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Dr Michael Fricker

Post-doctoral Research Fellow

School of Medicine and Public Health

Understanding the molecular basis of disease

Dr Michael Fricker started his academic career at the University of Cambridge, where he studied cell death in brain cells, first as a PhD student and then as a post-doctoral researcher. He’s now using those cell biology techniques to investigate the causes of asthma and chronic obstructive pulmonary disease (COPD) at the University of Newcastle.

“I would describe myself as a cell biologist – before I moved to the HMRI, most of my work was done in basic sciences, trying to understand the molecular mechanisms by which cells die.”

His research group at Cambridge was the first to identify a novel form of cell death, ‘phagoptosis’.

“A popular idea in cell death research is that cells die and then (and only then) they're eaten by neighbouring cells. We discovered that actually the eating process itself can drive death, so if you block the eating then you can rescue cells in certain situations.”

“This has important implications in medical research. In our bodies, an estimated 70 billion cells die per day. These death pathways are highly regulated as part of the body’s internal homeostasis mechanisms. Disruption of this regulation is manifested in a number of medical conditions – from neurodegeneration to cancer to asthma.”

New challenges

Michael moved to Newcastle in 2012, where he worked alongside Professor Phil Hansbro at UON’s Centre for Asthma & Respiratory Disease (now PRC for Healthy Lungs).

“It was quite a big change of field for me and a big challenge but I learned a lot."

“I have been able to apply some of my expertise in those basic cellular processes to our research on respiratory disease. So we have projects looking at different types of cell death in COPD – lung structures are destroyed and certain types of cell death can contribute to that as well as the ongoing inflammation in the lungs.”

Focus on severe asthma

Since 2016, Michael has been working with Professor Peter Gibson at the university’s Centre of Excellence for Severe Asthma, alongside translational health researchers and lab-based scientists alike.

“We’re working at both ends of the spectrum. I’m looking for biomarkers and we’re also looking at ways to translate this medical research into clinical practice.”

Asthma is an umbrella term which encompasses a number of subtypes of the disease. Severe asthma patients display the most extreme clinical symptoms, which are typically resistant to conventional drug treatments.

“We’re specifically targeting severe asthma because that's the area where there's the most unmet clinical need.”

There are a number of emerging asthma drugs on the market, and a number of them which have shown promise in clinical trials target ‘type 2 inflammation’. While approximately 50% of asthma patients exhibit this type of inflammation and are therefore likely to benefit from these drugs, there is a lot less known about the inflammatory processes observed in the rest of the asthmatic population.

“I'm aiming to understand some of those processes, develop biomarkers that report them and hopefully help to uncover new therapeutic targets. So what we're trying to do is develop ways of better managing the disease and better ways of using these new treatments that are coming through.”

Rethinking sputum subtypes

Currently, asthma subtypes and corresponding treatment pathways are designated using microscopy analysis of patient sputum samples.

“Conventional sputum analysis is performed using a microscope based cell count – so the only information that goes into that process is whatever is distinguishable by eye.”

Michael is currently researching ways to improve this subtyping process, with the ultimate goal of delivering personalised medicine to severe asthma patients.

“While we might count a few hundred cells under a microscope, if we were to run that same sample on a flow cytometer, we might count a couple of million cells. That way, we can look at rarer cells, like mast cells - which are linked to allergic inflammation.”

Flow cytometers can rapidly identify cells based on their size and density. Researchers can also label different cell types by using targeted stains which correspond to specific cell markers.

“It hasn't been used very much in clinical studies; in part because the technology is relatively new and in part because sputum is sticky stuff, which creates a further technical challenge. While it isn't suitable for mass clinical use at the moment, it's an evolving technology and we are generating some very promising results.”

Another application for flow cytometry in this context is the isolation of specific cells from patient samples. These cells can then be closely studied in the lab.

By investigating disease subtypes at the molecular level, Michael is hoping to identify specific biomarkers to guide treatment pathways.

“My overriding passion is the study of basic cellular processes and life at that cellular and molecular level. We can learn a lot about these basic processes through studying disease as well - and the two are fully interconnected.”

Understanding the molecular basis of disease

Michael Fricker is a post-doctoral research fellow within the Centre of Excellence for Severe Asthma.

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Career Summary

Biography

I am a post-doctoral research fellow within the Centre of Excellence for Severe Asthma based at the HMRI. My work focuses on discovering and validating novel cellular and molecular mechanisms of disease and biomarkers in asthma and Chronic Obstructive Pulmonary Disease (COPD). I completed my PhD in cellular neuroscience at the University of Cambridge, UK, in 2008 and subsequently held post-doctoral positions at the Beatson Institute for Cancer Research, Glasgow, UK and at the University of Cambridge. In 2012 I changed fields to study respiratory disease, and have applied my expertise in basic inflammatory and cell signaling processes to develop novel insights into chronic respiratory diseases such as asthma and COPD.

Research Expertise
Molecular analysis of cell death pathways including apoptosis, necrosis, necroptosis, phagoptosis, phagocytosis. Pathogenesis of Severe Asthma and COPD. Macrophages, mast cells and their roles in disease. Metabolic flux analysis. Mechanisms of neurodegeneration and neuroprotection.

