Associated Papers
Homozygous Familial Hypercholesterolemia in Canada: An Observational Study.
Brown L et al.
Jacc. Advances, 2023
Proprotein convertase subtilisin/kexin type 9 inhibitor non responses in an adult with a history of coronary revascularization: A case report.
Yang L et al.
World Journal of Clinical Cases, 2022
The Role of Registers in Increasing Knowledge and Improving Management of Children and Adolescents Affected by Familial Hypercholesterolemia: the LIPIGEN Pediatric Group.
Gazzotti M et al.
Frontiers in Genetics, 2022
35795214 (PubMed )
Supplement: DataSheet1.docx
Lomitapide for treatment of homozygous familial hypercholesterolemia: The Québec experience.
Aljenedil S et al.
Atherosclerosis, 2020
Molecular Characterization of Familial Hypercholesterolemia in a North American Cohort.
Garg A et al.
Journal of the Endocrine Society, 2020
Molecular modeling of LDLR aids interpretation of genomic variants.
Klee EW et al.
Journal of Molecular Medicine (berlin, Germany), 2019
30778614 (PubMed )
Supplement: 109_2019_1755_MOESM1_ESM.xlsx › TableS1
The ever-expanding saga of the proprotein convertases and their roles in body homeostasis: emphasis on novel proprotein convertase subtilisin kexin number 9 functions and regulation.
Seidah NG et al.
Current Opinion in Lipidology, 2018
New Sequencing technologies help revealing unexpected mutations in Autosomal Dominant Hypercholesterolemia.
Elbitar S et al.
Scientific Reports, 2018
The Proprotein Convertase Subtilisin/Kexin Type 9-resistant R410S Low Density Lipoprotein Receptor Mutation: A NOVEL MECHANISM CAUSING FAMILIAL HYPERCHOLESTEROLEMIA.
Susan-Resiga D et al.
The Journal of Biological Chemistry, 2017
Analysis of the frequency and spectrum of mutations recognised to cause familial hypercholesterolaemia in routine clinical practice in a UK specialist hospital lipid clinic.
Futema M et al.
Atherosclerosis, 2013
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