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Journal articles on the topic 'Complement factor I'

Author: Grafiati

Published: 4 June 2021

Last updated: 12 February 2022

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1

de la Fuente, M., M. J. Blanco, B. Pazos, M. I. Fernández, A. Carracedo, M. Sánchez-Salorio, R. M. Coco, C. Torrón, and A. M. Gómez. "Complement Factor H." Ophthalmology 114, no. 1 (January 2007): 193.e1–193.e2. http://dx.doi.org/10.1016/j.ophtha.2006.10.004.

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2

Altmann, Tom, Megan Torvell, Stephen Owens, Dipayan Mitra, Neil S. Sheerin, B. Paul Morgan, David Kavanagh, and Rob Forsyth. "Complement factor I deficiency." Neurology - Neuroimmunology Neuroinflammation 7, no. 3 (February 25, 2020): e689. http://dx.doi.org/10.1212/nxi.0000000000000689.

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ObjectiveTo raise awareness of complement factor I (CFI) deficiency as a potentially treatable cause of severe cerebral inflammation.MethodsCase report with neuroradiology, neuropathology, and functional data describing the mutation with review of literature.ResultsWe present a case of acute, fulminant, destructive cerebral edema in a previously well 11-year-old, demonstrating massive activation of complement pathways on neuropathology and compound heterozygote status for 2 pathogenic mutations in CFI which result in normal levels but completely abrogate function.ConclusionsOur case adds to a very small number of extant reports of this phenomenon associated with a spectrum of inflammatory histopathologies including hemorrhagic leukoencephalopathy and clinical presentations resembling severe acute disseminated encephalomyelitis. CFI deficiency can result in uncontrolled activation of the complement pathways in the brain resulting in devastating cerebral inflammation. The deficit is latent, but the catastrophic dysregulation of the complement system may be the result of a C3 acute phase response. Diagnoses to date have been retrospective. Diagnosis requires a high index of suspicion and clinician awareness of the limitations of first-line clinical tests of complement activity and activation. Simple measurement of circulating CFI levels, as here, may fail to diagnose functional deficiency with absent CFI activity. These diagnostic challenges may mean that the CFI deficiency is being systematically under-recognized as a cause of fulminant cerebral inflammation. Complement inhibitory therapies (such as eculizumab) offer new potential treatment, underlining the importance of prompt recognition, and real-time whole exome sequencing may play an important future role.

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3

Jiang, Haixiang, Eric Wagner, Huamei Zhang, and Michael M. Frank. "Complement 1 Inhibitor Is a Regulator of the Alternative Complement Pathway." Journal of Experimental Medicine 194, no. 11 (December 3, 2001): 1609–16. http://dx.doi.org/10.1084/jem.194.11.1609.

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We studied complement 1 inhibitor (C1-INH) as an inhibitor of the alternative complement pathway. C1-INH prevented lysis, induced by the alternative complement pathway, of paroxysmal nocturnal hemoglobinuria (PNH) erythrocytes in human serum. It inhibited the binding of both factors B and C3 to PNH and rabbit erythrocytes and blocked the ability of factor B to restore alternative-pathway function in factor B–depleted serum. C1-INH did not bind to factors B or D but did bind to immobilized C3b and cobra venom factor (CVF), a C3b analogue. C1-INH prevented factor B from binding to CVF-coated beads and dissociated bound factor B from such beads. Factor B and C1-INH showed cross competition in binding to CVF-coated beads. Factor D cleaved factor B into Bb and Ba in the presence of C3b. Cleavage was markedly inhibited when C3b was preincubated with C1-INH. C1-INH inhibited the formation of CVFBb and decreased the C3 cleavage. Removal of C1-INH from serum, in the presence of Mg-EGTA with an anti–C1-INH immunoabsorbant, markedly increased alternative-pathway lysis. C1-INH interacts with C3b to inhibit binding of factor B to C3b. At physiologic concentrations, it is a downregulator of the alternative pathway convertase.

