COPD
  • Cachexia
  • Cell Biology
  • Efferocytosis
  • Human Disease
  • Mast Cell
  • Microglia
  • Molecular Biology
  • Muscle
  • Necrosis
  • Neuroinflammation
  • Pulmonary disease

Fields of Research

Code Description Percentage
110203 Respiratory Diseases 50
060199 Biochemistry and Cell Biology not elsewhere classified 25
110999 Neurosciences not elsewhere classified 25

Professional Experience

UON Appointment

Title Organisation / Department
Research Associate University of Newcastle
School of Biomedical Sciences and Pharmacy
Australia

Academic appointment

Dates Title Organisation / Department
1/01/2009 - 1/04/2012 Post-doctoral researcher University of Cambridge
Department of Biochemistry
United Kingdom
1/01/2008 - 1/01/2009 Post-doctoral researcher Beatson Cancer Research Institute
Cancer Cell Death laboratory
United Kingdom
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Publications

For publications that are currently unpublished or in-press, details are shown in italics.


Chapter (1 outputs)

Year Citation Altmetrics Link
2011 Fricker M, Tolkovsky A, 'Necrosis, Apoptosis, and Autophagy: Mechanisms of Neuronal and Glial Cell Death', Cell Culture Techniques, Neuromethods, Springer, London, UK 305-330 (2011) [B1]

Journal article (15 outputs)

Year Citation Altmetrics Link
2015 Baxter PS, Bell KFS, Hasel P, Kaindl AM, Fricker M, Thomson D, et al., 'Synaptic NMDA receptor activity is coupled to the transcriptional control of the glutathione system', Nature Communications, 6 6761-6761 (2015)
DOI 10.1038/ncomms7761
2014 Hansbro PM, Hamilton MJ, Fricker M, Gellatly SL, Jarnicki AG, Zheng D, et al., 'Importance of mast cell Prss31/transmembrane tryptase/tryptase-¿ in lung function and experimental chronic obstructive pulmonary disease and colitis', Journal of Biological Chemistry, 289 18214-18227 (2014) [C1]

Protease serine member S31 (Prss31)/transmembrane tryptase/tryptase-¿ is a mast cell (MC)-restricted protease of unknown function that is retained on the outer leaflet of the pla... [more]

Protease serine member S31 (Prss31)/transmembrane tryptase/tryptase-¿ is a mast cell (MC)-restricted protease of unknown function that is retained on the outer leaflet of the plasma membrane when MCs are activated. We determined the nucleotide sequences of the Prss31 gene in different mouse strains and then used a Cre/loxP homologous recombination approach to create a novel Prss31 -/- C57BL/6 mouse line. The resulting animals exhibited no obvious developmental abnormality, contained normal numbers of granulated MCs in their tissues, and did not compensate for their loss of the membrane tryptase by increasing their expression of other granule proteases. When Prss31-null MCs were activated with a calcium ionophore or by their high affinity IgE receptors, they degranulated in a pattern similar to that of WT MCs. Prss31-null mice had increased baseline airway reactivity to methacholine but markedly reduced experimental chronic obstructive pulmonary disease and colitis, thereby indicating both beneficial and adverse functional roles for the tryptase. In a cigarette smokeinduced model of chronic obstructive pulmonary disease, WT mice had more pulmonary macrophages, higher histopathology scores, and more fibrosis in their small airways than similarly treated Prss31-null mice. In a dextran sodium sulfate-induced acute colitis model, WT mice lost more weight, had higher histopathology scores, and contained more Cxcl-2 and IL-6 mRNA in their colons than similarly treated Prss31-null mice. The accumulated data raise the possibility that inhibitors of this membrane tryptase may provide additional therapeutic benefit in the treatment of humans with these MC-dependent inflammatory diseases. © 2014 by The American Society for Biochemistry and Molecular Biology, Inc.

