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The Journal of Clinical Investigation|July 15, 1996
An intronic mutation in a lariat branchpoint sequence is a direct cause of an inherited human disorder (fish-eye disease)J A Kuivenhoven, H Weibusch, P H Pritchard, et al.
Journal of Lipid Research|July 1, 1993
Expression and characterization of recombinant human lecithin:cholesterol acyltransferaseJ S Hill, K O, X Wang, et al.
Proceedings of the National Academy of Sciences of the United States of America|June 1, 1991
A molecular defect causing fish eye disease: an amino acid exchange in lecithin-cholesterol acyltransferase (LCAT) leads to the selective loss of alpha-LCAT activityH Funke, A von Eckardstein, P H Pritchard, et al.
Clinical and Investigative Medicine. Medecine Clinique Et Experimentale|October 1, 1990
Characterization of a lipoprotein lipase class III type defect in hypertriglyceridemic catsL N Peritz, J D Brunzell, C Harvey-Clarke, et al.
Journal of Internal Medicine|April 1, 1992
Familial high-density-lipoprotein deficiency causing corneal opacities (fish eye disease) in a family of Dutch descentJ J Kastelein, P H Pritchard, D W Erkelens, et al.
Biochimica Et Biophysica Acta|February 24, 2000
Biochemical and compositional analyses of recombinant lecithin:cholesterol acyltransferase (LCAT) obtained from a hepatic sourceA F Ayyobi, A G Lacko, K Murray, et al.
Archives of Biochemistry and Biophysics|May 23, 2001
Probing the 121-136 domain of lecithin:cholesterol acyltransferase using antibodiesK R Murray, M P Nair, A F Ayyobi, et al.
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