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Journal articles on the topic 'Soluble complement receptor 1'

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Published: 4 June 2021
Last updated: 13 February 2022

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1

&NA;. "Myelin protected by soluble recombinant complement receptor 1." Inpharma Weekly &NA;, no. 944 (July 1994): 11. http://dx.doi.org/10.2165/00128413-199409440-00025.

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2

Luan, Nguyen M., Yuji Teramura, and Hiroo Iwata. "Immobilization of soluble complement receptor 1 on islets." Biomaterials 32, no. 20 (July 2011): 4539–45. http://dx.doi.org/10.1016/j.biomaterials.2011.03.017.

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3

Chávez-Cartaya, Rafael E., Gilda Pino DeSola, Les Wright, Neville V. Jamieson, and David J. G. White. "REGULATION OF THE COMPLEMENT CASCADE BY SOLUBLE COMPLEMENT RECEPTOR TYPE 1." Transplantation 59, no. 7 (April 1995): 1047–52. http://dx.doi.org/10.1097/00007890-199504150-00023.

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4

Swift, A. J., T. S. Collins, P. Bugelski, and J. A. Winkelstein. "Soluble human complement receptor type 1 inhibits complement-mediated host defense." Clinical and diagnostic laboratory immunology 1, no. 5 (1994): 585–89. http://dx.doi.org/10.1128/cdli.1.5.585-589.1994.

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5

Gillinov, A. Marc, Patrick A. DeValeria, Jerry A. Winkelstein, Ian Wilson, William E. Curtis, David Shaw, C. Grace Yeh, et al. "Complement inhibition with soluble complement receptor type 1 in cardiopulmonary bypass." Annals of Thoracic Surgery 55, no. 3 (March 1993): 619–24. http://dx.doi.org/10.1016/0003-4975(93)90264-i.

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6

Couser, W. G., R. J. Johnson, B. A. Young, C. G. Yeh, C. A. Toth, and A. R. Rudolph. "The effects of soluble recombinant complement receptor 1 on complement-mediated experimental glomerulonephritis." Journal of the American Society of Nephrology 5, no. 11 (May 1995): 1888–94. http://dx.doi.org/10.1681/asn.v5111888.

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Complement is a major mediator of tissue injury in several types of glomerulonephritis. However, no therapeutic agents that inhibit complement activation are available for human use. sCR1 (TP10, BRL 55736) is a recombinant, soluble human complement receptor 1 (CR1) molecule lacking transmembrane and cytoplasmic domains that inhibits C3 and C5 convertase activity by preferentially binding C4b and C3b. To test the efficacy of sCR1 on complement-mediated glomerulonephritis, rats were pretreated with sCR1 (60 mg/kg per day) before and during the induction of three models of complement-dependent glomerulonephritis (concanavalin A and antithymocyte serum models of proliferative glomerulonephritis, passive Heyman nephritis). Daily sCR1 and complement hemolytic activity levels were measured, and renal histology and urine protein excretion were examined. Mean serum sCR1 levels of 100 to 200 micrograms/mL were maintained with a reduction in complement hemolytic activity to less than 15% in most animals. In the antithymocyte serum model, sCR1-treated animals had significant reductions in mesangiolysis, glomerular platelet and macrophage infiltrates, and proteinuria at 48 h. In the concanavalin A model, sCR1 significantly reduced glomerular C3 and fibrin deposits, platelet infiltrates, and proteinuria at 48 h. In passive Heymann nephritis, proteinuria was also significantly reduced (199 +/- 8.5 versus 125 +/- 16 mg/day, P < 0.002) at 5 days. It was concluded that sCR1 significantly reduces both morphologic and functional consequences of several different types of complement-mediated glomerulonephritis and deserves evaluation as a potential therapeutic agent in complement-mediated immune glomerular disease in humans.
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7

Moulds, JM, and KE Rowe. "Neutralization of Knops system antibodies using soluble complement receptor 1." Transfusion 36, no. 6 (June 1996): 517–20. http://dx.doi.org/10.1046/j.1537-2995.1996.36696269510.x.

