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Results: 1-8 |
Results: 8
FAMILIAL MODERATE HYPERCHOLESTEROLEMIA CAUSED BY ASP235-]GLU MUTATIONOF THE LDL RECEPTOR GENE AND COOCCURRENCE OF A DE-NOVO DELETION OF THE LDL RECEPTOR GENE IN THE SAME FAMILY
Authors: KOIVISTO UM GYLLING H MIETTINEN TA KONTULA K
Citation: Um. Koivisto et al., FAMILIAL MODERATE HYPERCHOLESTEROLEMIA CAUSED BY ASP235-]GLU MUTATIONOF THE LDL RECEPTOR GENE AND COOCCURRENCE OF A DE-NOVO DELETION OF THE LDL RECEPTOR GENE IN THE SAME FAMILY, Arteriosclerosis, thrombosis, and vascular biology, 17(7), 1997, pp. 1392-1399
POLYMORPHISMS OF THE GENES ENCODING APOPROTEIN-A-I, APOPROTEIN-B, APOPROTEIN-C-III, AND APOPROTEIN-E AND LDL-RECEPTOR, AND CHOLESTEROL AND LDL METABOLISM DURING INCREASED CHOLESTEROL INTAKE - COMMON ALLELES OFTHE APOPROTEIN-E GENE SHOW THE GREATEST REGULATORY IMPACT
Authors: GYLLING H KONTULA K KOIVISTO UM MIETTINEN HE MIETTINEN TA
Citation: H. Gylling et al., POLYMORPHISMS OF THE GENES ENCODING APOPROTEIN-A-I, APOPROTEIN-B, APOPROTEIN-C-III, AND APOPROTEIN-E AND LDL-RECEPTOR, AND CHOLESTEROL AND LDL METABOLISM DURING INCREASED CHOLESTEROL INTAKE - COMMON ALLELES OFTHE APOPROTEIN-E GENE SHOW THE GREATEST REGULATORY IMPACT, Arteriosclerosis, thrombosis, and vascular biology, 17(1), 1997, pp. 38-44
A NOVEL DELETION INVERSION MUTATION IN THE LOW-DENSITY-LIPOPROTEIN RECEPTOR GENE AS A CAUSE OF HETEROZYGOUS FAMILIAL HYPERCHOLESTEROLEMIA/
Authors: KOIVISTO UM KONTULA K
Citation: Um. Koivisto et K. Kontula, A NOVEL DELETION INVERSION MUTATION IN THE LOW-DENSITY-LIPOPROTEIN RECEPTOR GENE AS A CAUSE OF HETEROZYGOUS FAMILIAL HYPERCHOLESTEROLEMIA/, Human mutation, 8(4), 1996, pp. 326-332
MOLECULAR CHARACTERIZATION OF MINOR GENE REARRANGEMENTS IN FINNISH PATIENTS WITH HETEROZYGOUS FAMILIAL HYPERCHOLESTEROLEMIA - IDENTIFICATION OF 2 COMMON MISSENSE MUTATIONS (GLY823-]ASP AND LEU380-]HIS) AND 8 RARE MUTATIONS OF THE LDL RECEPTOR GENE
Authors: KOIVISTO UM VIIKARI JS KONTULA K
Citation: Um. Koivisto et al., MOLECULAR CHARACTERIZATION OF MINOR GENE REARRANGEMENTS IN FINNISH PATIENTS WITH HETEROZYGOUS FAMILIAL HYPERCHOLESTEROLEMIA - IDENTIFICATION OF 2 COMMON MISSENSE MUTATIONS (GLY823-]ASP AND LEU380-]HIS) AND 8 RARE MUTATIONS OF THE LDL RECEPTOR GENE, American journal of human genetics, 57(4), 1995, pp. 789-797
A SINGLE-BASE SUBSTITUTION IN THE PROXIMAL SP1 SITE OF THE HUMAN LOW-DENSITY-LIPOPROTEIN RECEPTOR PROMOTER AS A CAUSE OF HETEROZYGOUS FAMILIAL HYPERCHOLESTEROLEMIA
Authors: KOIVISTO UM PALVIMO JJ JANNE OA KONTULA K
Citation: Um. Koivisto et al., A SINGLE-BASE SUBSTITUTION IN THE PROXIMAL SP1 SITE OF THE HUMAN LOW-DENSITY-LIPOPROTEIN RECEPTOR PROMOTER AS A CAUSE OF HETEROZYGOUS FAMILIAL HYPERCHOLESTEROLEMIA, Proceedings of the National Academy of Sciences of the United Statesof America, 91(22), 1994, pp. 10526-10530
A SINGLE-BASE SUBSTITUTION IN THE PROXIMAL SP1 SITE OF THE HUMAN LOW-DENSITY-LIPOPROTEIN RECEPTOR PROMOTER AS A CAUSE OF HETEROZYGOUS FAMILIAL HYPERCHOLESTEROLEMIA
Authors: KOIVISTO UM PALVIMO JJ JANNE OA KONTULA K
Citation: Um. Koivisto et al., A SINGLE-BASE SUBSTITUTION IN THE PROXIMAL SP1 SITE OF THE HUMAN LOW-DENSITY-LIPOPROTEIN RECEPTOR PROMOTER AS A CAUSE OF HETEROZYGOUS FAMILIAL HYPERCHOLESTEROLEMIA, Proceedings of the National Academy of Sciences of the United Statesof America, 91(22), 1994, pp. 10526-10530
DELETION OF EXON-15 OF THE LDL RECEPTOR GENE IS ASSOCIATED WITH A MILD FORM OF FAMILIAL HYPERCHOLESTEROLEMIA - FH-ESPOO
Authors: KOIVISTO PVI KOIVISTO UM KOVANEN PT GYLLING H MIETTINEN TA KONTULA K
Citation: Pvi. Koivisto et al., DELETION OF EXON-15 OF THE LDL RECEPTOR GENE IS ASSOCIATED WITH A MILD FORM OF FAMILIAL HYPERCHOLESTEROLEMIA - FH-ESPOO, Arteriosclerosis and thrombosis, 13(11), 1993, pp. 1680-1688
PREVALENCE AND GEOGRAPHICAL-DISTRIBUTION OF MAJOR LDL RECEPTOR GENE REARRANGEMENTS IN FINLAND
Authors: AALTOSETALA K KOIVISTO UM MIETTINEN TA GYLLING H KESANIEMI YA SAVOLAINEN M PYORALA K EBELING T MONONEN I TURTOLA H VIIKARI J KONTULA K
Citation: K. Aaltosetala et al., PREVALENCE AND GEOGRAPHICAL-DISTRIBUTION OF MAJOR LDL RECEPTOR GENE REARRANGEMENTS IN FINLAND, Journal of internal medicine, 231(3), 1992, pp. 227-234
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