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4

Zhang, Yuzhou, Adam Keenan, Margaret A. Lindorfer, Gabriella R. Pitcher, Ronald P. Taylor, John D. Lambris, and Richard J. H. Smith. "Activation of alternative complement pathway without complement factor D." Molecular Immunology 89 (September 2017): 173. http://dx.doi.org/10.1016/j.molimm.2017.06.153.

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5

Slade, Charlotte, Julian Bosco, Gary Unglik, Karl Bleasel, Mato Nagel, and Ingrid Winship. "Deficiency in Complement Factor B." New England Journal of Medicine 369, no. 17 (October 24, 2013): 1667–69. http://dx.doi.org/10.1056/nejmc1306326.

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6

Hamsten, Carl, Lillemor Skattum, Lennart Truedsson, Ulrika von Döbeln, Mathias Uhlén, Jochen M. Schwenk, Lennart Hammarström, Peter Nilsson, and Maja Neiman. "Heat differentiated complement factor profiling." Journal of Proteomics 126 (August 2015): 155–62. http://dx.doi.org/10.1016/j.jprot.2015.05.027.

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7

Aguilar, Andrea. "Complement factor H: beyond aHUS." Nature Reviews Nephrology 13, no. 3 (January 23, 2017): 136. http://dx.doi.org/10.1038/nrneph.2017.3.

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8

Rudduck, C., L. Beckman, G. Franzén, L. Jacobsson, and L. Lindström. "Complement Factor C4 in Schizophrenia." Human Heredity 35, no. 4 (1985): 223–26. http://dx.doi.org/10.1159/000153549.

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9

McCrae, Keith R. "Tissue factor needs a “complement”." Blood 110, no. 7 (October 1, 2007): 2228. http://dx.doi.org/10.1182/blood-2007-06-093757.

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10

Feng, Shuju, Michael H. Kroll, and Vahid Afshar-Kharghan. "Von Willebrand Factor Is a Cofactor in Complement Regulation." Blood 124, no. 21 (December 6, 2014): 109. http://dx.doi.org/10.1182/blood.v124.21.109.109.

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Complement, besides its involvement in eliminating microbes, participates in such diverse processes as synapse maturation, clearance of immune complexes, angiogenesis and tissue regeneration. Delicate balance between complement activation and regulation contributes to complement’s role in physiology. Any trigger that tips this balance can induce self-attack. Atypical hemolytic uremic syndrome (aHUS) is a systemic disease characterized by non-immune hemolytic anemia, thrombocytopenia, and renal impairment. In over 50% of cases, aHUS is known to be caused by uncontrolled activation of the complements. Von Willebrand factor (VWF) is a large multimeric glycoprotein that plays an important role in stopping the escape of blood from vessels following vascular injury. VWF and VWF cleavage enzyme ADAMTS13 gene defects have been identified in patients with aHUS, raising the possibility that VWF could have contributed to complement regulation. To examine the role of VWF in complement activation, we investigated whether VWF functions as a cofactor for FI-mediated C3b cleavage through in vitro assay. We found that C3b binds to VWF. In the presence of plasma-purified VWF (pVWF), FI cleaves C3b to 68kD and 43kD degradation products (iC3b) (Figure (A)). VWF alone, or FI alone, did not have any effect on C3b cleavage. C3b, not C3 or iC3b, was the mainly substrate for FI/VWF proteolysis. Increasing VWF concentration or prolonging the incubation time with VWF enhanced FI-mediated C3b cleavage. To remove the possibility that another plasma protein co-purified with pVWF that affects our results, we used recombinant VWF dimers purified from human embryonic kidney (HEK) 293 cell expressing VWF-Dpro cDNA, and detected a similar cofactor activity (Figure (B)).To investigate whether the size of VWF multimers have any effect on C3b cleavage, we compared the cofactor activity of pVWF, recombinant VWF dimers, and ULVWF multimers. While pVWF and dimer VWF enhanced C3b cleavage by FI, ULVWF did not have any effect on C3b cleavage (Figure (B)). In plasma, complement proteins Factor B and Factor D coexist with the inhibitory protein FI. To investigate the effect of VWF on complement activity in the presence of both pro-activation and inhibitory complement proteins, we incubated C3, FB, FD, and FI with VWF. In the presence of FB and FD, C3 be activated and resulted in the generation of C3a and C3b. Addition of recombinant VWF put a brake on complement activation and shifted C3 toward the generation of iC3b (Figure (C)). We conclude that normal plasma VWF, function as a cofactor, prevents complement activation through steers the complement pathway toward the generation of inactive iC3b. ULVWF multimers, as are present in patients with thrombotic microangiopathy, lack an inhibitory effect on complement and permit complement activation. Figure 1 Figure 1. Disclosures No relevant conflicts of interest to declare.

