Activating mutations in Kir6.2 and neonatal diabetes: new clinical syndromes, new scientific insights, and new therapy. by Hattersley, A, Ashcroft, F

What makes a good genetic association study? by Hattersley, A, McCarthy, M

What makes a good genetic association study? by Hattersley, A, McCarthy, M

Learning from molecular genetics: novel insights arising from the definition of genes for monogenic and type 2 diabetes. by McCarthy, M, Hattersley, A

Identifying routine clinical predictors of non-adherence to second line therapies in Type 2 diabetes: a retrospective cohort analysis in a large primary care database by Shields, B, Hattersley, A, Farmer, A

The role of the HNF4alpha enhancer in type 2 diabetes. by Mitchell, S, Gloyn, A, Owen, K, Hattersley, A, Frayling, T

Type II diabetes: clinical aspects of molecular biological studies. by Turner, R, Hattersley, A, Shaw, J, Levy, J

A survey of cytomegalovirus (CMV) DNA in primary sclerosing cholangitis (PSC) liver tissues using a sensitive polymerase chain reaction (PCR) based assay. by Mehal, W, Hattersley, A, Chapman, R, Fleming, K

The role of the HNF4α enhancer in type 2 diabetes variants of the HNF4α enhancer are not a common cause of susceptibility to type 2 diabetes by Mitchell, S, Gloyn, A, Owen, K, Hattersley, A, Frayling, T

Response to Comment on: McDonald et al. High-Sensitivity CRP Discriminates HNF1A-MODY From Other Subtypes of Diabetes. Diabetes Care 2011;34:1860-1862. by McDonald, T, Owen, K, Gloyn, A, Hattersley, A

Mutations in KCNJ11, which encodes Kir6.2, are a common cause of diabetes diagnosed in the first 6 months of life, with the phenotype determined by genotype. by Flanagan, SE, Edghill, E, Gloyn, A, Ellard, S, Hattersley, A

Permanent neonatal diabetes caused by an in-frame deletion in the N-terminus of Kir6.2 by Craig, T, Shimomura, K, Flanagan, S, Ellard, S, Hattersley, A, Ashcroft, F

[Insulin secretion in non-insulin-dependent diabetes] by Turner, R, Clark, A, Levy, J, Hattersley, A, Cook, J

The extent of K-ATP channel block by MgATP correlates with the clinical phenotype caused by gain-of-function KCNJ11 mutations by Proks, R, Girard, C, Gloyn, A, Hattersley, A, Ashcroft, F

Insulin secretion in non-insulin-dependent diabetes by Turner, R, Clark, A, Levy, J, Hattersley, A, Cook, J

Molecular basis of Kir6.2 mutations causing neonatal diabetes and neonatal diabetes with neurological features by Proks, P, Antcliff, J, Gloyn, A, Hattersley, A, Ashcroft, F

Permanent neonatal diabetes in an Asian infant. by Porter, JR, Shaw, N, Barrett, T, Hattersley, A, Ellard, S, Gloyn, A

Interaction between mutations in the slide helix of Kir6.2 associated with neonatal diabetes and neurological symptoms. by Männikkö, R, Jefferies, C, Flanagan, SE, Hattersley, A, Ellard, S, Ashcroft, F

Molecular basis of Kir6.2 mutations associated with neonatal diabetes or neonatal diabetes plus neurological features. by Proks, P, Antcliff, J, Lippiat, J, Gloyn, A, Hattersley, A, Ashcroft, F

Predicting post one-year durability of glucose-lowering monotherapies in patients with new-onset type 2 diabetes by Agbaje, O, Coleman, R, Hattersley, A, Pearson, E, Holman, R, MASTERMIND Consortium