DOI 10.1074/jbc.M114.548594
Citations Scopus - 4Web of Science - 3
Co-authors Paul Foster, Philip Hansbro
2014 Fricker M, Deane A, Hansbro PM, 'Animal models of chronic obstructive pulmonary disease', Expert Opinion on Drug Discovery, 9 629-645 (2014) [C1]

Introduction: Chronic obstructive pulmonary disease (COPD) is a leading global cause of mortality and chronic morbidity. Inhalation of cigarette smoke is the principal risk factor... [more]

Introduction: Chronic obstructive pulmonary disease (COPD) is a leading global cause of mortality and chronic morbidity. Inhalation of cigarette smoke is the principal risk factor for development of this disease. COPD is a progressive disease that is typically characterised by chronic pulmonary inflammation, mucus hypersecretion, airway remodelling and emphysema that collectively reduce lung function. There are currently no therapies that effectively halt or reverse disease progression. It is hoped that the development of animal models that develop the hallmark features of COPD, in a short time frame, will aid in the identifying and testing of new therapeutic approaches. Areas covered: The authors review the recent developments in mouse models of chronic cigarette smoke-induced COPD as well as the principal findings. Furthermore, the authors discuss the use of mouse models to understand the pathogenesis and the contribution of infectious exacerbations. They also discuss the investigations of the systemic co-morbidities of COPD (pulmonary hypertension, cachexia and osteoporosis). Expert opinion: Recent advances in the field mark a point where animal models recapitulate the pathologies of COPD patients in a short time frame. They also reveal novel insights into the pathogenesis and potential treatment of this debilitating disease. © 2014 Informa UK, Ltd.

DOI 10.1517/17460441.2014.909805
Citations Scopus - 6Web of Science - 8
Co-authors Philip Hansbro
2013 Fricker M, Vilalta A, Tolkovsky AM, Brown GC, 'Caspase Inhibitors Protect Neurons by Enabling Selective Necroptosis of Inflamed Microglia', JOURNAL OF BIOLOGICAL CHEMISTRY, 288 9145-9152 (2013) [C1]
DOI 10.1074/jbc.M112.427880
Citations Scopus - 14Web of Science - 15
2013 Fricker M, Vilalta A, Tolkovsky AM, Brown GC, 'Caspase Inhibitors Protect Neurons by Enabling Selective Necroptosis of Inflamed Microglia', JOURNAL OF BIOLOGICAL CHEMISTRY, 288 9145-9152 (2013) [C1]
DOI 10.1074/jbc.M112.427880
Citations Web of Science - 13
2013 Neher JJ, Emmrich JV, Fricker M, Mander PK, Thery C, Brown GC, 'Phagocytosis executes delayed neuronal death after focal brain ischemia', Proceedings of the National Academy of Sciences, 110 E4098-E4107 (2013) [C1]
DOI 10.1073/pnas.1308679110
Citations Scopus - 18
2012 Fricker M, Neher J, Zhao J-W, Thery C, Tolkovsky A, Brown G, 'MFG-E8 Mediates Primary Phagocytosis of Viable Neurons during Neuroinflammation', The Journal of Neuroscience, 32 2657-2666 (2012) [C1]
Citations Scopus - 33
2012 Fricker M, Oliva-Martin MJ, Brown G, 'Primary phagocytosis of viable neurons by microglia activated with LPS or Abeta is dependent on calreticulin/LRP phagocytic signalling.', Journal of Neuroinflammation, 9 196-e196 (2012) [C1]
Citations Scopus - 16Web of Science - 16
2010 Fricker M, O'Prey J, Tolkovsky A, Ryan K, 'Phosphorylation of Puma modulates its apoptotic function by regulating protein stability', Cell Death and Disease, 1 e59-e59 (2010) [C1]
Citations Scopus - 33Web of Science - 29
2010 Fricker M, Papadia S, Hardingham G, Tolkovsky A, 'Implication of TAp73 in the p53-independent pathway of Puma induction and Puma-dependent apoptosis in primary cortical neurons', Journal of Neurochemistry, 114 772-783 (2010) [C1]
Citations Scopus - 8
2010 Fricker M, Leveille F, Papadia S, Bell K, Soriano F, Martel M-A, et al., 'Suppression of the intrinsic apoptosis pathway by synaptic activity', The Journal of Neuroscience, 30 2623-2635 (2010) [C1]
Citations Scopus - 62
2009 Wilkinson S, O'Prey J, Fricker M, Ryan K, 'Hypoxia-selective macroautophagy and cell survival signaled by autocrine PDGFR activity', Genes and Development, 23 1283-1288 (2009) [C1]
Citations Scopus - 34Web of Science - 31
2005 Fricker M, Lograsso P, Ellis S, Wilkie N, Hunt P, Pollack S, 'Substituting c-Jun N-terminal kinase-3 (JNK3) ATP-binding site amino acid residues with their p38 counterparts affects binding of JNK-and p38-selective inhibitors', Archives of Biochemistry and Biophysics, 438 195-205 (2005) [C1]
2005 Fricker M, Wong HK, Wyttenbach A, Villunger A, Michalak E, Strasser A, Tolkovsky A, 'Mutually exclusive subsets of BH3-only proteins are activated by the p53 and c-Jun N-terminal kinase/c-Jun signaling pathways during cortical neuron apoptosis induced by arsenite', Molecular and Cellular Biology, 25 8732-8747 (2005) [C1]
2003 Beher D, Fricker M, Nadin A, Clarke E, Wrigley J, Li Y-M, et al., 'In vitro characterization of the presenilin-dependent y-secretase complex using a novel affinity ligand', Biochemistry, 42 8133-8142 (2003) [C1]
Show 12 more journal articles
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Grants and Funding

