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3.4.21.43: classical-complement-pathway C3/C5 convertase

This is an abbreviated version!
For detailed information about classical-complement-pathway C3/C5 convertase, go to the full flat file.

Word Map on EC 3.4.21.43

Reaction

Selective cleavage of Arg-/-Ser bond in complement component C3 alpha-chain to form C3a and C3b, and Arg-/- bond in complement component C5 alpha-chain to form C5a and C5b =

Synonyms

C3 convertase, C3/C5 convertase, C3b 2 Bb, C3b2Bb, C3bBb, C3bBbP, C4, C423, C4b,2a, C4b,2a,3b, C4b,C2a, C4b2a, C4b2a(C3b)n, C4b2a3b, C4b2aC3b, C4bC2a, C5 convertase, classical C3 convertase, classical C5 convertase, classical pathway C3 convertase, classical pathway C3/C5 convertase, classical pathway C5 convertase, complement C3 convertase, CP C3 convertase, CP C3/C5 convertase, CP C5 convertase, EAC1,C4b,C2a, EC 3.4.21.44, high affinity C5 convertase, soluble C3 convertase, surface-bound C3 convertase

ECTree

     3 Hydrolases
         3.4 Acting on peptide bonds (peptidases)
             3.4.21 Serine endopeptidases
                3.4.21.43 classical-complement-pathway C3/C5 convertase

Disease

Disease on EC 3.4.21.43 - classical-complement-pathway C3/C5 convertase

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DISEASE
TITLE OF PUBLICATION
LINK TO PUBMED
Arthritis
The complement system is activated in synovial fluid from subjects with knee injury and from patients with osteoarthritis.
Arthritis, Rheumatoid
The complement system is activated in synovial fluid from subjects with knee injury and from patients with osteoarthritis.
Colitis
Regulation of the alternative pathway of complement modulates injury and immunity in a chronic model of dextran sulphate sodium-induced colitis.
Diabetic Nephropathies
Loss of decay-accelerating factor triggers podocyte injury and glomerulosclerosis.
Glomerulonephritis
Accelerated decay of the cell bound C4b2a complex by serum of patients with membranoproliferative glomerulonephritis and acute poststreptococcal glomerulonephritis.
Mechanism of action of the C4 nephritic factor. Deregulation of the classical pathway of C3 convertase.
Regulation and deregulation of the fluid-phase classical pathway C3 convertase.
Glomerulonephritis, Membranoproliferative
Accelerated decay of the cell bound C4b2a complex by serum of patients with membranoproliferative glomerulonephritis and acute poststreptococcal glomerulonephritis.
Autoantibody to complement neoantigens in membranoproliferative glomerulonephritis.
Autoimmune forms of thrombotic microangiopathy and membranoproliferative glomerulonephritis: Indications for a disease spectrum and common pathogenic principles.
Infections
Regulation of the alternative pathway of complement modulates injury and immunity in a chronic model of dextran sulphate sodium-induced colitis.
Lupus Erythematosus, Systemic
Heterogeneity, polypeptide chain composition and antigenic reactivity of autoantibodies (F-42) that are directed against the classical pathway C3 convertase of complement and isolated from sera of patients with systemic lupus erythematosus.
Relative importance of C4 binding protein in the modulation of the classical pathway C3 convertase in patients with systemic lupus erythematosus.
Stabilization of the classical pathway C3 convertase C42, by a factor F-42, isolated from serum of patients with systemic lupus erythematosus.
Multiple Sclerosis
A systematic analysis of the complement pathways in patients with neuromyelitis optica indicates alteration but no activation during remission.
Neoplasms
The complement system is activated in synovial fluid from subjects with knee injury and from patients with osteoarthritis.
Sepsis
Autoantibody stabilization of the classical pathway C3 convertase leading to C3 deficiency and Neisserial sepsis: C4 nephritic factor revisited.