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GoPubMed Proteins lists recent and important papers and reviews for proteins. Page last changed on 19 Dec 2016.

Serpin peptidase inhibitor, clade G

C1 esterase inhibitor, CI in, C1-INH, C1 in
This gene encodes a highly glycosylated plasma protein involved in the regulation of the complement cascade. Its protein inhibits activated C1r and C1s of the first complement component and thus regulates complement activation. Deficiency of this protein is associated with hereditary angioneurotic oedema (HANE). Alternative splicing results in multiple transcript variants encoding the same isoform. [provided by RefSeq, Jul 2008] (from NCBI)
Top mentioned proteins: HAD, CAN, AGE, ESI, iMpact
Papers using C1 esterase inhibitor antibodies
Capillary leak syndrome in children who undergo cardiopulmonary bypass: clinical outcome in comparison with complement activation and C1 inhibitor.
Mehta Anand S., In PLoS ONE, 2000
... C1 inhibitor mouse monoclonal antibody was obtained from the AntibodyShop (Denmark), purified peroxidase-conjugated goat anti-human C1inh IgG was purchased from Cedarlane laboratories (Canada) ...
CLAMP: a biosensor kinetic data analysis program
Stover Cordula M., In PLoS ONE, 1997
... inhibitor mouse monoclonal antibody was obtained from the AntibodyShop (Demark) and purified peroxidase-conjugated goat anti-human C1inh IgG was purchased from Cedarlane laboratories (Canada) ...
Unique C1 inhibitor dysfunction in a kindred without angioedema. II. Identification of an Ala443⟹Val substitution and functional analysis of the recombinant mutant protein
Kawakami Masaya et al., In Archivum Immunologiae et Therapiae Experimentalis, 1994
... The parameters measured were C1-INH, C4, MBL concentration and MBL/MASP-2 complex ...
Papers on C1 esterase inhibitor
Cortical Plasticity and Reorganization in Pediatric Single-sided Deafness Pre- and Postcochlear Implantation: A Case Study.
Zeitler et al., Seattle, United States. In Otol Neurotol, Feb 2016
BACKGROUND: The extent to which sensory pathways reorganize in childhood SSD is not well understood and there is currently little evidence demonstrating the efficacy of CI in children with SSD.
Is a history of radiation therapy a contra-indication for carotid surgery?
DE Vries et al., Nieuwegein, Netherlands. In J Cardiovasc Surg (torino), Feb 2016
Prior CI in association with carotid artery stenosis poses potential challenges, when revascularization is considered.
Erythema Marginatum as an Early Symptom of Hereditary Angioedema: Case Report of 2 Newborns.
Farkas et al., Germany. In Pediatrics, Feb 2016
UNASSIGNED: Hereditary angioedema due to C1 inhibitor deficiency (C1-INH-HAE) is a rare genetic disease that causes recurrent swelling attacks that may affect various body tissues.
Nanofiltrated C1-esterase-inhibitor in the prophylactic treatment of bradykinin-mediated angioedema.
Strassen et al., Ulm, Germany. In Transfusion, Feb 2016
Current therapy consists of B2 bradykinin receptor antagonists, C1-esterase-inhibitor (C1-INH) concentrate, or the kallikrein inhibitor ecallantide.
Multicenter clinical trial of the Nucleus Hybrid S8 cochlear implant: Final outcomes.
Turner et al., Seattle, United States. In Laryngoscope, Feb 2016
METHODS: Eighty-seven subjects received a Nucleus Hybrid S8 CI in their poorer ear.
Genetic analysis of hereditary angioedema in a brazilian family by targeted next generation sequencing.
Pesquero et al., In Biol Chem, Feb 2016
Although many proteins may be involved in regulating the wide spectrum of HAE symptoms, most studies have only focused on C1-INH and FXII.
Interactions of visual hallucinations, rapid eye movement sleep behavior disorder and cognitive impairment in Parkinson's disease: A review.
Pal et al., Bengaluru, India. In Parkinsonism Relat Disord, Jan 2016
There is marked overlap in the risk factors for development of RBD, VH and CI in patients with PD. Results of clinical and epidemiological studies as well as studies based on neuroimaging, electrophysiology especially transcranial magnetic stimulation and neuropsycholgical evaluations in PD patients have suggested presence of certain common neurobiological process leading to emergence of RBD, VH and CI.
