Rhesus Recombinant C4B protein, ECD, His Tag (V2LY-0526-LY9654)

Name: Rhesus Recombinant C4B protein, ECD, His Tag
SKU: V2LY-0526-LY9654
Rating: 5 (1 reviews)

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Datasheet

SDS

Request for COA

Datasheet Target References Q & As Review & reward Protocols Associated Products

Basic Information

Expressed Host

HEK293 Cells

Protein Species

Rhesus

Tag

His Tag

Protein Construction

This product is Rhesus Recombinant C4B protein, ECD, His Tag consist of Amino Acid: 20-675 and predicts a molecular mass of 73.65 kDa.

Molecule Mass

73.65 kDa

Protein Domain

ECD

Sequence

Amino Acid: 20-675

Species

Rhesus

Formulations & Storage [For reference only, actual COA shall prevail!]

Purity

≥90% as determined by SDS-PAGE.

Endotoxin

Please contact us for more information.

Format

Lyophilized

Reconstitution

Allow the vial and reconstitution buffer to equilibrate to room temperature. Briefly centrifuge or tap down the vial to ensure that all lyophilized powder is collected at the bottom of the vial. For the reconstitution of this product, we recommend adding PBS or sterile water to achieve a final antibody concentration of 1 mg/mL. Allow the vial to reconstitute for 10-15 minutes at room temperature with gentle agitation. Avoid vigorous shaking that can cause foaming and antibody denaturation. Aliquot into volumes based on your experiment and store liquid protein at -20°C or -80°C for long time.

Buffer

Lyophilized from sterile Tris, NaCl, Glutathione, EDTA, DTT, PMSF, Glycerol

Preservative

None

Storage

Samples are stable for up to twelve months from date of receipt at -20°C to -80°C. Store it under sterile conditions at -20°C to -80°C. It is recommended that the protein be aliquoted for optimal storage. Avoid repeated freeze-thaw cycles.

More Infomation

Target

Full Name

complement component 4B (Chido blood group)

Function

Non-enzymatic component of the C3 and C5 convertases and thus essential for the propagation of the classical complement pathway. Covalently binds to immunoglobulins and immune complexes and enhances the solubilization of immune aggregates and the clearance of IC through CR1 on erythrocytes. C4A isotype is responsible for effective binding to form amide bonds with immune aggregates or protein antigens, while C4B isotype catalyzes the transacylation of the thioester carbonyl group to form ester bonds with carbohydrate antigens.
Derived from proteolytic degradation of complement C4, C4a anaphylatoxin is a mediator of local inflammatory process. It induces the contraction of smooth muscle, increases vascular permeability and causes histamine release from mast cells and basophilic leukocytes.

Biological Process

Complement activation Source: BHF-UCL
Complement activation, classical pathway Source: UniProtKB-KW
Detection of molecule of bacterial origin Source: BHF-UCL
Inflammatory response Source: UniProtKB-KW
Innate immune response Source: UniProtKB-KW
Opsonization Source: BHF-UCL
Positive regulation of apoptotic cell clearance Source: BHF-UCL
Regulation of complement activation Source: Reactome

Cellular Location

Secreted; Synapse; Axon; Dendrite

Involvement in disease

Systemic lupus erythematosus (SLE): Disease susceptibility is associated with variants affecting the gene represented in this entry. Interindividual copy-number variation (CNV) of complement component C4 and associated polymorphisms result in different susceptibilities to SLE. The risk of SLE susceptibility has been shown to be significantly increased among subjects with only two copies of total C4. A high copy number is a protective factor against SLE. A chronic, relapsing, inflammatory, and often febrile multisystemic disorder of connective tissue, characterized principally by involvement of the skin, joints, kidneys and serosal membranes. It is of unknown etiology, but is thought to represent a failure of the regulatory mechanisms of the autoimmune system. The disease is marked by a wide range of system dysfunctions, an elevated erythrocyte sedimentation rate, and the formation of LE cells in the blood or bone marrow.
Complement component 4B deficiency (C4BD): A rare defect of the complement classical pathway associated with the development of autoimmune disorders, mainly systemic lupus with or without associated glomerulonephritis.

