C1740

Sigma-Aldrich

Complement component C1q from human serum

≥95% (SDS-PAGE)

Número de CAS:
MDL number:
NACRES:
NA.61

Quality Level

biological source

human

assay

≥95% (SDS-PAGE)

form

liquid

application(s)

activity assay: suitable

shipped in

dry ice

storage temp.

−70°C

Gene Information

human ... C1QA(712), C1QB(713), C1QC(714)

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General description

C1q, together with C1r and C1s, in the ratio of 1:2:2, form the C1 complex which is the first component of the classical complement pathway. C1q is composed of 18 polypeptide chains (six A, six B, six C) (MW 460 kDa). All contain an 81-aa collagen-like region composed of (Gly-Xaa-Yaa) repeating sequences close to the N-terminus. Three chains (A1B1C1) form a triple helix with the C-terminus forming the globular heads which may be structurally and functionally distinct domains.

Application

Complement component C1q is an important regulator factor for platelet activation. This has been a topic for research, as platelet-leukocyte aggregates play an important role in inflammatory conditions such as coronary heart disease. In particular, C1q has been shown to inhibit collagen induced aggregation and enhance production of reactive oxygen species (ROS).

Biochem/physiol Actions

C1q deficiency, either because of rare homozygous genetic defect, or transcriptional/translational defects, is almost certainly a cause of systemic lupus erythematosus (SLE). The three C1q subunits are expressed through a novel mechanism of transcriptional synchronization.

Physical form

Supplied as a solution in 10 mM HEPES, 300 mM NaCl, pH 7.2

RIDADR

NONH for all modes of transport

WGK Germany

WGK 3

Flash Point F

Not applicable

Flash Point C

Not applicable

Certificado de Análisis
Elina Zotova et al.
Brain : a journal of neurology, 136(Pt 9), 2677-2696 (2013-08-15)
Inflammatory processes are important in the pathogenesis of Alzheimer's disease and in response to amyloid-β immunotherapy. We investigated the expression of multiple inflammatory markers in the brains of 28 non-immunized patients with Alzheimer's disease and 11 patients with Alzheimer's disease...
Consol Farrera et al.
Journal of immunology (Baltimore, Md. : 1950), 191(5), 2647-2656 (2013-08-02)
Neutrophil extracellular traps (NETs) facilitate the extracellular killing of pathogens. However, in recent years, excessive NET formation has been implicated in several pathological conditions. Indeed, NETs that are not removed from tissues or from the circulation might serve to trigger...
Andrew D Greenhalgh et al.
The Journal of neuroscience : the official journal of the Society for Neuroscience, 34(18), 6316-6322 (2014-05-03)
Macrophages in the injured spinal cord arise from resident microglia and infiltrating, peripherally derived monocytes. It is still not clear if macrophages derived from these two populations differ in their roles after CNS injury. The aims of this study are...
Nils Lachmann et al.
Transplantation, 95(5), 694-700 (2013-01-29)
Efforts to increase the specificity and sensitivity of human leukocyte antigen (HLA) antibody detection assays recently led to the establishment of two novel Luminex bead-based assays to detect complement-activating antibodies by the assessment of complement products C1q or C4d. Here...
Christian S Lobsiger et al.
Proceedings of the National Academy of Sciences of the United States of America, 110(46), E4385-E4392 (2013-10-31)
Accumulating evidence from mice expressing ALS-causing mutations in superoxide dismutase (SOD1) has implicated pathological immune responses in motor neuron degeneration. This includes microglial activation, lymphocyte infiltration, and the induction of C1q, the initiating component of the classic complement system that...

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