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8

Sadallah, Salima, Christoph Hess, Sylvie Miot, Olivier Spertini, Hans Lutz, and Jürg-Alfred Schifferli. "Elastase and metalloproteinase activities regulate soluble complement receptor 1 release." European Journal of Immunology 29, no. 11 (November 1999): 3754–61. http://dx.doi.org/10.1002/(sici)1521-4141(199911)29:11<3754::aid-immu3754>3.0.co;2-5.

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9

Cheung, Alfred K., Charles J. Parker, and Mary Hohnholt. "Soluble complement receptor type 1 inhibits complement activation induced by hemodialysis membranes in vitro." Kidney International 46, no. 6 (December 1994): 1680–87. http://dx.doi.org/10.1038/ki.1994.468.

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10

Lehmann, Thorsten G., Thomas A. Koeppel, Michael Kirschfink, Martha-Maria Gebhard, Christian Herfarth, Gerd Otto, and Stefan Post. "COMPLEMENT INHIBITION BY SOLUBLE COMPLEMENT RECEPTOR TYPE 1 IMPROVES MICROCIRCULATION AFTER RAT LIVER TRANSPLANTATION1,2." Transplantation 66, no. 6 (September 1998): 717–22. http://dx.doi.org/10.1097/00007890-199809270-00005.

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11

Pierre, Andrew F., Alexandre M. Xavier, Mingyao Liu, Stephen D. Cassivi, Thomas F. Lindsay, Henry C. Marsh, Arthur S. Slutsky, and Shaf H. Keshavjee. "EFFECT OF COMPLEMENT INHIBITION WITH SOLUBLE COMPLEMENT RECEPTOR 1 ON PIG ALLOTRANSPLANT LUNG FUNCTION1." Transplantation 66, no. 6 (September 1998): 723–32. http://dx.doi.org/10.1097/00007890-199809270-00006.

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12

Piddlesden, Sara J., Shisong Jiang, James L. Levin, Angela Vincent, and B. Paul Morgan. "Soluble complement receptor 1 (sCR1) protects against experimental autoimmune myasthenia gravis." Journal of Neuroimmunology 71, no. 1-2 (December 1996): 173–77. http://dx.doi.org/10.1016/s0165-5728(96)00144-0.

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13

Li, Jennifer S., James Jaggers, and Page AW Anderson. "The use of TP10, soluble complement receptor 1, in cardiopulmonary bypass." Expert Review of Cardiovascular Therapy 4, no. 5 (September 2006): 649–54. http://dx.doi.org/10.1586/14779072.4.5.649.

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14

Wymann, Sandra, Yun Dai, Anup G. Nair, Helen Cao, Glenn A. Powers, Anna Schnell, Genevieve Martin-Roussety, et al. "A novel soluble complement receptor 1 fragment with enhanced therapeutic potential." Journal of Biological Chemistry 296 (2021): 100200. http://dx.doi.org/10.1074/jbc.ra120.016127.

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15

Ghiran, Ionita, Sergi F. Barbashov, Lloyd B. Klickstein, Sander W. Tas, Jens C. Jensenius, and Anne Nicholson-Weller. "Complement Receptor 1/Cd35 Is a Receptor for Mannan-Binding Lectin." Journal of Experimental Medicine 192, no. 12 (December 18, 2000): 1797–808. http://dx.doi.org/10.1084/jem.192.12.1797.

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Mannan-binding lectin (MBL), a member of the collectin family, is known to have opsonic function, although identification of its cellular receptor has been elusive. Complement C1q, which is homologous to MBL, binds to complement receptor 1 (CR1/CD35), and thus we investigated whether CR1 also functions as the MBL receptor. Radioiodinated MBL bound to recombinant soluble CR1 (sCR1) that had been immobilized on plastic with an apparent equilibrium dissociation constant of 5 nM. N-acetyl-d-glucosamine did not inhibit sCR1–MBL binding, indicating that the carbohydrate binding site of MBL is not involved in binding CR1. C1q inhibited MBL binding to immobilized sCR1, suggesting that MBL and C1q might bind to the same or adjacent sites on CR1. MBL binding to polymorphonuclear leukocytes (PMNs) was associated positively with changes in CR1 expression induced by phorbol myristate acetate. Finally, CR1 mediated the adhesion of human erythrocytes to immobilized MBL and functioned as a phagocytic receptor on PMNs for MBL–immunoglobulin G opsonized bacteria. Thus, MBL binds to both recombinant sCR1 and cellular CR1, which supports the role of CR1 as a cellular receptor for the collectin MBL.
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16

Heller, Axel, Marc Kunz, Andreas Samakas, Michael Haase, Michael Kirschfink, and Thea Koch. "THE COMPLEMENT REGULATORS C1 INHIBITOR AND SOLUBLE COMPLEMENT RECEPTOR 1 ATTENUATE ACUTE LUNG INJURY IN RABBITS." Shock 13, no. 4 (April 2000): 285–90. http://dx.doi.org/10.1097/00024382-200004000-00006.