Teaching Expertise
I have extensive experience in leading small group tutorials covering a broad range of basic biochemical and genetic topics and their relation to disease. I have also assisted and led laboratory-based undergraduate practical classes, facilitating results analysis and discussion in large and small teaching groups. I have supervised two honours students and one masters student to completion and am currently co-supervising four PhD students.


Qualifications

  • PhD, University of Cambridge - UK

Keywords

  • Asthma
  • Biochemistry
  • COPD
  • Cachexia
  • Cell Biology
  • Cell Death
  • Efferocytosis
  • Human Disease
  • Inflammation
  • Macrophage
  • Mast Cell
  • Microglia
  • Neurodegeneration
  • Pulmonary disease

Fields of Research

Code Description Percentage
110999 Neurosciences not elsewhere classified 10
110203 Respiratory Diseases 60
060199 Biochemistry and Cell Biology not elsewhere classified 30

Professional Experience

UON Appointment

Title Organisation / Department
Post-doctoral Research Fellow University of Newcastle
School of Medicine and Public Health
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.

Highlighted Publications

Year Citation Altmetrics Link
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 - 26Web of Science - 25
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 - 18Web of Science - 19
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 - 26Web of Science - 29
Co-authors Philip Hansbro
2015 Brown GC, Vilalta A, Fricker M, 'Phagoptosis - Cell Death By Phagocytosis - Plays Central Roles in Physiology, Host Defense and Pathology.', Current molecular medicine, 15 842-851 (2015) [C1]
Citations Scopus - 6Web of Science - 5
2017 Fricker M, Heaney LG, Upham JW, 'Can biomarkers help us hit targets in difficult-to-treat asthma?', Respirology, 22 430-442 (2017)
DOI 10.1111/resp.13014

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]
Citations Scopus - 3

Journal article (18 outputs)

Year Citation Altmetrics Link
2017 Fricker M, Heaney LG, Upham JW, 'Can biomarkers help us hit targets in difficult-to-treat asthma?', Respirology, 22 430-442 (2017)
DOI 10.1111/resp.13014
2016 Neniskyte U, Fricker M, Brown GC, 'Amyloid ß induces microglia to phagocytose neurons via activation of protein kinase Cs and NADPH oxidase', International Journal of Biochemistry and Cell Biology, 81 346-355 (2016) [C1]

© 2016Alzheimer's disease is characterized by brain plaques of amyloid beta and by neuronal loss, but it is unclear how amyloid beta causes neuronal loss and how to prevent this ... [more]

© 2016Alzheimer's disease is characterized by brain plaques of amyloid beta and by neuronal loss, but it is unclear how amyloid beta causes neuronal loss and how to prevent this loss. We have previously shown that amyloid beta causes neuronal loss by inducing microglia to phagocytose neurons, and here we investigated whether protein kinase Cs and NADPH oxidase were involved in this. The loss of neurons induced by amyloid beta in co-cultures of primary glia and neurons was completely prevented by inhibiting protein kinase Cs with Gö6976 or Gö6983. Directly activating protein kinase Cs with phorbol myristate acetate stimulated microglial phagocytosis, and induced neuronal loss mediated by MFG-E8/vitronectin receptor pathway of microglial phagocytosis. Blocking phagocytosis by MFG-E8 knockout or receptor inhibition left live neurons, indicating microglial phagocytosis was the cause of neuronal death. Phorbol myristate acetate stimulated the microglial NADPH oxidase, and inhibiting the oxidase prevented neuronal loss. A physiological activator of NADPH oxidase, fMLP, also induced neuronal loss dependent on microglia. Amyloid beta-induced neuronal loss was blocked by NADPH oxidase inhibitors, superoxide dismutase or Toll-like receptor function-blocking antibodies. The results indicate that amyloid beta induces microglial phagocytosis of neurons via activating protein kinase Cs and NADPH oxidase, and that activating the kinases or oxidase is sufficient to induce neuronal loss by microglial phagocytosis. Thus inhibiting protein kinase Cs or NADPH oxidase might be beneficial in Alzheimer's disease or other brain pathologies involving inflammatory neuronal loss mediated by microglia.

DOI 10.1016/j.biocel.2016.06.005
Citations Scopus - 1
2016 Gang L, Hsu A, Cooley MA, Jarnicki AG, Nair PM, Haw TJ, et al., 'Fibulin-1 regulates the pathogenesis of tissue remodeling in respiratory diseases', Journal of Clinical Investigation Insight, 1 (2016) [C1]
DOI 10.1172/jci.insight.86380
Citations Web of Science - 2
Co-authors Jay Horvat, Alan Hsu, Darryl Knight, Philip Hansbro, Marjorie Walker, Peter Wark
2015 Brown GC, Vilalta A, Fricker M, 'Phagoptosis - Cell Death By Phagocytosis - Plays Central Roles in Physiology, Host Defense and Pathology.', Current molecular medicine, 15 842-851 (2015) [C1]
Citations Scopus - 6Web of Science - 5
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 (2015) [C1]
DOI 10.1038/ncomms7761
Citations Scopus - 17Web of Science - 17
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 - 18Web of Science - 19
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 - 26Web of Science - 29
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 - 26Web of Science - 25
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 - 53Web of Science - 52
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 - 52Web of Science - 46
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 - 30Web of Science - 25
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 - 38Web of Science - 34
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 - 12Web of Science - 11
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 - 74Web of Science - 73
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 - 42Web of Science - 38
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]
Citations Scopus - 7
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]
Citations Scopus - 58Web of Science - 55
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]
Citations Scopus - 67
Show 15 more journal articles

