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Human Complement component 3 Protein 3318

$315.00$1,050.00

Summary

  • Expression: HEK293
  • Pure: Yes (HPLC)
  • Amino Acid Range: Ser23-Asn1663
SKU: 3318parent Categories: , Tag:
Weight 1 lbs
Dimensions 9 × 5 × 2 in
accession

P01024

express system

HEK293

product tag

C-His

purity

> 95% as determined by Tris-Bis PAGE;> 95% as determined by HPLC

background

Complement component 3 (C3), a pivotal molecule in the complement system, is an essential immune mediator in various diseases, including psoriasis. C3 deficiency promoted imiquimod-induced skin cell apoptosis and supported greater proportions of IFN-γ T cells in the inflamed tissues.

molecular weight

The protein has a predicted MW of 188.52 kDa. Due to enzyme lysis and glycosylation, the protein migrates to 67-68 kDa, 110-115 kDa and 140-160 kDa based on Tris-Bis PAGE result.

available size

100 µg, 500 µg

endotoxin

Less than 1EU per μg by the LAL method.

Human Complement component 3 Protein 3318

protein
Size and concentration
100, 500µg and lyophilized
Form
Lyophilized
Storage Instructions
Valid for 12 months from date of receipt when stored at -80°C. Recommend to aliquot the protein into smaller quantities for optimal storage. Please minimize freeze-thaw cycles.
Storage buffer
Shipped at ambient temperature.
Purity
> 95% as determined by Tris-Bis PAGE
target relevance
Complement component 3 (C3), a pivotal molecule in the complement system, is an essential immune mediator in various diseases, including psoriasis. C3 deficiency promoted imiquimod-induced skin cell apoptosis and supported greater proportions of IFN-γ T cells in the inflamed tissues.
Protein names
Complement C3 (C3 and PZP-like alpha-2-macroglobulin domain-containing protein 1) [Cleaved into: Complement C3 beta chain; C3-beta-c (C3bc); Complement C3 alpha chain; C3a anaphylatoxin; Acylation stimulating protein (ASP) (C3adesArg); Complement C3b alpha' chain; Complement C3c alpha' chain fragment 1; Complement C3dg fragment; Complemen
Gene names
C3,C3 CPAMD1
Mass
9606Da
Function
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.; Derived from proteolytic degradation of complement C3, C3a anaphylatoxin is a mediator of local inflammatory process. In chronic inflammation, acts as a chemoattractant for neutrophils (By similarity). It induces the contraction of smooth muscle, increases vascular permeability and causes histamine release from mast cells and basophilic leukocytes.; [C3-beta-c]: Acts as a chemoattractant for neutrophils in chronic inflammation.; [Acylation stimulating protein]: Adipogenic hormone that stimulates triglyceride (TG) synthesis and glucose transport in adipocytes, regulating fat storage and playing a role in postprandial TG clearance. Appears to stimulate TG synthesis via activation of the PLC, MAPK and AKT signaling pathways. Ligand for C5AR2. Promotes the phosphorylation, ARRB2-mediated internalization and recycling of C5AR2 (PubMed:10432298, PubMed:15833747, PubMed:16333141, PubMed:19615750, PubMed:2909530, PubMed:8376604, PubMed:9059512).
Subellular location
Secreted.
Tissues
Plasma. The acylation stimulating protein (ASP) is expressed in adipocytes and released into the plasma during both the fasting and postprandial periods.
Structure
C3 precursor is first processed by the removal of 4 Arg residues, forming two chains, beta and alpha, linked by a disulfide bond. C3 convertase activates C3 by cleaving the alpha chain, releasing C3a anaphylatoxin and generating C3b (beta chain + alpha' chain). Forms the pro-C3-convertase enzyme complex by interacting with Complement factor B Bb fragment (Bb), which is then stabilized by binding CFP, allowing the complex to become active (PubMed:28264884, PubMed:31507604). The interaction with Bb is dependent on Mg2+ (PubMed:31507604). C3b interacts with CR1 (via Sushi 8 and Sushi 9 domains) (PubMed:2972794, PubMed:8175757). C3b interacts with CFH (PubMed:21285368). C3d interacts with CFH (PubMed:21285368, PubMed:21317894). C3dg interacts with CR2 (via the N-terminal Sushi domains 1 and 2). During pregnancy, C3dg exists as a complex (probably a 2:2:2 heterohexamer) with AGT and the proform of PRG2. Interacts with VSIG4. Interacts (both C3a and ASP) with C5AR2; the interaction occurs with higher affinity for ASP, enhancing the phosphorylation and activation of C5AR2, recruitment of ARRB2 to the cell surface and endocytosis of GRP77.; (Microbial infection) C3b interacts with herpes simplex virus 1 (HHV-1) and herpes simplex virus 2 (HHV-2) envelope glycoprotein C; this interaction inhibits the activation of the complement system.; (Microbial infection) Interacts with Staphylococcus aureus immunoglobulin-binding protein Sbi; this interaction prevents the association between C3dg and CR2.; (Microbial infection) Interacts with Staphylococcus aureus protein Fib.
Post-translational modification
C3b is rapidly split in two positions by factor I and a cofactor to form iC3b (inactivated C3b) and C3f which is released. Then iC3b is slowly cleaved (possibly by factor I) to form C3c (beta chain + alpha' chain fragment 1 + alpha' chain fragment 2), C3dg and C3f. Other proteases produce other fragments such as C3d or C3g. C3a is further processed by carboxypeptidases to release the C-terminal arginine residue generating the acylation stimulating protein (ASP). Levels of ASP are increased in adipocytes in the postprandial period and by insulin and dietary chylomicrons.; Phosphorylated by FAM20C in the extracellular medium.; (Microbial infection) C3 is cleaved by Staphylococcus aureus aureolysin; this cleavage renders C3a and C3b inactive. C3b is rapidly degraded by host factors CFH and CFI preventing its deposition on the bacterial surface while C3a is further inactivated by aureolysin.; (Microbial infection) Complement C3 beta chain is cleaved and inactivated by S.pyogenes SpeB.; (Microbial infection) Cleaved by N.meningitidis NalP between Leu-744 and Gly-754, generating a slightly shorter C3 alpha form and a slightly longer C3 beta form. The C3b-like fragment is degraded in the presence of the complement regulators CFH and CFI, preventing its deposition on the bacterial surface.
Target Relevance information above includes information from UniProt accession: P01024
The UniProt Consortium

HPLC of Human Complement component 3 Protein
The purity of Human Complement component 3 is greater than 95% as determined by SEC-HPLC.
SDS-PAGE gel of Human Complement component 3 Protein
Human Complement component 3 on Tris-Bis PAGE under reduced condition. The purity is greater than 95%.

Publications

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Published literature highly relevant to the biological target of this product and referencing this antibody or clone are retrieved from PubMed database provided by The United States National Library of Medicine at the National Institutes of Health.

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