Complement C1 (Complement 1)

The first complement component to act in the activation of CLASSICAL COMPLEMENT PATHWAY. It is a calcium-dependent trimolecular complex made up of three subcomponents: COMPLEMENT C1Q; COMPLEMENT C1R; and COMPLEMENT C1S at 1:2:2 ratios. When the intact C1 binds to at least two antibodies (involving C1q), C1r and C1s are sequentially activated, leading to subsequent steps in the cascade of COMPLEMENT ACTIVATION.

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Networked: 96 relevant articles (1 outcomes, 7 trials/studies)

Relationship Network

Bio-Agent Context: Research Results

Experts

1.	Cunnion, Kenji M: 5 articles (01/2021 - 01/2016)
2.	Hair, Pamela S: 5 articles (01/2021 - 01/2016)
3.	Krishna, Neel K: 4 articles (01/2021 - 01/2016)
4.	Kapferer-Seebacher, Ines: 4 articles (01/2019 - 11/2017)
5.	Zschocke, Johannes: 4 articles (01/2019 - 11/2017)
6.	Amberger, Albert: 3 articles (01/2019 - 01/2019)
7.	Bally, Isabelle: 3 articles (01/2019 - 01/2019)
8.	Dalonneau, Fabien: 3 articles (01/2019 - 01/2019)
9.	Gaboriaud, Christine: 3 articles (01/2019 - 01/2019)
10.	Gröbner, Rebekka: 3 articles (01/2019 - 01/2019)

Related Diseases

1.	Hereditary Angioedemas 08/01/2021 - "Hereditary angioedema (HAE) is a rare condition, mostly due to genetic deficiency of complement C1 inhibitor (C1-INH). " 09/01/2014 - "Hereditary angioedema is caused by a deficiency (type I) or dysfunction (type II) in complement C1 inhibitor. " 06/01/2013 - "Hereditary angioedema (HAE) is a genetic syndrome caused by a functional deficit in complement C1 inhibitor that results in recurrent episodes of nonpruritic swelling of the hands, feet, arms, legs, trunk, face, genitalia, bowels, and larynx beginning in childhood or adolescence and continuing throughout the patient's lifetime. " 05/01/1998 - "Hereditary angioneurotic edema (HAE) is an infrequent autosomal dominant disorder characterized by a decrease in the levels or a dysfunction of the complement C1 inhibitor factor (C1 inh). " 05/01/1991 - "Patients with hereditary angioneurotic edema (HANE) have serum levels of functionally active inhibitor of the first component of complement (C1 INH) between 5 and 30% of normal, instead of the 50% expected from the single normal allele. "
2.	Angioedema 05/28/1987 - "During the past 25 years, three forms of deficiency of the inhibitor of the first component of complement (C1 inhibitor) with angioedema have been recognized; two forms are hereditary and one is acquired. " 10/01/2013 - "Approximately 2% of angioedema (AE) patients have a hereditary or an acquired deficiency of the complement 1 (C1) esterase inhibitor (C1 INH) gene. " 08/01/1986 - "The first component of complement (C1) inhibitor plays a critical role in the regulation of the classical complement pathway and the contact system, and the deficiency of C1 inhibitor protein or function is associated with recurrent angioedema. " 12/01/1993 - "Acquired complement component 1 (C1) inhibitor deficiency with consequent angioedema is a rare condition that may indicate an underlying neoplasm of B-lymphocytes or plasma cells. " 06/01/2008 - "[Angiotensin-converting enzyme inhibitor-related angioedema: emergency treatment with complement C1 inhibitor concentrate]."
3.	Neoplasms (Cancer) 01/01/2018 - "The Mortality-Incidence Ratio complement [1 - MIR] is an appropriate tool for approximating observed five-year survival for the ten types of cancers studied. " 01/01/2014 - "Murine CRT is then translocated to the external membrane where, together with rTcCRT, complement C1 is captured, thus promoting tumor phagocytosis. " 09/28/2023 - "The combination of markers, including the complement C1 complex, JCHAIN, and CD5L, resulted in a prediction model with an AUC of 0.96 for the identification of multiple myeloma patients across various cancer patients. " 01/01/2022 - "Background: Complement component 1 Q subcomponent binding protein (C1QBP) plays a vital role in the progression and metabolism of cancer. " 01/01/2018 - "The Mortality-Incidence Ratio complement [1 - MIR] is an indicator validated in various populations to estimate five-year cancer survival, but its validity remains unreported in Peru. "
4.	Systemic Lupus Erythematosus (Libman-Sacks Disease) 08/01/2010 - "Recent studies have tested genetic variation at the C1QA, C1QB and C1QC (complement component 1, q subcomponent, A chain, complement component 1, q subcomponent, B chain and complement component 1, q subcomponent, c chain) loci in relation to systemic lupus erythematosus (SLE) risk. " 10/01/2016 - "Recently, autoantibodies against C1q, a component of complement 1, were reported to be correlated with complement activation in systemic lupus erythematosus. " 01/01/1995 - "A large proportion of systemic lupus erythematosus (SLE) patients develop glomerulonephritis, coincident with the appearance of autoantibodies to C1q, the Fc-recognizing collagen-like subcomponent of the first component of complement, C1. "
5.	Obesity 05/01/2007 - "These data suggests that both adipose and immune cells are the sources for abnormal adipose tissue production of C1 complement and decorin in obesity. " 05/01/2007 - "In this study, we investigated adipose expression and regulation of C1 complement subcomponents and C1 activation regulator decorin in obesity and insulin resistance. " 10/01/2009 - "Three candidate genes not previously associated with obesity or type 2 diabetes, sushi domain containing 2, collagen and calcium-binding EGF domains 1 and periostin (Postn), as well as one gene known to be associated, complement component 1, were shown by RT-PCR to be differentially expressed in skeletal muscle of P. "

Related Drugs and Biologics

1.	Bradykinin Receptor Antagonists
2.	Bradykinin
3.	Carrier Proteins (Binding Protein)
4.	Proteins (Proteins, Gene)
5.	Complement System Proteins (Complement)
6.	Decorin
7.	Leukemia Inhibitory Factor
8.	Small Interfering RNA (siRNA)
9.	Complement C4 (Complement Component 4)
10.	Complement C1 Inhibitor Protein (C1 Esterase Inhibitor)

Related Therapies and Procedures

1.	Emergency Treatment
2.	Drug Therapy (Chemotherapy)