Fernando Morales

MutL traps MutS at a DNA mismatch

Mechanisms, regulation and functions of the unfolded protein response

Semi-automated quantification of C9orf72 expansion size reveals inverse correlation between hexanucleotide repeat number and disease duration in frontotemporal degeneration

Applications of genome editing technology in the targeted therapy of human diseases: mechanisms, advances and prospects

MRC Centre for Neuromuscular Diseases 1st (1st December 2010), and 2nd (2nd May 2012) myotonic dystrophy workshops, London, UK and the myotonic dystrophy standards of care and national registry meeting, Newcastle, UK July 2011

Prevalence of Muscular Dystrophies: A Systematic Literature Review

Decoding ALS: from genes to mechanism

The Unfolded Protein Response: Detecting and Responding to Fluctuations in the Protein-Folding Capacity of the Endoplasmic Reticulum

Genetics of Huntington disease

Extrahelical (CAG)/(CTG) triplet repeat elements support proliferating cell nuclear antigen loading and MutLα endonuclease activation

Disease-associated CAG{middle dot}CTG triplet repeats expand rapidly in non-dividing mouse cells, but cell cycle arrest is insufficient to drive expansion

Somatic instability of the expanded CTG triplet repeat in myotonic dystrophy type 1 is a heritable quantitative trait and modifier of disease severity

High levels of somatic DNA diversity at the myotonic dystrophy type 1 locus are driven by ultra-frequent expansion and contraction mutations