Summary

Number of grants 5
Total funding $57,000

Click on a grant title below to expand the full details for that specific grant.


20152 grants / $24,000

Determining the role of necroptosis in the pathogenesis of COPD.$22,000

Funding body: Rebecca L Cooper Medical Research Foundation Ltd

Funding body Rebecca L Cooper Medical Research Foundation Ltd
Project Team Doctor Michael Fricker
Scheme Research Grant
Role Lead
Funding Start 2015
Funding Finish 2015
GNo G1500294
Type Of Funding Grant - Aust Non Government
Category 3AFG
UON Y

European Congress of Immunology, Austria 6-9 September$2,000

Funding body: University of Newcastle - Faculty of Health and Medicine

Funding body University of Newcastle - Faculty of Health and Medicine
Project Team Doctor Michael Fricker
Scheme Travel Grant
Role Lead
Funding Start 2015
Funding Finish 2015
GNo G1500927
Type Of Funding Internal
Category INTE
UON Y

20131 grants / $20,000

DP73 Digital colour and monochrome camera + cellSens software + Xcite120 fluorescence lamp illuminator$20,000

Funding body: NHMRC (National Health & Medical Research Council)

Funding body NHMRC (National Health & Medical Research Council)
Project Team Laureate Professor Paul Foster, Doctor Alan Hsu, Professor Phil Hansbro, Professor Joerg Mattes, Doctor Katie Baines, Associate Professor Jodie Simpson, Professor Rakesh Kumar, Doctor Nicole Hansbro, Doctor Steven Maltby, Doctor Ming Yang, Doctor Gerard Kaiko, Doctor Jay Horvat, Doctor Simon Keely, Doctor Andrew Jarnicki, Doctor Michael Fricker
Scheme Equipment Grant
Role Investigator
Funding Start 2013
Funding Finish 2013
GNo G1201186
Type Of Funding Other Public Sector - Commonwealth
Category 2OPC
UON Y

20122 grants / $13,000

Elucidation of mechanisms of cachexia in COPD$10,000

Funding body: University of Newcastle

Funding body University of Newcastle
Project Team Doctor Michael Fricker
Scheme Early Career Researcher Grant
Role Lead
Funding Start 2012
Funding Finish 2012
GNo G1200889
Type Of Funding Internal
Category INTE
UON Y

Investigating the role of MIC-1 in causing cachexia associated with chronic obstructive pulmonary disease$3,000

Funding body: University of Newcastle

Funding body University of Newcastle
Project Team Doctor Michael Fricker
Scheme New Staff Grant
Role Lead
Funding Start 2012
Funding Finish 2012
GNo G1200869
Type Of Funding Internal
Category INTE
UON Y
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Research Supervision

Current Supervision

Commenced Research Title / Program / Supervisor Type
2015 Contribution of Cell Death to the Pathogenesis of Chronic Obstructive Pulmonary Disease (COPD)
Microbiology, Faculty of Health and Medicine
Co-Supervisor
2014 Utilisation of Microbial Products as New Therapies for COPD/Emphysema
Microbiology, Faculty of Health and Medicine
Co-Supervisor

Past Supervision

Year Research Title / Program / Supervisor Type
2011 CRT/LRP phagocytic signaling between microglia and neurons
Biochemistry & Cell Biology, University of Cambridge
Principal Supervisor
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Dr Michael Fricker

Position

Research Associate
School of Biomedical Sciences and Pharmacy
Faculty of Health and Medicine

Contact Details

Email michael.fricker@newcastle.edu.au
Phone (02) 4042 0207

Office

Room 2408
Building Hunter Medical Research Institute
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