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Dr Craig Hughes,
Prof J M Gibbins
Applications accepted all year round
Self-Funded PhD Students Only
Reading
United Kingdom
Biochemistry
Cell Biology
Molecular Biology
Pathology
Pharmacology
Structural Biology
About the Project
Project Overview:
The risk of heart attack or stroke is elevated in obesity and in people with metabolic disorders such as diabetes. The reason for this increased risk is not fully understood and is a focus of this project.
How platelets become activated, and to what extent they become activated is the governing factor determining whether a thrombus forms, or whether it will block a vessel. Tyrosine kinases play an essential role in the activation of platelets. This project will investigate how some of these kinases are regulated and therefore how they regulate platelet activation. Drugs which target these kinases are already an area of interest to the pharmaceutical industry for treatment of some cancers and some autoimmune diseases. What application these drugs may have in the treatment of cardiovascular disease remains to be discovered.
Reading Platelet Group:
The Reading Platelet Group is part of the Institute for Cardiovascular and Metabolic Research and is formed from the laboratories of 5 Principal Investigators, all collaborating on several projects. We provide a multidisciplinary interactive research environment; an excellent opportunity for training in a wide range of basic molecular and cell biology methods including flow cytometry, immunoprecipitation, functional assays such as platelet aggregometry and real-time flow-adhesion, as well as specialist training in microscopy techniques such as confocal.
School of Biological Sciences, University of Reading:
The University of Reading, located west of London, England, provides world-class research education programs. The University’s main Whiteknights Campus is set in 130 hectares of beautiful parkland, a 30-minute train ride to central London and 40 minutes from London Heathrow airport.
Our School of Biological Sciences conducts high-impact research, tackling current global challenges faced by society and the planet. Our research ranges from understanding and improving human health and combating disease, through to understanding evolutionary processes and uncovering new ways to protect the natural world. In 2020, we moved into a stunning new ~£60 million Health & Life Sciences building. This state-of-the-art facility is purpose-built for science research and teaching. It houses the Cole Museum of Zoology, a café and social spaces.
In the School of Biological Sciences, you will be joining a vibrant community of ~180 PhD students representing ~40 nationalities. Our students publish in high-impact journals, present at international conferences, and organise a range of exciting outreach and public engagement activities.
During your PhD at the University of Reading, you will expand your research knowledge and skills, receiving supervision in one-to-one and small group sessions. You will have access to cutting-edge technology and learn the latest research techniques. We also provide dedicated training in important transferable skills that will support your career aspirations. If English is not your first language, the University's excellent International Study and Language Institute will help you develop your academic English skills.
The University of Reading is a welcoming community for people of all faiths and cultures. We are committed to a healthy work-life balance and will work to ensure that you are supported personally and academically.
Eligibility:
Applicants should have a good degree (minimum of a UK Upper Second (2:1) undergraduate degree or equivalent) in Biomedical Science/Biochemistry or a strongly-related discipline. Applicants will also need to meet the University’s English Language requirements. We offer pre-sessional courses that can help with meeting these requirements.
How to apply:
Submit an application for a PhD in Biomedical
Sciences at http://www.reading.ac.uk/pgapply.
Further information:
http://www.reading.ac.uk/biologicalsciences/SchoolofBiologicalSciences/PhD/sbs-phd.aspx
Enquiries:
Dr. Craig Hughes, email: c.e.hughes@reading.ac.uk
Dr Hughes’ profile: Dr Craig Hughes – University of Reading
Funding Notes
We welcome applications from self-funded students worldwide for this project.
If you are applying to an international funding scheme, we encourage you to get in contact as we may be able to support you in your application.
If you are applying to an international funding scheme, we encourage you to get in contact as we may be able to support you in your application.
References
Maternal and offspring high-fat diet leads to platelet hyperactivation in male mice offspring’ Gaspar RS, Unsworth AJ, Al-Dibouni A, Bye A, Sage T, Stewart M, Wells S, Cox RD, Gibbins JM, Sellayah D, Hughes CE. Scientific Reports 2021 11:1473.
‘Low dose Btk inhibitors selectively block platelet activation by CLEC-2’ Nicolson PLR, Nock SH, Hinds J, Garcia-Quintanilla L, Smith CW, Campos J, Brill A, Pike JA, Kahn
AO, Poulter NS, Kavanagh D, Watson S, Watson C, Clifford H, Huissoon A, Pollitt AY, Eble J, Pratt G, Watson SP, Hughes CE. Haematologica 2021 106(1):208-219.
‘Inhibition of Btk by Btk-specific concentrations of ibrutinib and acalabrutinib delays but does not block platelet aggregation to GPVI’ Nicolson PLR, Hughes CE, Watson S, Nock SH, Hardy AT, Watson CN, Montague SJ, Malcor JD, Thomas MR, Pollitt AY, Tomlinson MG, Pratt G, and Watson S.P. (2018) Haematologica 2018 103(12):2097-2108.
‘Immobilized fibrinogen activates human platelets through GPVI’ Mangin PH, Onselaer MB, Receveur N, Le Lay N, Hardy AT, Wilson C, Sanchez X, Loyau S, Dupuis A, Babar AK, Miller JLC, Philippou H, Hughes CE, Herr AB, Ariëns RAS, Mezzano D, Jandrot-Perrus M, Gachet C, Watson SP. Hematologica 2018 103(5) 898-907.