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11

Zhu, Li, Ya-Ling Zhai, Feng-Mei Wang, Ping Hou, Ji-Cheng Lv, Da-Min Xu, Su-Fang Shi, et al. "Variants in Complement Factor H and Complement Factor H-Related Protein Genes, CFHR3 and CFHR1, Affect Complement Activation in IgA Nephropathy." Journal of the American Society of Nephrology 26, no. 5 (September 9, 2014): 1195–204. http://dx.doi.org/10.1681/asn.2014010096.

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12

LESLIE. "Complement activation by leukocytes from patients with complement factor I deficiency." Molecular Immunology 30 (September 1993): 28. http://dx.doi.org/10.1016/0161-5890(93)90271-c.

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13

Makou, Elisavet, Andrew P. Herbert, and Paul N. Barlow. "Functional Anatomy of Complement Factor H." Biochemistry 52, no. 23 (May 31, 2013): 3949–62. http://dx.doi.org/10.1021/bi4003452.

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14

Skerka, Christine, Qian Chen, Veronique Fremeaux-Bacchi, and Lubka T. Roumenina. "Complement factor H related proteins (CFHRs)." Molecular Immunology 56, no. 3 (December 2013): 170–80. http://dx.doi.org/10.1016/j.molimm.2013.06.001.

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15

Grossman, Tamar, Michele Carrer, Robert Johnson, Lijiang Shen, Lisa Hettrick, Scott Henry, Brett Monia, and Michael McCaleb. "Antisense therapy targeting complement factor B." Molecular Immunology 102 (October 2018): 156. http://dx.doi.org/10.1016/j.molimm.2018.06.082.

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16

Durey, Marie-Agnes Dragon, Aditi Sinha, Shambhuprasad Kotresh Togarsimalemath, and Arvind Bagga. "Anti-complement-factor H-associated glomerulopathies." Nature Reviews Nephrology 12, no. 9 (July 25, 2016): 563–78. http://dx.doi.org/10.1038/nrneph.2016.99.

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17

Medjeral-Thomas, Nicholas, and Matthew C. Pickering. "The complement factor H-related proteins." Immunological Reviews 274, no. 1 (October 26, 2016): 191–201. http://dx.doi.org/10.1111/imr.12477.

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18

Gorevic, Peter D. "Rheumatoid Factor, Complement, and Mixed Cryoglobulinemia." Clinical and Developmental Immunology 2012 (2012): 1–6. http://dx.doi.org/10.1155/2012/439018.

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Low serum level of complement component 4 (C4) that occurs in mixed cryoglobulinemia (MC) may be due to in vivo or ex vivo activation of complement by the classical pathway. Potential activators include monoclonal IgM rheumatoid factor (RF), IgG antibodies, and the complexing of the two in the cold, perhaps modulated by the rheology and stoichiometry of cryocomplexes in specific microcirculations. There is also the potential for activation of complement by the alternative and lectin pathways, particularly in the setting of chronic infection and immune stimulation caused by hepatitis C virus (HCV). Engagement of C1q and interaction with specific cell surface receptors serve to localize immune complexes (ICs) to the sites of pathology, notably the cutaneous and glomerular microcirculations. Defective or saturated clearance of ICs by CR1and/or Fc receptors may explain persistence in the circulation. The phlogistic potential of cryoprecipitable ICs depends upon the cleavage of complement components to generate fragments with anaphylatoxin or leukocyte mobilizing activity, and the assembly of the membrane attack complex (C5b-9) on cell surfaces. A research agenda would include further characterization of the effector arm of complement activation in MC, and elucidation of activation mechanisms due to virus and viral antigens in HCV infection.