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17

LAVER, ALISON J., MARTIN HIBBS, and RICHARD A. G. SMITH. "Activation of complement by DMSO and ethanol and its inhibition by soluble complement receptor type 1." Biochemical Society Transactions 23, no. 2 (May 1, 1995): 167S. http://dx.doi.org/10.1042/bst023167s.

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18

Gibb, Alison L., Anne M. Freeman, Richard A. G. Smith, Stuart Edmonds, and Edith Sim. "The interaction of soluble human complement receptor type 1 (sCR1, BRL55730) with human complement component C4." Biochimica et Biophysica Acta (BBA) - Molecular Basis of Disease 1180, no. 3 (January 1993): 313–20. http://dx.doi.org/10.1016/0925-4439(93)90056-7.

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19

PRUITT, SCOTT K., WILLIAM M. BALDWIN, HENRY C. MARSH, SHU S. LIN, C. Grace Yeh, and R. RANDAL BOLLINGER. "THE EFFECT OF SOLUBLE COMPLEMENT RECEPTOR TYPE 1 ON HYPERACUTE XENOGRAFT REJECTION." Transplantation 52, no. 5 (November 1991): 868–72. http://dx.doi.org/10.1097/00007890-199111000-00022.

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20

Luan, Nguyen Minh, and Hiroo Iwata. "Xenotransplantation of islets enclosed in agarose microcapsule carrying soluble complement receptor 1." Biomaterials 33, no. 32 (November 2012): 8075–81. http://dx.doi.org/10.1016/j.biomaterials.2012.07.048.

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21

Jung, Stefan, Klaus V. Toyka, and Hans-Peter Hartung. "Soluble complement receptor type 1 inhibits experimental autoimmune neuritis in Lewis rats." Neuroscience Letters 200, no. 3 (November 1995): 167–70. http://dx.doi.org/10.1016/0304-3940(95)12115-k.

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22

Pruitt, Scott K., and R. Randal Bollinger. "The effect of soluble complement receptor type 1 on hyperacute allograft rejection." Journal of Surgical Research 50, no. 4 (April 1991): 350–55. http://dx.doi.org/10.1016/0022-4804(91)90202-w.

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23

Weiser, Martin R., Simon A. L. Gibbs, Francis D. Moore, and Herbert B. Hechtman. "Complement inhibition by soluble complement receptor type 1 fails to moderate cerulein-induced pancreatitis in the rat." International Journal of Pancreatology 19, no. 2 (April 1996): 129–34. http://dx.doi.org/10.1007/bf02805226.

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24

Sadallah, S. "Increased levels of soluble complement receptor 1 in serum patients with liver diseases." Hepatology 24, no. 1 (July 1996): 118–22. http://dx.doi.org/10.1053/jhep.1996.v24.pm0008707249.

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25

Kallio, E. A., K. B. Lemstro¨m, J. M. Tikkanen, U. S. Ryan, P. J. Ha¨yry, and P. K. Koskinen. "Effect of soluble complement receptor type 1 (sCR1) on experimental obliterative bronchiolitis (OB)." Journal of Heart and Lung Transplantation 18, no. 1 (January 1999): 52–53. http://dx.doi.org/10.1016/s1053-2498(99)80077-1.

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26

Danielsson, Carina, Manuel Pascual, Lars French, Gertraud Steiger, and Jürg-Alfred Schifferli. "Soluble complement receptor type 1 (CD35) is released from leukocytes by surface cleavage." European Journal of Immunology 24, no. 11 (November 1994): 2725–31. http://dx.doi.org/10.1002/eji.1830241123.

