Dr Tom Webb

Dr Tom WebbLecturer in Cardiovascular Genomics

BSc (Genetics) 2001, University of Sheffield
PhD 2005, MRC Human Genetics Unit, Edinburgh

Email: tw126@le.ac.uk

Address: Department of Cardiovascular Sciences, University of Leicester, Cardiovascular Research Centre, Glenfield General Hospital, Leicester, LE3 9QP.

Personal details

BSc (Genetics) 2001, University of Sheffield

PhD 2005, MRC Human Genetics Unit, Edinburgh

Membership of learned societies

Member of the Genetics Society
The British Society for Cardiovascular Research 
The European Society of Cardiology 
The European Society of Human Genetics

Publications

Key publications

Webb TR, Parfitt DA, Gardner JC, Martinez A, Bevilacqua D, Davidson AE, Zito I, Thiselton DL, Ressa JH, Apergi M, Schwarz N, Kanuga N, Michaelides M, Cheetham ME, Gorin MB, Hardcastle AJ. Deep intronic mutation in OFD1, identified by targeted genomic next-generation sequencing, causes a severe form of X-linked retinitis pigmentosa (RP23). Hum Mol Genet. 2012 Jun 13.

Webb TR, Matarin M, Gardner JC, Kelberman D, Hassan H, Ang W, Michaelides M, Ruddle JB, Pennell CE, Yazar S, Khor CC, Anung T,  Yogarajah M, Robson AG, Holder GE,  Cheetham ME, Traboulsi EI, Moore AT, Sowden JC, Sisodiya SM, Mackey DA, Tuft SJ, and Hardcastle AJ. X-linked Megalocornea caused by mutations in CHRDL1 identifies an essential role for Ventroptin in anterior segment development. Am J Hum Genet. 2012 Feb 10;90(2):247-59.

Gardner JC, Webb TR, Kanuga N, Robson AG, Holder GE, Stockman A, Ripamonti C, Ebenezer ND, Ogun O, Devery S, Wright GA, Maher ER, Cheetham ME, Moore AT, Michaelides M, and Hardcastle AJ. 2010. X-linked cone dystrophy caused by mutation of the red and green cone opsins. Am J Hum Genet. 87(1). 26-39.

Chan LF, Webb TR, Cooray SN, Guasti L, Chapple JP, Chung TT Egertova M, Elphick M, Cheetham ME, Metherall LA, and Clark AJL. 2009. MRAP and MRAP2 are bidirectional regulators of the Melanocortin receptor family. Proc Natl Acad Sci. 106(15). 6146-51.

Recent papers

Research

Understanding the molecular and cellular mechanisms of genetic variants associated with coronary artery disease.

Over the last few years, large-scale genetic association studies have identified the genetic loci that cause coronary artery disease (CAD). An important finding from these studies has been that many of these loci do not work through known coronary risk factors suggesting that novel pathways contribute to a risk of CAD. Our research involves the use of genetic, molecular and cellular approaches to study CAD risk loci. Our primary approach is to use homologous recombination and nuclease-based genome editing technologies to generate human disease cell models. Genome editing permits the precise introduction of individual disease-associated genetic variants into human cell lines allowing the functional consequences of individual disease-associated genetic variants to be identified. Genome editing can also be used to create human knock-out cell lines, delete larger segments of DNA, such as regulatory elements, or to create reporter cell lines.

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