نتایج جستجو برای: ldlr locus

تعداد نتایج: 69565  

Journal: :acta medica iranica 0
seyed hamid jamaldini department of genetics, genetic research center, university of social welfare and rehabilitation sciences, tehran, iran. mojgan babanejad department of genetics, genetic research center, university of social welfare and rehabilitation sciences, tehran, iran. reza mozaffari department of genetics, cardiogenetic research center, tehran, iran-department of genetics, shahid rajaie cardiovascular medical & research center, tehran, iran. nooshin nikzat department of genetics, genetic research center, university of social welfare and rehabilitation sciences, tehran, iran. khadijeh jalalvand department of genetics, genetic research center, university of social welfare and rehabilitation sciences, tehran, iran. azadeh badiei department of genetics, genetic research center, university of social welfare and rehabilitation sciences, tehran, iran.

coronary artery disease (cad) is the leading cause of mortality in many parts of the world. genome-wide association studies (gwas) have identified several genetic variants associated with cad in low-density lipoprotein receptor (ldlr) locus. this study was evaluated the possible association of genetic markers at ldlr locus with cad irrespective to lipid profile and as well as the association of...

2007
Michele M.P. Lufino Roberto Manservigi Richard Wade-Martins

Episomal gene expression vectors offer a safe and attractive alternative to integrating vectors. Here we describe the development of a high capacity episomal vector system exploiting human episomal retention sequences to provide efficient vector maintenance and regulated gene expression through the delivery of a genomic DNA locus. The iBAC-S/MAR vector is capable of the infectious delivery and ...

Journal: :Journal of lipid research 1999
L Haddad I N Day S Hunt R R Williams S E Humphries P N Hopkins

Monogenically inherited hypercholesterolemia is most commonly caused by mutations at the low density lipoprotein receptor (LDLR) locus causing familial hypercholesterolemia (FH) or at the apolipoprotein B (APOB) locus causing the disorder familial defective apoB (FDB). Probands from 47 kindreds with a strict clinical diagnosis of FH were selected from the Cardiovascular Genetics Research Lipid ...

Journal: :PLoS ONE 2008
Patrick Linsel-Nitschke Anika Götz Jeanette Erdmann Ingrid Braenne Peter Braund Christian Hengstenberg Klaus Stark Marcus Fischer Stefan Schreiber Nour Eddine El Mokhtari Arne Schaefer Jürgen Schrezenmeier Diana Rubin Anke Hinney Thomas Reinehr Christian Roth Jan Ortlepp Peter Hanrath Alistair S. Hall Massimo Mangino Wolfgang Lieb Claudia Lamina Iris M. Heid Angela Doering Christian Gieger Annette Peters Thomas Meitinger H.-Erich Wichmann Inke R. König Andreas Ziegler Florian Kronenberg Nilesh J. Samani Heribert Schunkert

BACKGROUND Rare mutations of the low-density lipoprotein receptor gene (LDLR) cause familial hypercholesterolemia, which increases the risk for coronary artery disease (CAD). Less is known about the implications of common genetic variation in the LDLR gene regarding the variability of cholesterol levels and risk of CAD. METHODS Imputed genotype data at the LDLR locus on 1 644 individuals of a...

Journal: :Journal of medical genetics 1998
W K Lee L Haddad M J Macleod A M Dorrance D J Wilson D Gaffney M H Dominiczak C J Packard I N Day S E Humphries A F Dominiczak

Familial hypercholesterolaemia (FH) is an autosomal codominant disorder characterised by high levels of LDL cholesterol and a high incidence of coronary artery disease. Our aims were to track the low density lipoprotein receptor (LDLR) gene in individual families with phenotypic FH and to identify and characterise any mutations of the LDLR gene that may be common in the west of Scotland FH popu...

Journal: :Science 2001
C K Garcia K Wilund M Arca G Zuliani R Fellin M Maioli S Calandra S Bertolini F Cossu N Grishin R Barnes J C Cohen H H Hobbs

Atherogenic low density lipoproteins are cleared from the circulation by hepatic low density lipoprotein receptors (LDLR). Two inherited forms of hypercholesterolemia result from loss of LDLR activity: autosomal dominant familial hypercholesterolemia (FH), caused by mutations in the LDLR gene, and autosomal recessive hypercholesterolemia (ARH), of unknown etiology. Here we map the ARH locus to ...

Journal: :Circulation. Cardiovascular genetics 2011
Puneetpal Singh Mario Di Napoli Monica Singh

BACKGROUND In humans, the E4 allele of the apolipoprotein E gene is associated with increased coronary heart disease risk. Surprisingly, in rodents, apolipoprotein E4 only accelerates the atherosclerotic process when transgenic for the human low-density lipoprotein receptor (LDLR) protein. We therefore investigated whether the LDLR locus interacted with the apolipoprotein E gene genotype on cor...

Journal: :Current opinion in lipidology 2012
Vincenzo Sorrentino Noam Zelcer

PURPOSE OF REVIEW The hepatic low-density lipoprotein receptor (LDLR) pathway is essential for clearing circulating LDL and is an important therapeutic target for treating cardiovascular disease. Abundance of the LDLR is subject to both transcriptional and nontranscriptional control. Here, we highlight a new post-transcriptional mechanism for controlling LDLR function via ubiquitination of the ...

Journal: :Arteriosclerosis, thrombosis, and vascular biology 2005
Sara Bretschger Seidelmann Carl De Luca Rudolph L Leibel Jan L Breslow Alan R Tall Carrie L Welch

OBJECTIVE The purpose of this study was to examine genetic factors responsible for metabolic syndrome and atherosclerosis in a setting of low-density lipoprotein (LDL) receptor deficiency in a cross between C57BL/6J (B6) and PERA/Ei (PERA) inbred mouse strains. METHODS AND RESULTS Comparison of metabolic phenotypes in B6 and PERA strains revealed the PERA genetic background to be dramatically...

2016
Alastair G Kerr Lawrence CS Tam Ashley B Hale Milena Cioroch Gillian Douglas Keith M Channon Richard Wade-Martins

Familial hypercholesterolemia (FH) is a life-threatening genetic disorder characterized by elevated levels of plasma low-density lipoprotein cholesterol (LDL-cholesterol). Current attempts at gene therapy for FH have been limited by the use of strong heterologous promoters which lack genomic DNA elements essential for regulated expression. Here, we have combined a minigene vector expressing the...

نمودار تعداد نتایج جستجو در هر سال

با کلیک روی نمودار نتایج را به سال انتشار فیلتر کنید