Conference (5 outputs)

Year Citation Altmetrics Link
2016 Hansbro PM, Liu G, Cooley MA, Jarnicki AG, Hsu AC, Nair PM, et al., 'Fibulin-1 Plays Critical Roles In The Pathogenesis Of Pulmonary Diseases', AMERICAN JOURNAL OF RESPIRATORY AND CRITICAL CARE MEDICINE (2016)
Co-authors Philip Hansbro, Alan Hsu, Peter Wark, Jay Horvat, Darryl Knight
2016 Gellatly S, Dennis P, Jarnicki A, Lachner N, Wood D, Fricker M, et al., 'HEALTHY GUT MICROBIOTA AMELIORATES EXPERIMENTAL CHRONIC OBSTRUCTIVE PULMONARY DISEASE', RESPIROLOGY (2016)
Co-authors Simon Keely, Philip Hansbro
2016 Pathinayake PS, Hsu AC-Y, Parsons K, Loo S-L, Fricker M, Wood LG, et al., 'Effect of oxidative stress and rhinovirus infection on mitochondrial/endoplasmic reticular function in human primary bronchial epithelial cells', EUROPEAN JOURNAL OF IMMUNOLOGY (2016)
Co-authors Lisa Wood, Peter Wark, Alan Hsu, Philip Hansbro
2015 Hardingham GE, Baxter P, Bell K, Hasel P, Kaindl A, Thomson D, et al., 'SYNAPTIC NMDA RECEPTOR ACTIVITY IS COUPLED TO THE TRANSCRIPTIONAL CONTROL OF THE GLUTATHIONE SYSTEM IN THE DEVELOPING FOREBRAIN', SCHIZOPHRENIA BULLETIN (2015) [E3]
2015 Emmrich J, Vilalta A, Fricker M, Neher J, Brown G, 'Microglia phagocytose stressed neurons resulting in delayed neuronal death by phagoptosis after brain ischaemia or inflammation', JOURNAL OF NEUROCHEMISTRY (2015) [E3]
Show 2 more conferences
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Grants and Funding

Summary

Number of grants 6
Total funding $62,000

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


20171 grants / $5,000

Utilisation of microbial products as novel therapies for COPD$5,000

Funding body: Hunter Medical Research Institute

Funding body Hunter Medical Research Institute
Project Team Professor Phil Hansbro, Doctor Shaan Gellatly, Doctor Michael Fricker, Mr Kurtis Budden
Scheme Greaves Family Postgraduate Scholarship in Medical Research
Role Investigator
Funding Start 2017
Funding Finish 2017
GNo G1700348
Type Of Funding Grant - Aust Non Government
Category 3AFG
UON Y

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, Professor Jodie Simpson, Professor Rakesh Kumar, Doctor Nicole Hansbro, Doctor Steven Maltby, Doctor Ming Yang, Doctor Gerard Kaiko, Doctor Jay Horvat, Associate Professor 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

Number of supervisions

Completed2
Current5

Total current UON EFTSL

PhD0.9

Current Supervision

Commenced Level of Study Research Title Program Supervisor Type
2017 PhD Investigating Aberrant Inflammatory Signaling in Asthma PhD (Medicine), Faculty of Health and Medicine, The University of Newcastle Co-Supervisor
2016 PhD Mechanisms and Therapeutic Targeting of Oxidative Stress in Lung Disease PhD (Immunology & Microbiol), Faculty of Health and Medicine, The University of Newcastle Co-Supervisor
2015 PhD The effects of Galectin-3 on alveolar macrophage function in asthma Medical Science, University of Newcastle - Faculty of Health and Medicine, School of Medicine and Public Health Co-Supervisor
2015 PhD Contribution of Cell Death to the Pathogenesis of Chronic Obstructive Pulmonary Disease (COPD) PhD (Immunology & Microbiol), Faculty of Health and Medicine, The University of Newcastle Co-Supervisor
2014 PhD Utilisation of Microbial Products as New Therapies for COPD/Emphysema PhD (Immunology & Microbiol), Faculty of Health and Medicine, The University of Newcastle Co-Supervisor

Past Supervision

Year Level of Study Research Title Program Supervisor Type
2016 Honours Altered macrophage signaling in COPD Medical Science, The University of Newcastle - Faculty of Health and Medicine Co-Supervisor
2011 Masters CRT/LRP phagocytic signaling between microglia and neurons Biochemistry & Cell Biology, University of Cambridge Principal Supervisor
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Dr Michael Fricker

Position

Post-doctoral Research Fellow
School of Medicine and Public Health
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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