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27

Hamacher, J., S. Sadallah, J. A. Schifferli, J. Villard, and L. P. Nicod. "Soluble complement receptor type 1 (CD35) in bronchoalveolar lavage of inflammatory lung diseases." European Respiratory Journal 11, no. 1 (January 1, 1998): 112–19. http://dx.doi.org/10.1183/09031936.98.11010112.

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28

Ruggieri, Elizabeth V., Peter J. Bugelski, Johanne M. Kaplan, Daniel Everitt, John Lipani, Diane K. Jorkasky, Steven C. Boike, Frederick DeClement, Francis D. Moore, and Danuta J. Herzyk. "Relationships between antibodies against human soluble complement receptor 1 (hsCR1) from various species." Journal of Clinical Immunology 16, no. 2 (March 1996): 97–106. http://dx.doi.org/10.1007/bf01540956.

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29

Sivasankar, B., K. R. Raju, V. Anand, S. Malu, S. Padmanabhan, S. C. Tiwari, Nibhriti Das, and L. M. Srivastava. "Levels of plasma soluble complement receptor 1 (sCR1) in normal Indian adult population." Indian Journal of Clinical Biochemistry 14, no. 2 (July 1999): 237–40. http://dx.doi.org/10.1007/bf02867924.

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30

Kyriakides, Constantinos, William Austen, Yong Wang, Joanne Favuzza, Lester Kobzik, Francis D. Moore, and Herbert B. Hechtman. "Membrane attack complex of complement and neutrophils mediate the injury of acid aspiration." Journal of Applied Physiology 87, no. 6 (December 1, 1999): 2357–61. http://dx.doi.org/10.1152/jappl.1999.87.6.2357.

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A significant role for the alternative complement pathway in acid aspiration has been demonstrated by the observation that C3 genetic knockout mice are protected from injury. Utilizing C5-deficient mice, we now test the role of the terminal complement components in mediating injury. Lung permeability in C5-deficient mice was 64% less than in wild-type animals and was similar to wild-type mice treated with soluble complement receptor type 1, which gave a 67% protection. Injury was fully restored in C5-deficient mice reconstituted with wild-type serum. The role of neutrophils was established in immunodepleted wild-type animals that showed a 58% protection. Injury was further reduced (90%) with the addition of soluble complement receptor type 1, indicating an additive effect of neutrophils and complement. Similarly, an additional protection was noted in C5-deficient neutropenic mice, indicating that neutrophil-mediated injury does not require C5a. Thus acid aspiration injury is mediated by the membrane attack complex and neutrophils. Neutrophil activity is independent of C5a.
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31

Weisman, H., T. Bartow, M. Leppo, H. Marsh, G. Carson, M. Concino, M. Boyle, K. Roux, M. Weisfeldt, and D. Fearon. "Soluble human complement receptor type 1: in vivo inhibitor of complement suppressing post-ischemic myocardial inflammation and necrosis." Science 249, no. 4965 (July 13, 1990): 146–51. http://dx.doi.org/10.1126/science.2371562.

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32

Li, L. M., J. B. Li, Y. Zhu, and G. Y. Fan. "Soluble complement receptor type 1 inhibits complement system activation and improves motor function in acute spinal cord injury." Spinal Cord 48, no. 2 (September 8, 2009): 105–11. http://dx.doi.org/10.1038/sc.2009.104.

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33

Kaczorowski, Susan L., Joanne K. Schiding, Carol A. Toth, and Patrick M. Kochanek. "Effect of Soluble Complement Receptor-1 on Neutrophil Accumulation after Traumatic Brain Injury in Rats." Journal of Cerebral Blood Flow & Metabolism 15, no. 5 (September 1995): 860–64. http://dx.doi.org/10.1038/jcbfm.1995.107.

