Literature summary for 3.4.21.42 extracted from

Shi, J.; Rose, E.L.; Singh, A.; Hussain, S.; Stagliano, N.E.; Parry, G.C.; Panicker, S.
TNT003, an inhibitor of the serine protease C1s, prevents complement activation induced by cold agglutinins (2014), Blood, 123, 4015-4022.

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Inhibitors

Inhibitors	Comment	Organism	Structure
TNT003	a mouse monoclonal antibody targeting the CP-specific serine protease C1s. TNT003 prevents cold agglutinin-mediated deposition of complement opsonins that promote phagocytosis of red blood cells. By preventing classical pathway activation, TNT003 also prevents cold agglutinin-driven generation of anaphylatoxins	Homo sapiens

Localization

Localization	Comment	Organism	GeneOntology No.	Textmining
extracellular	-	Homo sapiens	-	-

Organism

Organism	UniProt	Comment	Textmining
Homo sapiens	P09871	-	-

Source Tissue

Source Tissue	Comment	Organism	Textmining
blood serum	-	Homo sapiens	-

Synonyms

Synonyms	Comment	Organism
serine protease C1s	-	Homo sapiens

General Information

General Information	Comment	Organism
physiological function	C1s is involved in the classical pathway of complement, whose activation is often associated with autoimmune disorders in which disease pathology is linked to the presence of an autoantibody. One such disorder is cold agglutinin disease, an autoimmune hemolytic anemia in which autoantibodies (cold agglutinins) bind to red blood cells at low temperatures. Anemia occurs as a result of autoantibody-mediated classical pathway activation on the surface of the erythrocyte, leading to the deposition of complement opsonins that drive extravascular hemolysis in the liver, overview. Classical pathway activity in cold agglutinin disease patients terminates prior to activation of the terminal cascade	Homo sapiens

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Release 2023.1 (January 2023)