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19

Wiggs, Janey L. "Complement Factor H and Macular Degeneration." Archives of Ophthalmology 124, no. 4 (April 1, 2006): 577. http://dx.doi.org/10.1001/archopht.124.4.577.

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20

Geertinger, Preben, and Henning Sørensen. "COMPLEMENT AS A FACTOR IN ARTERIOSCLEROSIS." Acta Pathologica Microbiologica Scandinavica Section A Pathology 78A, no. 3 (August 15, 2009): 284–88. http://dx.doi.org/10.1111/j.1699-0463.1970.tb03303.x.

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21

Zipfel, Peter F. "Complement Factor H: Physiology and Pathophysiology." Seminars in Thrombosis and Hemostasis 27, no. 03 (2001): 191–200. http://dx.doi.org/10.1055/s-2001-15248.

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22

Mhatre, A., and W. P. Aston. "Isolation of bovine complement factor H." Veterinary Immunology and Immunopathology 14, no. 4 (April 1987): 357–75. http://dx.doi.org/10.1016/0165-2427(87)90038-9.

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23

YAMAUCHI, Y. "Zymogen forms of complement factor D." Molecular Immunology 30 (September 1993): 63. http://dx.doi.org/10.1016/0161-5890(93)90413-6.

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24

Lachmann, Peter J. "The story of complement factor I." Immunobiology 224, no. 4 (July 2019): 511–17. http://dx.doi.org/10.1016/j.imbio.2019.05.003.

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25

WHO-IUIS nomenclature sub-committee. "Nomenclature for human complement factor B." Journal of Immunological Methods 163, no. 1 (July 1993): 9–11. http://dx.doi.org/10.1016/0022-1759(93)90233-w.

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26

Boudhabhay, Idris, and Lubka T. Roumenina. "Complement factor H: a guardian within?" Kidney International 100, no. 4 (October 2021): 747–49. http://dx.doi.org/10.1016/j.kint.2021.07.023.

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27

Fakhouri, Fadi, Elena Goicoechea de Jorge, Frédérique Brune, Philippe Azam, H. Terence Cook, and Matthew C. Pickering. "Treatment with human complement factor H rapidly reverses renal complement deposition in factor H-deficient mice." Kidney International 78, no. 3 (August 2010): 279–86. http://dx.doi.org/10.1038/ki.2010.132.

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28

Gitterman, Daniel P., Talat H. Malik, Allan Bradley, and Matthew C. Pickering. "Generation of mice with deficiency of complement factor H and the complement factor H-related proteins." Immunobiology 221, no. 10 (October 2016): 1221. http://dx.doi.org/10.1016/j.imbio.2016.06.215.

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29

De Córdoba, S. Rodríguez, and E. Goicoechea De Jorge. "Translational Mini-Review Series on Complement Factor H: Genetics and disease associations of human complement factor H." Clinical & Experimental Immunology 151, no. 1 (December 7, 2007): 1–13. http://dx.doi.org/10.1111/j.1365-2249.2007.03552.x.

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30

Goicoechea de Jorge, E., J. J. E. Caesar, T. H. Malik, M. Patel, M. Colledge, S. Johnson, S. Hakobyan, et al. "Dimerization of complement factor H-related proteins modulates complement activation in vivo." Proceedings of the National Academy of Sciences 110, no. 12 (March 4, 2013): 4685–90. http://dx.doi.org/10.1073/pnas.1219260110.

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31

Ali, Youssif M., Robert B. Sim, Wilhelm Schwaeble, and Mona I. Shaaban. "Enterococcus faecalis Escapes Complement-Mediated Killing via Recruitment of Complement Factor H." Journal of Infectious Diseases 220, no. 6 (May 6, 2019): 1061–70. http://dx.doi.org/10.1093/infdis/jiz226.