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As part of the acute inflammatory response, neutrophils accumulate in the central nervous system after injury. Recently, a soluble human recombinant complement receptor (sCR1; BRL 55730; T Cell Sciences, Inc., Cambridge, MA, U.S.A.) has been developed that inhibits the activation of both the classical and the alternative pathways of complement. sCR1 attenuates the effects of the acute inflammatory response in several models of injury outside the central nervous system. The role of complement in traumatic brain injury, however, remains undefined. We hypothesized that treatment with sCR1 would attenuate neutrophil accumulation in the brain after cerebral trauma. Using a randomized, blinded protocol, 18 anesthetized Sprague–Dawley rats were pretreated with sCR1 or saline (control) at both 2 h and 2 min before trauma (weight drop) to the exposed right parietal cortex. A third dose of sCR1 (or saline) was given 6 h after trauma. Coronal brain sections centered on the site of trauma were obtained at 24 h after trauma and analyzed for myeloperoxidase (MPO) activity as a marker of neutrophil accumulation. Complete blood counts with differential were obtained before treatment with sCR1 and at 24 h after trauma. At 24 h after trauma, brain MPO activity was reduced by 41% in sCR1-treated rats compared with control rats [0.1599 ± 0.102 versus 0.27(2 ± 0.178 U/g (mean ± SD); p = 0.02]. The neutrophil count in peripheral blood increased approximately twofold in both groups. Neutrophil accumulation occurring in the brain after trauma is inhibited by sCR1 treatment. This suggests that complement activation is involved in the local inflammatory response to traumatic brain injury and plays an important role in neutrophil accumulation in the injured brain.
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34

von Dobschuetz, E., O. Bleiziffer, S. Pahernik, M. Dellian, T. Hoffmann, and K. Messmer. "Soluble complement receptor 1 preserves endothelial barrier function and microcirculation in postischemic pancreatitis in the rat." American Journal of Physiology-Gastrointestinal and Liver Physiology 286, no. 5 (May 2004): G791—G796. http://dx.doi.org/10.1152/ajpgi.00407.2003.

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Components of the activated complement cascade are considered to play a pivotal role in ischemia-reperfusion-induced organ injury. With the use of intravital epifluorescence microscopy, we investigated the effect of complement inhibition by the recombinant soluble complement receptor 1 (sCR1; TP10) on the effect of macromolecular microvascular permeability, functional capillary perfusion, and leukocyte endothelium interaction in postischemic pancreatitis. Anaesthetized Sprague-Dawley rats were subjected to 60 min of normothermic pancreatic ischemia induced by microclipping of the blood-supplying arteries of the organ. Rats who received sCR1 (15 mg/kg body wt iv; n = 7) during reperfusion showed a significant reduction of permeability (1.77 ± 1.34 × 10-8 cm/s; n = 7) of tetramethylrhodamine isothiocyanate-labeled albumin injected 90 min after the onset of reperfusion compared with vehicletreated animals (6.95 ± 1.56 × 10-8 cm/s; n = 7). At 120 min after the onset of reperfusion, the length of red blood cell-perfused capillaries (functional capillary density) was significantly improved (from 279 ± 15.7 to 330 ± 3.7 cm-1; n = 7) and the number of leukocytes adherent to postcapillary venules was significantly reduced (from 314 ± 87 to 163 ± 71 mm-2; n = 7) by sCR1 compared with vehicle treatment. Complement inhibition by sCR1 effectively ameliorates pancreatic ischemia-reperfusion-induced microcirculatory disturbances and might be considered for treatment of postischemic pancreatitis.
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35

Ramaglia, Valeria, Ruud Wolterman, Maryla de Kok, Miriam Ann Vigar, Ineke Wagenaar-Bos, Rosalind Helen Mary King, Brian Paul Morgan, and Frank Baas. "Soluble Complement Receptor 1 Protects the Peripheral Nerve from Early Axon Loss after Injury." American Journal of Pathology 172, no. 4 (April 2008): 1043–52. http://dx.doi.org/10.2353/ajpath.2008.070660.

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36

Nomura, Nakao, Henry W. Lim, James L. Levin, and Shigeru Sassa. "Effect of soluble complement receptor type 1 on porphyrin-induced phototoxicity in guinea pigs." Journal of Photochemistry and Photobiology B: Biology 42, no. 1 (January 1998): 28–31. http://dx.doi.org/10.1016/s1011-1344(97)00112-7.

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37

Pruitt, Scott K., Allan D. Kirk, R. Randal Bollinger, Henry C. Marsh, Bradley H. Collins, James L. Levin, James R. Mault, et al. "THE EFFECT OF SOLUBLE COMPLEMENT RECEPTOR TYPE 1 ON HYPERACUTE REJECTION OF PORCINE XENOGRAFTS." Transplantation 57, no. 3 (February 1994): 363–70. http://dx.doi.org/10.1097/00007890-199402150-00009.