‘Severe platelet dysfunction in NHL patients receiving ibrutinib is absent in patients receiving acalabrutinib’ Bye AP, Unsworth AJ, Desborough MJ, Hildyard CAT, Appleby N, Bruce D, Kriek N, Nock SH, Sage T, Hughes CE*, and Gibbins JM* (*joint). Blood Advances 2017 1(26) 2610-23.
‘Fibrin activates GPVI in human and mouse platelets’ Alshehri OM*, Hughes CE*, Montague S, Watson SK, Frampton J, Bender M, Watson SP (*joint first authors). Blood 2015 126(13) 1601-8.
‘The N-terminal SH2 domain of Syk is required for (hem)ITAM but not integrin signalling in mouse platelets’ Hughes CE, Finney BA, Koentgen F, Lowe KL, Watson SP. Blood 2015 125(1) 144-54.
‘Critical role for an acidic amino acid region in platelet signalling by the hemITAM (hemi-Immunoreceptor Tyrosine-based Activation Motif) containing receptor CLEC-2 (C-type Lectin receptor-2)’ Hughes CE, Sinha U, Pandey A, Eble JA, O'Callaghan CA, Watson SP. JBC 2013 288(7) 5127-35
‘G6f-like is an ITAM-containing collagen receptor in thrombocytes’ Hughes CE, Radhakrishnan UP, Egginton S, Dijkstra JM, Jagadeeswaran P, Watson SP. PLOS ONE 2012 7(12) e52622
‘CLEC-2 is not required for platelet aggregation at arteriolar shear’ Hughes CE, Navarro-Núñez L, Finney BA, Mourão-Sá D, Pollitt AY, Watson SP. JTH 2010 8(10) 2328-32
‘CLEC-2 activates Syk through dimerisation’ Hughes CE, Pollitt AY, Mori J, Eble JA, Tomlinson MG, Hartwig JH, O’Callaghan CA, Fütterer K, Watson SP. Blood 2010 115(14) 2947-55
‘Low dose Btk inhibitors selectively block platelet activation by CLEC-2’ Nicolson PLR, Nock SH, Hinds J, Garcia-Quintanilla L, Smith CW, Campos J, Brill A, Pike JA, Kahn
AO, Poulter NS, Kavanagh D, Watson S, Watson C, Clifford H, Huissoon A, Pollitt AY, Eble J, Pratt G, Watson SP, Hughes CE. Haematologica 2021 106(1):208-219.
‘Inhibition of Btk by Btk-specific concentrations of ibrutinib and acalabrutinib delays but does not block platelet aggregation to GPVI’ Nicolson PLR, Hughes CE, Watson S, Nock SH, Hardy AT, Watson CN, Montague SJ, Malcor JD, Thomas MR, Pollitt AY, Tomlinson MG, Pratt G, and Watson S.P. (2018) Haematologica 2018 103(12):2097-2108.
‘Immobilized fibrinogen activates human platelets through GPVI’ Mangin PH, Onselaer MB, Receveur N, Le Lay N, Hardy AT, Wilson C, Sanchez X, Loyau S, Dupuis A, Babar AK, Miller JLC, Philippou H, Hughes CE, Herr AB, Ariëns RAS, Mezzano D, Jandrot-Perrus M, Gachet C, Watson SP. Hematologica 2018 103(5) 898-907.
‘Severe platelet dysfunction in NHL patients receiving ibrutinib is absent in patients receiving acalabrutinib’ Bye AP, Unsworth AJ, Desborough MJ, Hildyard CAT, Appleby N, Bruce D, Kriek N, Nock SH, Sage T, Hughes CE*, and Gibbins JM* (*joint). Blood Advances 2017 1(26) 2610-23.
‘Fibrin activates GPVI in human and mouse platelets’ Alshehri OM*, Hughes CE*, Montague S, Watson SK, Frampton J, Bender M, Watson SP (*joint first authors). Blood 2015 126(13) 1601-8.
‘The N-terminal SH2 domain of Syk is required for (hem)ITAM but not integrin signalling in mouse platelets’ Hughes CE, Finney BA, Koentgen F, Lowe KL, Watson SP. Blood 2015 125(1) 144-54.
‘Critical role for an acidic amino acid region in platelet signalling by the hemITAM (hemi-Immunoreceptor Tyrosine-based Activation Motif) containing receptor CLEC-2 (C-type Lectin receptor-2)’ Hughes CE, Sinha U, Pandey A, Eble JA, O'Callaghan CA, Watson SP. JBC 2013 288(7) 5127-35
‘G6f-like is an ITAM-containing collagen receptor in thrombocytes’ Hughes CE, Radhakrishnan UP, Egginton S, Dijkstra JM, Jagadeeswaran P, Watson SP. PLOS ONE 2012 7(12) e52622
‘CLEC-2 is not required for platelet aggregation at arteriolar shear’ Hughes CE, Navarro-Núñez L, Finney BA, Mourão-Sá D, Pollitt AY, Watson SP. JTH 2010 8(10) 2328-32
‘CLEC-2 activates Syk through dimerisation’ Hughes CE, Pollitt AY, Mori J, Eble JA, Tomlinson MG, Hartwig JH, O’Callaghan CA, Fütterer K, Watson SP. Blood 2010 115(14) 2947-55
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