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Adrian Clark DSc, FRCP, FMedSci
Professor of Medicine & Centre Lead for Endocrinology
Centre for Endocrinology

Contact Details:

a.j.clark@qmul.ac.uk

Professor Clark graduated in Medicine in 1976 and after training in general internal medicine worked as Registrar in Endocrinology at Hammersmith Hospital and Research Registrar at the Unit for Metabolic Medicine at Guys. He then began a period of five years training in molecular biology and receptor biology at the National Institutes of Health in Bethesda, USA working under Ira Pastan on the cloning of the EGF receptor and later under Kevin Catt on the angiotensin receptor. He was appointed to an MRC funded Senior Lectureship at Barts in 1991 where he established the Molecular Endocrinology laboratory. Professor Clark became Professor of Molecular Endocrinology in 1996 and Professor of Medicine in 2001. In addition to his role in the William Harvey, Professor Clark is Editor-in-Chief of the Journal of Endocrinology. He was awarded the Society for Endocrinology Medal in 1997 and the Clinical Endocrinology Trust Lectureship in 2007.

Current research interests

  • ACTH insensitivity
    We were the first to describe mutations in the ACTHreceptor as a cause of familial glucocorticoid deficiency (FGD), and more recently described a second gene, MRAP, as a cause of this syndrome. In collaboration with Angela Huebner’s group we identified the locus for triple A syndrome and later the gene encoding the protein ALADIN that is mutated in these patients. Current research centres on elucidating the function of the MRAP protein and identification of further genetic causes of FGD.

  • Fetal and childhood growth
    We have maintained a longstanding interest in conjunction with Martin Savage in novel mechanisms of growth hormone receptor impairment and IGF-I deficiency and their consequences. We lead and administer the NESTEGG study, a large cross-European study aimed at identifying the genetic basis of fetal and childhood growth.

  •  Fetal programming
    Our research focuses on investigating the hypothesis that epigenetic modification of the genome during fetal life is the fundamental underlying process in fetal programming in response to nutritional and other environmental insults.  Our work focuses specifically on mechanisms that lead to hypertension and insulin resistance.


Key publications

 

  • Cooray SN, Do Vale IA, Leung K-Y, Webb T, Chapple JP, Cheetham ME, Elphick MR and Clark AJL. (2008) The Melanocortin 2 Receptor Accessory protein exists as a homodimer and is essential for the function of the Melanocortin 2 Receptor in the mouse Y1 cell line. Endocrinology 149:1935-41.

  • Chung TT, Webb TR, Chan LF, Cooray SN, Metherell LA, King PJ, Chapple JP and Clark AJL (2008) The majority of ACTH receptor mutations found in Familial Glucocorticoid Deficiency type 1 lead to defective trafficking of the receptor to the cell surface. Journal of Clinical Endocrinology and Metabolism 93:4948-4954.

  • Webb TR, Chan L, Cooray SN, Cheetham ME, Chapple JP and Clark AJL. (2009) Distinct MRAP domains are required for MC2R interaction and promotion of receptor trafficking. Endocrinology 150:720-6.

  • Chan LF, Webb TR, Chung T-T, Meimaridou E, Cooray SN, Guasti L, Chapple JP, , Egertová M, Elphick MR, Cheetham ME, Metherell LA and Clark AJL. (2009) MRAP and MRAP2 are bidirectional regulators of the Melanocortin receptor family. Proceedings of the National Academy of Sciences USA 106: 6146-51.
  • Bogdarina I, Welham S, King PJ, Burns SP, Clark AJL (2007) . Epigenetic modification of the Renin-Angiotensin System in fetal programming of hypertension. Circulation Research, 100: 520-526.

  • Metherell LA, Chapple JP, Cooray S, David A, Becker C, Rüschendorf F, Naville D, Begeot M,   Khoo B, Nürnberg P, Huebner A, Cheetham ME & Clark AJL. (2005) Mutations in MRAP, encoding a novel interacting partner of the ACTH receptor, cause Familial Glucocorticoid Deficiency Type 2. Nature Genetics 37: 166 -170.
  • Storr HL, Clark AJL, Priestley JV & Michael GJ. (2005) Identification of the sites of expression of AAAS mRNA in the rat using in situ hybridization. Neuroscience 131: 113 -123.
  • Swords FM, Baig AH, Malchoff DM, Malchoff CD, Thorner MO, King PJ, Hunyady L & Clark AJL. (2003) Impaired desensitization of a mutant Adrenocorticotropin Receptor associated with apparent constitutive activity. Molecular Endocrinology 16: 2746 – 2753.

 

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Professor Adrian Clark
 

Senior Staff:

Laboratory Manager:

  • Thomas Milligan

Research Staff:

  • Irina Bogdarina
  • Sadani Cooray
  • Teng Teng Chung
  • Rebecca Gorrigan

PhD Students:

  • Claire Hughes

 

 

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