PTM

Prior to secretion, the single-chain precursor is enzymatically cleaved to yield non-identical chains alpha, beta and gamma. During activation, the alpha chain is cleaved by C1 into C4a and C4b, and C4b stays linked to the beta and gamma chains. Further degradation of C4b by C1 into the inactive fragments C4c and C4d blocks the generation of C3 convertase. The proteolytic cleavages often are incomplete so that many structural forms can be found in plasma.

Chua, G. T., Zhou, D., Ho, A. C. C., Chan, S. H. S., Yu, C. Y., & Lau, Y. L. (2020). A case report of complement C4B deficiency in a patient with steroid and IVIG-refractory anti-NMDA receptor encephalitis. BMC neurology, 20(1), 1-4.

Zarantonello, A., Presumey, J., Simoni, L., Yalcin, E., Fox, R., Hansen, A., ... & Andersen, G. R. (2020). An ultrahigh-affinity complement C4b-specific nanobody inhibits in vivo assembly of the classical pathway proconvertase. The Journal of Immunology, 205(6), 1678-1694.

Wang, H., Li, Y., Shi, G., Wang, Y., Lin, Y., Wang, Q., ... & Deng, H. (2020). A novel antitumor strategy: simultaneously inhibiting angiogenesis and complement by targeting VEGFA/PIGF and C3b/C4b. Molecular Therapy-Oncolytics, 16, 20-29.

Sharp, T. H., Boyle, A. L., Diebolder, C. A., Kros, A., Koster, A. J., & Gros, P. (2019). Insights into IgM-mediated complement activation based on in situ structures of IgM-C1-C4b. Proceedings of the National Academy of Sciences, 116(24), 11900-11905.

Mulvihill, E., Ardoin, S., Thompson, S. D., Zhou, B., Yu, G. R., King, E., ... & Yu, C. Y. (2019). Elevated serum complement levels and higher gene copy number of complement C4B are associated with hypertension and effective response to statin therapy in childhood-onset systemic lupus erythematosus (SLE). Lupus science & medicine, 6(1), e000333.

Hertz, C. E., Bayarri-Olmos, R., Kirketerp-Møller, N., van Putten, S., Pilely, K., Skjoedt, M. O., & Garred, P. (2018). Chimeric proteins containing MAP-1 and functional domains of C4b-binding protein reveal strong complement inhibitory capacities. Frontiers in immunology, 9, 1945.

Liesmaa, I., Paakkanen, R., Järvinen, A., Valtonen, V., & Lokki, M. L. (2018). Clinical features of patients with homozygous complement C4A or C4B deficiency. PloS one, 13(6), e0199305.

Haleem, K. S., Ali, Y. M., Yesilkaya, H., Kohler, T., Hammerschmidt, S., Andrew, P. W., ... & Lynch, N. J. (2018). The pneumococcal surface proteins PspA and PspC sequester host C4-binding protein to inactivate complement C4b on the bacterial surface. Infection and immunity, 87(1), e00742-18.

Nissilä, E., Korpela, K., Lokki, A. I., Paakkanen, R., Jokiranta, S., de Vos, W. M., ... & Meri, S. (2017). C4B gene influences intestinal microbiota through complement activation in patients with paediatric‐onset inflammatory bowel disease. Clinical & Experimental Immunology, 190(3), 394-405.

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Please try the standard protocols which include: protocols, troubleshooting and guide.

Enzyme-linked Immunosorbent Assay (ELISA)
Flow Cytometry
Immunofluorescence (IF)
Immunohistochemistry (IHC)
Immunoprecipitation (IP)
Western Blot (WB)
Enzyme Linked Immunospot (ELISpot)
Proteogenomic
Other Protocols

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For research use only. Not intended for any clinical use.

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