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AbstractBackgroundEnterococcus faecalis is considered to be the most important species of enterococci responsible for blood stream infections in critically ill patients. In blood, the complement system is activated via the classical pathway (CP), the lectin pathway (LP), or the alternative pathway (AP), and it plays a critical role in opsonophagocytosis of bacteria including E faecalis.MethodsIn a mouse model of enterococcus peritonitis, BALB-C mice were challenged with a high dose of E faecalis 12 hours after intraperitoneal administration of anti-Factor H (FH) antibodies or isotype control. Four hours later, control mice developed higher bacterial burden in blood and organs compared with mice treated with anti-FH antibodies.ResultsWe demonstrate that complement recognition molecules C1q, CL-11, and murine ficolin-A bind the enterococcus and drive the CP and the LP in human and mouse. We further describe that E faecalis evades the AP by recruitment of FH on its surface. Our results show a strong C3b deposition on E faecalis via both the CP and the LP but not through the AP.ConclusionsThese findings indicate that E faecalis avoids the complement phagocytosis by the AP via sequestering complement FH from the host blood.

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32

MARQUART*, H. V., J. M. RASMUSSEN, and R. G. Q. LESLIE. "Complement‐activating ability of leucocytes from patients with‘qc complement factor I deficiency." Immunology 91, no. 3 (July 1997): 486–92. http://dx.doi.org/10.1046/j.1365-2567.1997.00273.x.

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33

Chen, Qian, Michael Wiesener, Hannes U. Eberhardt, Andrea Hartmann, Barbara Uzonyi, Michael Kirschfink, Kerstin Amann, et al. "Complement factor H–related hybrid protein deregulates complement in dense deposit disease." Journal of Clinical Investigation 124, no. 1 (December 16, 2013): 145–55. http://dx.doi.org/10.1172/jci71866.

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34

Akcan, Uğur, Sercan Karabulut, Cem İsmail Küçükali, Sibel Çakır, and Erdem Tüzün. "Bipolar disorder patients display reduced serum complement levels and elevated peripheral blood complement expression levels." Acta Neuropsychiatrica 30, no. 2 (April 12, 2017): 70–78. http://dx.doi.org/10.1017/neu.2017.10.

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ObjectiveBipolar disorder (BD) patients have recently been shown to exhibit increased proinflammatory cytokine levels indicating the role of inflammation in this disease. As inflammatory responses often include complement level alterations and complement production is influenced by cytokines, we aimed to find out whether complement system is activated in BD in a time-dependent manner and complement factors are involved in BD pathogenesis.MethodsSerum C4, factor B, sC5b-9 and neuron-specific enolase levels were measured by enzyme-linked immunosorbent assay, whereas peripheral blood mononuclear cell messenger RNA (mRNA) expression levels of C1q, C4, factor B and CD55 were measured by real-time polymerase chain reaction in chronic BD patients (n=22), first episode BD patients (n=24) and healthy controls (n=19).ResultsSerum complement levels were significantly reduced in chronic BD patients as compared with first episode BD patients and healthy controls. Serum levels of complement factors showed significant inverse correlation with disease duration, severity of manic symptoms and serum neuron-specific enolase levels. In chronic BD patients, peripheral blood mononuclear cell mRNA expression levels of C1q, C4 and factor B were significantly elevated, whereas the mRNA expression level of the complement inhibitor CD55 was significantly reduced.ConclusionsOur results suggest that complement factor levels are reduced in BD presumably due to overconsumption of the complement system and complement production is increased at mRNA level possibly as a compensation measure. Complement factors might potentially be used as indicators of disease severity, neuronal loss and cognitive dysfunction.

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35

Edey, Matthew, Lisa Strain, Roy Ward, Saeed Ahmed, Trevor Thomas, and Timothy H. J. Goodship. "Is complement factor H a susceptibility factor for IgA nephropathy?" Molecular Immunology 46, no. 7 (April 2009): 1405–8. http://dx.doi.org/10.1016/j.molimm.2008.12.002.

