A type III complement factor D deficiency: Structural insights for inhibition of the alternative pathway

Conversely, in both mutant simulations, the distance remained larger, consistent with His41 pointing away from the active site. [...]in addition to disruption of key FB-binding residues, mutations R176P and R176A appear to stabilize the self-inhibited conformation of free FD. Overactivation of AP is...

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Published inJournal of allergy and clinical immunology Vol. 142; no. 1; pp. 311 - 314.e6
Main Authors Sng, Christopher C.T., O'Byrne, Sorcha, Prigozhin, Daniil M., Bauer, Matthias R., Harvey, Jennifer C., Ruhle, Michelle, Challis, Ben G., Lear, Sara, Roberts, Lee D., Workman, Sarita, Janowitz, Tobias, Magiera, Lukasz, Doffinger, Rainer, Buckland, Matthew S., Jodrell, Duncan J., Semple, Robert K., Wilson, Timothy J., Modis, Yorgo, Thaventhiran, James E.D.
Format Journal Article
LanguageEnglish
Published United States Elsevier Inc 01.07.2018
Elsevier Limited
Mosby
Subjects
Online AccessGet full text
ISSN0091-6749
1097-6825
1085-8725
1097-6825
DOI10.1016/j.jaci.2018.01.048

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Abstract Conversely, in both mutant simulations, the distance remained larger, consistent with His41 pointing away from the active site. [...]in addition to disruption of key FB-binding residues, mutations R176P and R176A appear to stabilize the self-inhibited conformation of free FD. Overactivation of AP is implicated in numerous inflammatory disorders, including age-related macular degeneration. [...]blockade of the AP by targeting the rate-limiting enzyme, FD, is an attractive approach to controlling disease progression. Furthermore, circulating concentrations of leptin and adiponectin, adipokines that regulate insulin sensitivity, were normal, as were fasting lipid profiles in both subjects. [...]glucose homeostasis is not impaired in the context of genetic, and therefore lifelong, FD deficiency. [...]research will be required to understand the role of FD in glucose homeostasis and FD-deficient family pedigrees offer a useful clinical insight to this question.Methods Informed consent statement All study participants gave their informed consent as appropriate under approved protocols from local institutional review boards.
AbstractList Conversely, in both mutant simulations, the distance remained larger, consistent with His41 pointing away from the active site. [...]in addition to disruption of key FB-binding residues, mutations R176P and R176A appear to stabilize the self-inhibited conformation of free FD. Overactivation of AP is implicated in numerous inflammatory disorders, including age-related macular degeneration. [...]blockade of the AP by targeting the rate-limiting enzyme, FD, is an attractive approach to controlling disease progression. Furthermore, circulating concentrations of leptin and adiponectin, adipokines that regulate insulin sensitivity, were normal, as were fasting lipid profiles in both subjects. [...]glucose homeostasis is not impaired in the context of genetic, and therefore lifelong, FD deficiency. [...]research will be required to understand the role of FD in glucose homeostasis and FD-deficient family pedigrees offer a useful clinical insight to this question.Methods Informed consent statement All study participants gave their informed consent as appropriate under approved protocols from local institutional review boards.
Author Thaventhiran, James E.D.
Bauer, Matthias R.
Challis, Ben G.
O'Byrne, Sorcha
Ruhle, Michelle
Buckland, Matthew S.
Semple, Robert K.
Modis, Yorgo
Sng, Christopher C.T.
Magiera, Lukasz
Harvey, Jennifer C.
Janowitz, Tobias
Wilson, Timothy J.
Roberts, Lee D.
Workman, Sarita
Doffinger, Rainer
Prigozhin, Daniil M.
Jodrell, Duncan J.
Lear, Sara
AuthorAffiliation k Department of Medicine, University of Cambridge, Addenbrooke's Hospital, Cambridge, United Kingdom
h Leeds Institute of Cardiovascular and Metabolic Medicine, Leeds Institute of Genetics, Health and Therapeutics (LIGHT) Laboratories, University of Leeds, Leeds, United Kingdom
c Molecular Immunity Unit, Department of Medicine, Medical Research Council (MRC) Laboratory of Molecular Biology, Cambridge, United Kingdom
d Division of Structural Studies, MRC Laboratory of Molecular Biology, Cambridge, United Kingdom
l MRC Toxicology Unit, University of Leicester, Leicester, United Kingdom
e Department of Immunology, Royal Free London National Health Service Foundation Trust, London, United Kingdom
f Walter and Eliza Hall Institute of Medical Research, Parkville, Australia
j Department of Microbiology, Miami University, Oxford, Ohio
a Cancer Research UK Cambridge Institute, Cambridge, United Kingdom
b Department of Clinical Immunology, Cambridge University Hospitals National Health Service Trust, Add
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Snippet Conversely, in both mutant simulations, the distance remained larger, consistent with His41 pointing away from the active site. [...]in addition to disruption...
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SubjectTerms Alternative pathway
Complement factor D
Complement Factor D - chemistry
Complement Factor D - deficiency
Complement Factor D - genetics
Complement Pathway, Alternative
Female
Hereditary Complement Deficiency Diseases
Humans
Immunologic Deficiency Syndromes - genetics
Inflammatory diseases
Macular degeneration
Male
Metabolism
Mutation
Pedigree
Protein Conformation
Simulation
Young Adult
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Title A type III complement factor D deficiency: Structural insights for inhibition of the alternative pathway
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