Optimizing hereditary angioedema management through tailored treatment approaches.
Longhurst et al., London, United Kingdom. In Expert Rev Clin Immunol, Jan 2016
Hereditary angioedema (HAE) is a rare but serious and potentially life threatening autosomal dominant condition caused by low or dysfunctional C1 esterase inhibitor (C1-INH) or uncontrolled contact pathway activation.
Serial change of C1 inhibitor in patients with sepsis-a preliminary report.
Shimazu et al., Suita, Japan. In Am J Emerg Med, Jan 2016
OBJECTIVE: C1 inhibitor (C1INH) regulates not only the complement system but also the plasma kallikrein-kinin, fibrinolytic, and coagulation systems.
Current treatment options for hereditary angioedema due to C1 inhibitor deficiency.
Cicardi et al., Milano, Italy. In Expert Opin Pharmacother, Nov 2015
INTRODUCTION: Hereditary angioedema (HAE) usually results from C1 inhibitor (C1-INH) deficiency or dysfunction.
Oral medicine case book 64: Some aspects of the pathophysiology of angioedema with special reference to the upper aerodigestive tract.
Feller et al., In Sadj, 2014
Deficiency or loss of functional activity of the complement component C1 esterase inhibitor (C1-INH) affects multiple systems, including the kallikrein-kinin, complement, coagulation and fibrinolytic pathways, and in the context of angioedema, the result is increased production and release of bradykinin and other vasoactive substances such as C3a.
Recombinant tissue plasminogen activator for acute ischaemic stroke: an updated systematic review and meta-analysis.
Cohen et al., Edinburgh, United Kingdom. In Lancet, 2012
We estimated summary odds ratios (ORs) and 95% CI in the primary analysis for prespecified outcomes within 7 days and at the final follow-up of all patients treated up to 6 h after stroke.
Identification of new biomarkers for Down's syndrome in maternal plasma.
Chitty et al., London, United Kingdom. In J Proteomics, 2012
analysis of the 10-14 weeks' plasma samples showed the presence of a protein of mass 100.3 kDa that was elevated in the Down's syndrome group compared to the controls. This protein was identified as being plasma protease C1 inhibitor.
C1-esterase inhibitor protects against early vein graft remodeling under arterial blood pressure.
Niessen et al., Amsterdam, Netherlands. In Atherosclerosis, 2012
C1inh significantly protects against early vein graft remodeling, including loss of endothelium and intimal thickening.
Hereditary and acquired complement component 1 esterase inhibitor deficiency: a review for the hematologist.
Johnston et al., Milano, Italy. In Acta Haematol, 2011
A deficiency of complement component 1 (C1) esterase inhibitor leads to overproduction of vasoactive kinins that cause angioedema. Review.
Human pasteurized C1-inhibitor concentrate for the treatment of hereditary angioedema due to C1-inhibitor deficiency.
Bork, Mainz, Germany. In Expert Rev Clin Immunol, 2011
Human pasteurized C1-inhibitor concentrate for the treatment of hereditary angioedema due to C1-inhibitor deficiency.
Acquired angioedema with C1 inhibitor deficiency associated with anticardiolipin antibodies.
Vacca et al., In Int J Immunopathol Pharmacol, 2011
Case Report: Report acquired angioedema with C1 inhibitor deficiency associated with anticardiolipin antibodies.
Role of delayed nuclear envelope breakdown and mitosis in Wolbachia-induced cytoplasmic incompatibility.
Sullivan et al., Santa Cruz, United States. In Science, 2002
When Wolbachia were present in the egg, synchrony was restored, which explains suppression of CI in these crosses.
C1-Esterase inhibitor: an anti-inflammatory agent and its potential use in the treatment of diseases other than hereditary angioedema.
Hack et al., Bern, Switzerland. In Pharmacol Rev, 2000
C1-esterase inhibitor (C1-Inh) therapy was introduced in clinical medicine about 25 years ago as a replacement therapy for patients with hereditary angioedema caused by a deficiency of C1-Inh.
An IgG autoantibody which inactivates C1-inhibitor.
Feighery et al., In Nature, 1986
This is the first report of an immunoglobulin G (IgG) autoantibody reactive with C1-inhibitor (C1-Inh), a pivotal inhibitor of the inflammatory response which is known to inactivate proteins of the complement, kinin, fibrinolytic and 'contact phase' systems.
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