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36

XU, H., M. CHEN, and JV FORRESTER. "Complement factor H and factor B expression in RPE cells." Acta Ophthalmologica 86 (September 4, 2008): 0. http://dx.doi.org/10.1111/j.1755-3768.2008.4133.x.

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37

Lynch, Anne M., Alan G. Palestine, Brandie D. Wagner, Jennifer L. Patnaik, Ashley A. Frazier-Abel, Marc T. Mathias, Frank S. Siringo, Vernon Michael Holers, and Naresh Mandava. "Complement factors and reticular pseudodrusen in intermediate age-related macular degeneration staged by multimodal imaging." BMJ Open Ophthalmology 5, no. 1 (January 2020): e000361. http://dx.doi.org/10.1136/bmjophth-2019-000361.

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ObjectiveSystemic activation of the complement system in intermediate age-related macular degeneration (AMD) is understudied. Moreover, links between the presence of reticular pseudodrusen (RPD) and systemic complement dysregulation have not been studied. The aim of this study was to determine if there is a difference in plasma complement factor levels in intermediate AMD compared with controls, and if complement levels are related to the presence of RPD.Methods and analysisLevels of complement factors C1q (µg/mL), C4 (µg/mL), C2 (µg/mL), Mannose Binding Lectin (ng/mL), C4b (µg/mL), C3 (µg/mL), factor B (µg/mL), factor D (µg/mL), properdin (µg/mL), C3a (ng/mL), iC3b/C3b (ng/mL), Ba (ng/mL), factor H (µg/mL), factor I (µg/mL), C5 (µg/mL), C5a (pg/mL) and SC5b-9 (ng/mL) were measured in plasma.Results109 cases and 65 controls were included in the study. Thirty-nine (36%) cases had RPD. Significantly lower systemic levels of: C1q (OR 0.96, 95% CI 0.94 to 0.98), factor B (OR 0.98, 95% CI 0.96 to 0.99), iC3b/C3b (OR 0.97, 95% CI 0.95 to 0.98), factor H (OR 0.99, 95% CI 0.98 to 0.99), factor I (OR 0.83, 95% CI 0.77 to 0.89) and C5 (OR 0.94, 95% CI 0.90 to 0.98) were found in cases versus controls. Significantly elevated levels of: C2 (OR 1.29, 95% CI 1.07 to 1.59), C3a (OR 1.03, 95% CI 1.01 to 1.05) Ba (OR 1.03, 95% CI 1.01 to 1.05) and C5a (OR 1.04, 95% CI 1.02 to 1.07) were found in cases versus controls. Systemic levels of complement factors measured were not related to the presence of RPD.ConclusionsLevels of several systemic complement pathway factors were found to be altered in intermediate AMD. Systemic levels of complement factors were not related to RPD.

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38

Williams, Michael A., David Haughton, Michael Stevenson, David Craig, A. Peter Passmore, and Giuliana Silvestri. "Plasma Complement factor H in Alzheimer's Disease." Journal of Alzheimer's Disease 45, no. 2 (March 18, 2015): 369–72. http://dx.doi.org/10.3233/jad-142742.

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39

Zipfel, Peter F., Christine Skerka, Jessica Caprioli, Tamara Manuelian, Hartmut H. Neumann, Marina Noris, and Giuseppe Remuzzi. "Complement factor H and hemolytic uremic syndrome." International Immunopharmacology 1, no. 3 (March 2001): 461–68. http://dx.doi.org/10.1016/s1567-5769(00)00047-3.

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40

Mathieson, Peter. "Complement factor H and haemolytic uraemic syndrome." Lancet 359, no. 9308 (March 2002): 801–2. http://dx.doi.org/10.1016/s0140-6736(02)07866-2.