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38

Sadallah, S., E. Giostra, G. Mentha, and J. A. Schifferli. "Increased levels of soluble complement receptor 1 in serum of patients with liver diseases." Hepatology 24, no. 1 (July 1996): 118–22. http://dx.doi.org/10.1002/hep.510240120.

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39

Luan, Nguyen Minh, Yuji Teramura, and Hiroo Iwata. "Layer-by-layer co-immobilization of soluble complement receptor 1 and heparin on islets." Biomaterials 32, no. 27 (September 2011): 6487–92. http://dx.doi.org/10.1016/j.biomaterials.2011.05.048.

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40

Smith, Edward F., Donald E. Griswold, John W. Egan, Leonard M. Hillegass, Richard A. G. Smith, Martin J. Hibbs, and Robert C. Gagnon. "Reduction of myocardial reperfusion injury with human soluble complement receptor type 1 (BRL 55730)." European Journal of Pharmacology 236, no. 3 (June 1993): 477–81. http://dx.doi.org/10.1016/0014-2999(93)90487-3.

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41

Li, Jennifer S., Stephen P. Sanders, April E. Perry, Sandra S. Stinnett, James Jaggers, Paula Bokesch, Laurie Reynolds, Rashid Nassar, and Page A. W. Anderson. "Pharmacokinetics and safety of TP10, soluble complement receptor 1, in infants undergoing cardiopulmonary bypass." American Heart Journal 147, no. 1 (January 2004): 173–80. http://dx.doi.org/10.1016/j.ahj.2003.07.004.

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42

Sim, R. B. "Large-scale isolation of complement receptor type 1 (CR1) from human erythrocytes. Proteolytic fragmentation studies." Biochemical Journal 232, no. 3 (December 15, 1985): 883–89. http://dx.doi.org/10.1042/bj2320883.

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A large-scale procedure for the isolation of complement receptor type 1 (CR1, the C3b receptor) from human erythrocytes is described. Two of the four known phenotypes of CR1 are detectable in the isolated material. Amino acid and hexosamine analysis of the A phenotype (Mr 240 000) indicates a polypeptide chain length of about 2030 amino acids and a carbohydrate content of 8%. Both N- and O-linked sugars appear to be present. Trypsin digestion of isolated CR1 shows that it is degraded rapidly and extensively, and no stable products of Mr greater than 25000 are found. The ability of the receptor to bind to solid-phase ligand is destroyed after a single cleavage by trypsin. The capacity of the receptor to act as a cofactor for Factor I-mediated cleavage of soluble C3b is, however, only gradually decreased by proteolysis, and 30% of this activity remains after extensive degradation. The same pattern of loss of binding to solid-phase ligand, with partial retention of interaction with soluble ligand, is also characteristic of the complement proteins Factor H and C4bp, which are functionally related to CR1.
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43

HAMER, Isabelle, Jean-Pierre PACCAUD, Dominique BELIN, Christine MAEDER, and Jean-Louis CARPENTIER. "Soluble form of complement C3b/C4b receptor (CR1) results from a proteolytic cleavage in the C-terminal region of CR1 transmembrane domain." Biochemical Journal 329, no. 1 (January 1, 1998): 183–90. http://dx.doi.org/10.1042/bj3290183.

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The complement C3b/C4b receptor (CR1) is an integral protein, anchored in the plasma membrane through a hydrophobic domain of 25 amino acids, but is also found in the plasma in soluble form (sCR1). A recombinant, soluble form of CR1 has been demonstrated to reduce complement-dependent tissue injury in animal models of ischaemia/reperfusion. In view of the important pathophysiological relevance of sCR1, we have investigated the mechanisms governing CR1 release by using various mutated and chimaeric receptors transiently expressed in COS cells. Pulse-chase experiments revealed that (1) sCR1 is produced by a proteolytic process, (2) the cleavage site lies within the C-terminus of CR1 transmembrane domain, (3) the proteolytic process involves a fully glycosylated CR1 form and (4) this process takes place in late secretory vesicles or at the plasma membrane.
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44

Lazar, H. L., T. Keilani, C. A. Fitzgerald, O. M. Shapira, C. T. Hunter, R. J. Shemin, H. C. Marsh, and U. S. Ryan. "Beneficial Effects of Complement Inhibition With Soluble Complement Receptor 1 (TP10) During Cardiac Surgery: Is There a Gender Difference?" Circulation 116, no. 11_suppl (September 11, 2007): I—83—I—88. http://dx.doi.org/10.1161/circulationaha.106.677914.

