Anne K. Soutar spends much of her time researching LDL receptor, Endocrinology, Internal medicine, Familial hypercholesterolemia and Apolipoprotein B. Her LDL receptor research is multidisciplinary, relying on both Mutation and Receptor. Her In vivo research extends to Endocrinology, which is thematically connected.
Her research in Familial hypercholesterolemia intersects with topics in Genetics and Hyperlipoproteinemia Type II. Her Genetics study integrates concerns from other disciplines, such as Amyloidosis and Amyloid. Her Apolipoprotein B research incorporates themes from Hydroxymethylglutaryl-CoA Reductase Inhibitors and Pediatrics.
Her scientific interests lie mostly in LDL receptor, Internal medicine, Endocrinology, Genetics and Low-density lipoprotein. Her LDL receptor research includes themes of Receptor and Molecular biology. Her research on Internal medicine frequently connects to adjacent areas such as Reductase.
Her Endocrinology study often links to related topics such as In vivo. Her Low-density lipoprotein research includes elements of Catabolism, Very low-density lipoprotein, Low-density lipoprotein receptor-related protein 8 and Northern blot. Anne K. Soutar has researched Apolipoprotein B in several fields, including Heterozygote advantage and Blood plasma.
Her main research concerns LDL receptor, PCSK9, Internal medicine, Genetics and Molecular biology. The study incorporates disciplines such as Exon, Allele and Apolipoprotein B in addition to LDL receptor. Her biological study spans a wide range of topics, including Mutation, Mutant, Proprotein convertase, Multiplex ligation-dependent probe amplification and Kexin.
Anne K. Soutar combines subjects such as Endocrinology, Surgery and Bioinformatics with her study of Internal medicine. Her Endocrinology study incorporates themes from Hydroxymethylglutaryl-CoA reductase and Reductase. Her work focuses on many connections between Genetics and other disciplines, such as Ldlr gene, that overlap with her field of interest in Mutation detection and Functional analysis.
Anne K. Soutar focuses on PCSK9, LDL receptor, Internal medicine, Endocrinology and Mutation. She combines topics linked to Apolipoprotein B with her work on LDL receptor. Her Internal medicine study combines topics from a wide range of disciplines, such as Oncology, Bioinformatics and Target enrichment.
Specifically, her work in Endocrinology is concerned with the study of Cholesterol. Her work carried out in the field of Mutation brings together such families of science as Gene duplication, Lipid metabolism and Multiplex ligation-dependent probe amplification. Her study looks at the intersection of Familial hypercholesterolemia and topics like Lipoprotein with Exon and Low-density lipoprotein.
This overview was generated by a machine learning system which analysed the scientist’s body of work. If you have any feedback, you can contact us here.
Human lysozyme gene mutations cause hereditary systemic amyloidosis
M. B. Pepys;P. N. Hawkins;D. R. Booth;D. M. Vigushin.
Mechanisms of Disease: genetic causes of familial hypercholesterolemia
Anne K Soutar;Rossi P Naoumova.
Nature Reviews Cardiology (2007)
Defects of receptor-mediated low density lipoprotein catabolism in homozygous familial hypercholesterolemia and hypothyroidism in vivo.
Gilbert R. Thompson;Anne K. Soutar;Florentin A. Spengel;Arvind Jadhav.
Proceedings of the National Academy of Sciences of the United States of America (1981)
Severe Hypercholesterolemia in Four British Families With the D374Y Mutation in the PCSK9 Gene: Long-Term Follow-Up and Treatment Response
Rossi P. Naoumova;Isabella Tosi;Dilip Patel;Clare Neuwirth.
Arteriosclerosis, Thrombosis, and Vascular Biology (2005)
Evidence for effect of mutant PCSK9 on apolipoprotein B secretion as the cause of unusually severe dominant hypercholesterolaemia
Xi-Ming Sun;Emily R. Eden;Isabella Tosi;Clare K. Neuwirth.
Human Molecular Genetics (2005)
Simultaneous measurement of apolipoprotein B turnover in very-low- and low-density lipoproteins in familial hypercholesterolaemia
A.K. Soutar;N.B. Myant;G.R. Thompson.
Apolipoprotein AI mutation Arg-60 causes autosomal dominant amyloidosis.
A K Soutar;P N Hawkins;D M Vigushin;G A Tennent.
Proceedings of the National Academy of Sciences of the United States of America (1992)
Characterization and tissue-specific expression of the human 'very low density lipoprotein (VLDL) receptor' mRNA.
Julie C. Webb;Dilip D. Patel;Michael D. Jones;Brian L. Knight.
Human Molecular Genetics (1994)
Phenotypic variation in heterozygous familial hypercholesterolemia: a comparison of Chinese patients with the same or similar mutations in the LDL receptor gene in China or Canada.
Simon N. Pimstone;Xi-Ming Sun;Christele du Souich;Jiri J. Frohlich.
Arteriosclerosis, Thrombosis, and Vascular Biology (1998)
Phase transitions in bilamellar vesicles. Measurements by pyrene excimer fluorescence and effect on transacylation by lecithin: cholesterol acyltransferase.
Anne K. Soutar;Henry J. Pownall;Angela S. Hu;Louis C. Smith.
If you think any of the details on this page are incorrect, let us know.
We appreciate your kind effort to assist us to improve this page, it would be helpful providing us with as much detail as possible in the text box below: