About: Peter F Zipfel

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An Entity of Type : wikibase:Item, within Data Space : wikidata.demo.openlinksw.com associated with source document(s)

researcher

Attributes	Values
rdf:type	Item
description	researcher (en) investigador (es) wetenschapper (nl) дослідник (uk) эрдэмтэн (mn) изилдөөчү (ky) 研究者 (zh) հետազոտող (hy)
rdfs:label	Peter F Zipfel (en) Peter F Zipfel (nl) Peter F. Zipfel (it)
skos:prefLabel	Peter F Zipfel (en) Peter F Zipfel (nl) Peter F. Zipfel (it)
name	Peter F Zipfel (en) Peter F Zipfel (nl) Peter F. Zipfel (it)
given name	wds:Q87623772-E352E4B6-253E-4ED0-A10C-73071F8A6EDB
given name	Peter
instance of	wds:Q87623772-3786B157-AA4C-450C-A921-C0B72982E7B9
instance of	Homo sapiens
Loop ID	wds:Q87623772-0DAF5357-47A8-44E4-9C42-D5465345FE81
Loop ID	25074
skos:altLabel	Peter Zipfel (en)
occupation	wds:Q87623772-EC2BDAEB-E92E-410C-8250-82CD36C740A1
employer	wds:Q87623772-C734F86B-C12E-4502-95ED-413198668A30
sex or gender	wds:Q87623772-BB2F5A58-60FB-4917-990D-E2B885DA0115
ISNI	wds:Q87623772-9994AB11-128A-4469-A206-E278CBAA28F8
VIAF ID	wds:Q87623772-DB7416DF-EF51-4D6E-AAD6-7B551A9805C2
GND ID	wds:Q87623772-93f6ce56-a559-43dc-b26d-6012b1823bfd
IdRef ID	wds:Q87623772-68C367E9-290C-4D8E-A0CB-0ACDF32BB915
National Library of Israel J9U ID	wds:Q87623772-C95DACF8-C20E-4627-992F-9B65BD75186C
VIAF ID	http://viaf.org/viaf/12635440
GND ID	https://d-nb.info/gnd/110935810
IdRef ID	http://www.idref.fr/127288643/id
occupation	researcher
employer	Leibniz Institute for Natural Product Research and Infection Biology
sex or gender	male
ISNI	0000000034921626
VIAF ID	12635440
GND ID	110935810
IdRef ID	127288643
National Library of Israel J9U ID	987007444899805171
ORCID iD	wds:Q87623772-25110F48-5909-43F1-BE2A-D3000039D90C
Dimensions author ID	wds:Q87623772-1137E4FC-6EEE-40CF-B1BA-C0A37AAD98D5
ORCID iD	https://orcid.org/0000-0002-6149-2411
ORCID iD	0000-0002-6149-2411
Dimensions author ID	01003046545.18
is about of	https://www.wikidata.org/wiki/Special:EntityData/Q87623772
is author of	Mutations in factor H reduce binding affinity to C3b and heparin and surface attachment to endothelial cells in hemolytic uremic syndrome The complement factor H R1210C mutation is associated with atypical hemolytic uremic syndrome Complement factor H binds malondialdehyde epitopes and protects from oxidative stress Monomeric C-reactive protein modulates classic complement activation on necrotic cells Dihydrolipoamide dehydrogenase of Pseudomonas aeruginosa is a surface-exposed immune evasion protein that binds three members of the factor H family and plasminogen Complement regulator-acquiring surface protein 1 of Borrelia burgdorferi binds to human bone morphogenic protein 2, several extracellular matrix proteins, and plasminogen. The Staphylococcus aureus protein Sbi acts as a complement inhibitor and forms a tripartite complex with host complement Factor H and C3b Successful (?) therapy of hemolytic-uremic syndrome with factor H abnormality Mutations in factor H reduce binding affinity to C3b and heparin and surface attachment to endothelial cells in hemolytic uremic syndrome Complement C3b/C3d and cell surface polyanions are recognized by overlapping binding sites on the most carboxyl-terminal domain of complement factor H The role of complement in AMD. DEAP-HUS: deficiency of CFHR plasma proteins and autoantibody-positive form of hemolytic uremic syndrome New insights into disease-specific absence of complement factor H related protein C in mouse models of spontaneous autoimmune diseases Comparative and functional genomics provide insights into the pathogenicity of dermatophytic fungi LfhA, a novel factor H-binding protein of Leptospira interrogans Human pathogenic Borrelia spielmanii sp. nov. resists complement-mediated killing by direct binding of immune regulators factor H and factor H-like protein 1 Genetic screening in haemolytic uraemic syndrome Conidial Dihydroxynaphthalene Melanin of the Human Pathogenic Fungus Aspergillus fumigatus Interferes with the Host Endocytosis Pathway The vesicle transport protein Vac1p is required for virulence of Candida albicans Relative role of genetic complement abnormalities in sporadic and familial aHUS and their impact on clinical phenotype Factor H and atypical hemolytic uremic syndrome: mutations in the C-terminus cause structural changes and defective recognition functions Factor H autoantibodies in atypical hemolytic uremic syndrome correlate with CFHR1/CFHR3 deficiency Autoantibodies in haemolytic uraemic syndrome (HUS). Complement inhibitor eculizumab in atypical hemolytic uremic syndrome Combination of factor H mutation and properdin deficiency causes severe C3 glomerulonephritis Complement and diseases: defective alternative pathway control results in kidney and eye diseases Binding of the human complement regulators CFHR1 and factor H by streptococcal collagen-like protein 1 (Scl1) via their conserved C termini allows control of the complement cascade at multiple levels Complement regulator Factor H mediates a two-step uptake of Streptococcus pneumoniae by human cells The host immune regulator factor H interacts via two contact sites with the PspC protein of Streptococcus pneumoniae and mediates adhesion to host epithelial cells The interactive Factor H-atypical hemolytic uremic syndrome mutation database and website: update and integration of membrane cofactor protein and Factor I mutations with structural models Streptococcus pneumoniae evades complement attack and opsonophagocytosis by expressing the pspC locus-encoded Hic protein that binds to short consensus repeats 8-11 of factor H. Immune evasion of the human pathogen Pseudomonas aeruginosa: elongation factor Tuf is a factor H and plasminogen binding protein Leptospiral endostatin-like protein A is a bacterial cell surface receptor for human plasminogen Complement Resistance of Borrelia burgdorferi Correlates with the Expression of BbCRASP-1, a Novel Linear Plasmid-encoded Surface Protein That Interacts with Human Factor H and FHL-1 and Is Unrelated to Erp Proteins Plasminogen is a complement inhibitor Haemophilus influenzae uses the surface protein E to acquire human plasminogen and to evade innate immunity. Secreted Aspergillus fumigatus protease Alp1 degrades human complement proteins C3, C4, and C5. Identification and functional characterization of complement regulator-acquiring surface protein 1 of the Lyme disease spirochetes Borrelia afzelii and Borrelia garinii Binding of human complement regulators FHL-1 and factor H to CRASP-1 orthologs of Borrelia burgdorferi The opportunistic human pathogenic fungus Aspergillus fumigatus evades the host complement system Standardisation of the factor H autoantibody assay Immune evasion of Borrelia burgdorferi: mapping of a complement-inhibitor factor H-binding site of BbCRASP-3, a novel member of the Erp protein family Functional characterization of BbCRASP-2, a distinct outer membrane protein of Borrelia burgdorferi that binds host complement regulators factor H and FHL-1 Where next with atypical hemolytic uremic syndrome? The autoimmune disease DEAP-hemolytic uremic syndrome Deletion of complement factor H-related genes CFHR1 and CFHR3 is associated with atypical hemolytic uremic syndrome An imbalance of human complement regulatory proteins CFHR1, CFHR3 and factor H influences risk for age-related macular degeneration (AMD) Anti factor H autoantibodies block C-terminal recognition function of factor H in hemolytic uremic syndrome Factor H family proteins and human diseases Complement evasion of pathogens: common strategies are shared by diverse organisms

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