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Complement C3a Protein | C3a protein

Human Complement C3a

Gene Names
C3; ASP; C3a; C3b; AHUS5; ARMD9; CPAMD1
Purity
Greater than 98.0% as determined by SDS-PAGE.
Synonyms
Complement C3a; Human Complement C3a; Complement C3a Human; Complement C3; C3 and PZP-like alpha-2-macroglobulin domain-containing protein 1; C3; CPAMD1; C3a Human; C3a protein
Ordering
For Research Use Only!
Host
Human Plasma
Purity/Purification
Greater than 98.0% as determined by SDS-PAGE.
Form/Format
C3a solution contains Phosphate buffered saline, pH7.2.
Sterile Filtered solution.
Human Virus Test
Plasma from each donor has been tested and found negative for antibody to HIV-1, HIV-2, HCV, HTLV-I &II and HBSAG.
Preparation and Storage
C3a Human is stable at 4 degree C if entire vial will be used within 2-4 weeks.
Store, frozen below -20 degree C for longer periods of time.
For long term storage it is recommended to add a carrier protein (0.1% HSA or BSA).
Avoid multiple freeze-thaw cycles.
Related Product Information for C3a protein
Introduction: Native human C3a is created by cleavage of human C3 protein by a human C3 convertase. C3a is a member of the anaphylatoxin family of three proteins (C3a, C4a and C5a) created by the activation of complement. C3a mediates various inflammatory responses including smooth muscle contraction, increased vascular permeability, vasodilation and release of histamine from mast cells and basophils. C3a (In contrast to C5a) does not exhibit significant neutrophil stimulating activities and does not induce chemotaxis, granule release or superoxide production. C3a acts through the C3a Receptor which is a G-protein coupled receptor found mainly on peripheral tissues, lymphoid cells and in the central nervous system. These activities of C3a are inactivated by removal of the C-terminal arginine which happens rapidly in plasma due to the action of carboxypeptidase N.
Description: Human Complement C3a produced in Human plasma is an non glycosylated polypeptide chain containing 77 amino acids having a molecular weight of 9,089 daltons.
Product Categories/Family for C3a protein

NCBI and Uniprot Product Information

NCBI GI #
NCBI GeneID
718
UniProt Accession #
Molecular Weight
187,148 Da
NCBI Official Full Name
Complement component 3
NCBI Official Synonym Full Names
complement component 3
NCBI Official Symbol
C3
NCBI Official Synonym Symbols
ASP; C3a; C3b; AHUS5; ARMD9; CPAMD1
NCBI Protein Information
complement C3; prepro-C3; C3a anaphylatoxin; complement component C3; complement component C3a; complement component C3b; acylation-stimulating protein cleavage product; C3 and PZP-like alpha-2-macroglobulin domain-containing protein 1
UniProt Protein Name
Complement C3
UniProt Gene Name
C3
UniProt Synonym Gene Names
CPAMD1; ASP
UniProt Entry Name
CO3_HUMAN

NCBI Description

Complement component C3 plays a central role in the activation of complement system. Its activation is required for both classical and alternative complement activation pathways. People with C3 deficiency are susceptible to bacterial infection. [provided by RefSeq, Feb 2009]

Uniprot Description

C3: C3 plays a central role in the activation of the complement system. Its processing by C3 convertase is the central reaction in both classical and alternative complement pathways. After activation C3b can bind covalently, via its reactive thioester, to cell surface carbohydrates or immune aggregates. Defects in C3 are the cause of complement component 3 deficiency (C3D). A rare defect of the complement classical pathway. Patients develop recurrent, severe, pyogenic infections because of ineffective opsonization of pathogens. Some patients may also develop autoimmune disorders, such as arthralgia and vasculitic rashes, lupus-like syndrome and membranoproliferative glomerulonephritis. Genetic variation in C3 is associated with susceptibility to age-related macular degeneration type 9 (ARMD9). ARMD is a multifactorial eye disease and the most common cause of irreversible vision loss in the developed world. In most patients, the disease is manifest as ophthalmoscopically visible yellowish accumulations of protein and lipid that lie beneath the retinal pigment epithelium and within an elastin- containing structure known as Bruch membrane. Defects in C3 are a cause of susceptibility to hemolytic uremic syndrome atypical type 5 (AHUS5). An atypical form of hemolytic uremic syndrome. It is a complex genetic disease characterized by microangiopathic hemolytic anemia, thrombocytopenia, renal failure and absence of episodes of enterocolitis and diarrhea. In contrast to typical hemolytic uremic syndrome, atypical forms have a poorer prognosis, with higher death rates and frequent progression to end-stage renal disease. Susceptibility to the development of atypical hemolytic uremic syndrome can be conferred by mutations in various components of or regulatory factors in the complement cascade system. Other genes may play a role in modifying the phenotype. Increased levels of C3 and its cleavage product ASP, are associated with obesity, diabetes and coronary heart disease. Short-term endurance training reduces baseline ASP levels and subsequently fat storage.

Protein type: Secreted, signal peptide; Secreted; Inhibitor

Chromosomal Location of Human Ortholog: 19p13.3-p13.2

Cellular Component: extracellular space; plasma membrane; extracellular region

Molecular Function: protein binding; endopeptidase inhibitor activity; C5L2 anaphylatoxin chemotactic receptor binding; receptor binding

Biological Process: regulation of immune response; complement activation, alternative pathway; signal transduction; fatty acid metabolic process; complement activation; G-protein coupled receptor protein signaling pathway; positive regulation of angiogenesis; positive regulation of activation of membrane attack complex; positive regulation of G-protein coupled receptor protein signaling pathway; positive regulation of type IIa hypersensitivity; regulation of complement activation; innate immune response; immune response; positive regulation of protein amino acid phosphorylation; inflammatory response; complement activation, classical pathway

Disease: Complement Component 3 Deficiency, Autosomal Recessive; Hemolytic Uremic Syndrome, Atypical, Susceptibility To, 5; Macular Degeneration, Age-related, 9

Research Articles on C3a

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Product Notes

The C3a c3 (Catalog #AAA147381) is a Protein produced from Human Plasma and is intended for research purposes only. The product is available for immediate purchase. It is sometimes possible for the material contained within the vial of "Complement C3a, Protein" to become dispersed throughout the inside of the vial, particularly around the seal of said vial, during shipment and storage. We always suggest centrifuging these vials to consolidate all of the liquid away from the lid and to the bottom of the vial prior to opening. Please be advised that certain products may require dry ice for shipping and that, if this is the case, an additional dry ice fee may also be required.

Precautions

All products in the AAA Biotech catalog are strictly for research-use only, and are absolutely not suitable for use in any sort of medical, therapeutic, prophylactic, in-vivo, or diagnostic capacity. By purchasing a product from AAA Biotech, you are explicitly certifying that said products will be properly tested and used in line with industry standard. AAA Biotech and its authorized distribution partners reserve the right to refuse to fulfill any order if we have any indication that a purchaser may be intending to use a product outside of our accepted criteria.

Disclaimer

Though we do strive to guarantee the information represented in this datasheet, AAA Biotech cannot be held responsible for any oversights or imprecisions. AAA Biotech reserves the right to adjust any aspect of this datasheet at any time and without notice. It is the responsibility of the customer to inform AAA Biotech of any product performance issues observed or experienced within 30 days of receipt of said product. To see additional details on this or any of our other policies, please see our Terms & Conditions page.

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