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41

Assirelli, E., P. Dolzani, L. Pulsatelli, O. Addimanda, G. Lisignoli, E. Mariani, and R. Meliconi. "Complement factor expression in osteoarthritis joint compartments." Osteoarthritis and Cartilage 24 (April 2016): S383—S384. http://dx.doi.org/10.1016/j.joca.2016.01.686.

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42

NONAKA, M. "Molecular cloning of lamprey complement factor B." Molecular Immunology 30 (September 1993): 38. http://dx.doi.org/10.1016/0161-5890(93)90313-z.

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43

Roversi, Pietro, Stefanos A. Tsiftsoglou, Robert B. Sim, and Susan M. Lea. "Crystallographic studies of human complement factor I." Molecular Immunology 44, no. 1-3 (January 2007): 233–34. http://dx.doi.org/10.1016/j.molimm.2006.07.203.

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44

Nilsson, Sara C., Robert B. Sim, Susan M. Lea, Veronique Fremeaux-Bacchi, and Anna M. Blom. "Complement factor I in health and disease." Molecular Immunology 48, no. 14 (August 2011): 1611–20. http://dx.doi.org/10.1016/j.molimm.2011.04.004.

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45

Geserick, G., P. Otremba, H. Schröder, B. Stradmann-Bellinghausen, and P. M. Schneider. "Reference Typing Report for Complement Factor B." Experimental and Clinical Immunogenetics 15, no. 4 (1998): 261–63. http://dx.doi.org/10.1159/000019080.

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46

Fontaine, M., M. J. Demares, V. Koistinen, A. J. Day, C. Davrinche, R. B. Sim, and J. Ripoche. "Truncated forms of human complement factor H." Biochemical Journal 258, no. 3 (March 15, 1989): 927–30. http://dx.doi.org/10.1042/bj2580927.

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By the use of Western-blot analyses with polyclonal anti-(Factor H) antibodies, two low-Mr protein species of Mr 41,000 and 37,000 under non-reducing conditions and 43,000 and 40,000 under reducing conditions are consistently detected together with the well-known 155,000-Mr Factor H in human plasma and serum. These two additional species are also found in plasma, urine and synovial fluids. The 41,000-Mr species but not the 37,00-Mr species is detected by a monoclonal anti-(Factor H) antibody directed at the N-terminal part of Factor H. The 37,000-Mr species but not the 41,000-Mr species is detected by a monoclonal anti-(Factor H) antibody directed at the C-terminal part of Factor H. The 41,000-Mr and 37,000-Mr species are different from the well-characterized 36,000-Mr N-terminal tryptic fragment of Factor H. They are likely to represent translational products of the short Factor H mRNA species of 1.8 kb and 1.2-1.5 kb occurring in human liver that we have recently described.

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47

Martin, S. C. "Phosphorylation of complement factor C3 in vivo." Biochemical Journal 261, no. 3 (August 1, 1989): 1051–54. http://dx.doi.org/10.1042/bj2611051.

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Complement factor C3, the central protein of the complement system, was found to be phosphorylated both in EDTA- and heparin-anticoagulated whole blood and in coagulating blood. Complement S protein (vitronectin) was also found to be phosphorylated under these conditions. Further, purified C3 was found to be a phosphoprotein in vivo, containing 0.15 mol of alkali-labile phosphate/mol of protein. The ATP concentration in plasma was measured and found to be about 2 microM.

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48

Tamano, Mariko, Yoshinobu Fuke, Morito Endo, Isao Ohsawa, Takayuki Fujita, and Hiroyuki Ohi. "Urinary Complement Factor H in Renal Disease." Nephron 92, no. 3 (2002): 705–7. http://dx.doi.org/10.1159/000064090.

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Rossi, Gabriele. "Meningococcaemia, complement system, and factor V Leiden." Lancet 363, no. 9415 (April 2004): 1166. http://dx.doi.org/10.1016/s0140-6736(04)15916-3.

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Bitzer, Michael, and Christiane M. Erley. "Meningococcaemia, complement system, and factor V Leiden." Lancet 363, no. 9415 (April 2004): 1166. http://dx.doi.org/10.1016/s0140-6736(04)15918-7.

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