Results 31 to 40 of about 70,452 (309)

A non-redundant role of complement protein C1q in normal and adverse pregnancy

open access: yesExploration of Immunology, 2022
Complement component 1q (C1q) is the recognition molecule of the classical pathway of the complement system that can bind to an array of closely spaced antigen-bound immunoglobulin G (IgG) and IgM antibodies.
Chiara Agostinis   +4 more
doaj   +1 more source

C1q and SRPX2 regulate microglia mediated synapse elimination during early development in the visual thalamus but not the visual cortex

open access: yesGlia, 2021
The classical complement cascade mediates synapse elimination in the visual thalamus during early brain development. However, whether the primary visual cortex also undergoes complement‐mediated synapse elimination during early visual system development ...
Qifei Cong   +5 more
semanticscholar   +1 more source

Complement, C1q, and C1q-Related Molecules Regulate Macrophage Polarization [PDF]

open access: yesFrontiers in Immunology, 2014
Complement is a critical system of enzymes, regulatory proteins, and receptors that regulates both innate and adaptive immune responses. Natural mutations in complement molecules highlight their requirement in regulation of a variety of human conditions including infectious disease and autoimmunity.
Suzanne S. Bohlson   +4 more
openaire   +4 more sources

CD93 is Selectively Expressed on Human Myeloma Cells but Not on B Lymphocytes [PDF]

open access: yesIranian Journal of Immunology, 2019
Background: CD93 has originally been known as a C1q receptor, and many studies have demonstrated that CD93 is expressed on hematopoietic stem cells, B cell progenitors, myeloid and monocytic cells.
Shohreh Fakhari   +4 more
doaj   +1 more source

Development of C1q Affinity Chromatography for the Study of C1q–IgG Interactions

open access: yesThe Journal of Immunology, 2023
Abstract The classical complement system represents a central effector mechanism of Abs initiated by the binding of C1q to target bound IgG. Human C1q contains six heterotrimeric globular head groups that mediate IgG interaction, resulting in an avidity-driven binding event involving multiple IgG molecules binding a single C1q ...
Michael J E Marshall   +7 more
openaire   +4 more sources

A Novel Serum Protein Similar to C1q, Produced Exclusively in Adipocytes (*)

open access: yesJournal of Biological Chemistry, 1995
We describe a novel 30-kDa secretory protein, Acrp30 (adipocyte complement-related protein of 30 kDa), that is made exclusively in adipocytes and whose mRNA is induced over 100-fold during adipocyte differentiation.
P. Scherer   +4 more
semanticscholar   +1 more source

Peptide inhibitor of complement C1 (PIC1), a novel suppressor of classical pathway activation: mechanistic studies and clinical potential

open access: yesFrontiers in Immunology, 2014
The classical pathway of complement plays multiple physiological roles including modulating immunological effectors initiated by adaptive immune responses as well as an essential homeostatic role in the clearance of damaged self-antigens.
Julia A Sharp   +5 more
doaj   +1 more source

SLE: Novel Postulates for Therapeutic Options

open access: yesFrontiers in Immunology, 2020
Genetic deficiency in C1q is a strong susceptibility factor for systemic lupus erythematosus (SLE). There are two major hypotheses that potentially explain the role of C1q in SLE.
Kinga K. Hosszu   +3 more
doaj   +1 more source

Paths reunited: initiation of the classical and lectin pathways of complement activation [PDF]

open access: yes, 2010
Understanding the structural organisation and mode of action of the initiating complex of the classical pathway of complement activation (C1) has been a central goal in complement biology since its isolation almost 50 years ago.
Keeble, Anthony H.   +4 more
core   +1 more source

C1q-targeted inhibition of the classical complement pathway prevents injury in a novel mouse model of acute motor axonal neuropathy [PDF]

open access: yes, 2016
Introduction Guillain-Barré syndrome (GBS) is an autoimmune disease that results in acute paralysis through inflammatory attack on peripheral nerves, and currently has limited, non-specific treatment options.
Barrie, Jennifer A.   +8 more
core   +2 more sources

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