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45

Pruitt, Scott K., R. Randal Bollinger, Bradley H. Collins, Henry C. Marsh, James L. Levin, Alfred R. Rudolph, William M. Baldwin, and Fred Sanfilippo. "EFFECT OF CONTINUOUS COMPLEMENT INHIBITION USING SOLUBLE COMPLEMENT RECEPTOR TYPE 1 ON SURVIVAL OF PIG-TO-PRIMATE CARDIAC XENOGRAFTS1." Transplantation 63, no. 6 (March 1997): 900–902. http://dx.doi.org/10.1097/00007890-199703270-00017.

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46

Kyriakides, Constantinos, Yong Wang, William G. Austen, Joanne Favuzza, Lester Kobzik, Francis D. Moore, and Herbert B. Hechtman. "Sialyl Lewisx hybridized complement receptor type 1 moderates acid aspiration injury." American Journal of Physiology-Lung Cellular and Molecular Physiology 281, no. 6 (December 1, 2001): L1494—L1499. http://dx.doi.org/10.1152/ajplung.2001.281.6.l1494.

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Abstract:
The potentially enhanced anti-inflammatory effects of the sialyl Lewisx(sLex)-decorated version of soluble complement receptor type 1 (sCR1) in moderating acid aspiration injury are examined. HCl was instilled in tracheostomy tubes placed in mice, and extravasation of 125I-labeled albumin in bronchoalveolar lavage (BAL) fluid was used to calculate the vascular permeability index (PI). Neutrophil counts in BAL fluid and immunohistochemistry were performed. PI was moderated by 82% after treatment with sCR1sLexcompared with 54% in sCR1-untreated mice ( P < 0.05). Respective reductions in PI in mice treated 0.5 and 1 h after acid aspiration with sCR1sLex of 70 and 57% were greater than the decreases in PI of 45 and 38% observed in respective sCR1-treated groups ( P < 0.05). BAL fluid neutrophil counts in sCR1sLex-treated mice were significantly less than those in sCR1-treated animals, which were similar to those in untreated mice. Immunohistochemistry stained for sCR1 only on the pulmonary vascular endothelium of sCR1sLex- but not sCR1-treated mice. In conclusion, sCR1sLex moderates permeability by antagonizing complement activation and neutrophil adhesion. Delayed complement and neutrophil antagonism significantly reduces injury.
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47

Heckl-??streicher, Brigitte, Annette Wosnik, and Michael Kirschfink. "PROTECTION OF PORCINE ENDOTHELIAL CELLS FROM COMPLEMENT-MEDIATED CYTOTOXICITY BY THE HUMAN COMPLEMENT REGULATORS CD59, C1 INHIBITOR, AND SOLUBLE COMPLEMENT RECEPTOR TYPE 1." Transplantation 62, no. 11 (December 1996): 1693–96. http://dx.doi.org/10.1097/00007890-199612150-00032.

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48

Chai, Paul J., Rashid Nassar, Annette E. Oakeley, Damian M. Craig, George Quick, James Jaggers, Stephen P. Sanders, Ross M. Ungerleider, and Page A. W. Anderson. "Soluble Complement Receptor-1 Protects Heart, Lung, and Cardiac Myofilament Function From Cardiopulmonary Bypass Damage." Circulation 101, no. 5 (February 8, 2000): 541–46. http://dx.doi.org/10.1161/01.cir.101.5.541.

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49

GOODFELLOW, R. M., A. S. WILLIAMS, J. L. LEVIN, B. D. WILLIAMS, and B. P. MORGAN. "Local therapy with soluble complement receptor 1 (sCR1) suppresses inflammation in rat mono-articular arthritis." Clinical & Experimental Immunology 110, no. 1 (September 1997): 45–52. http://dx.doi.org/10.1111/j.1365-2249.1997.511e-ce1408.x.

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50

Szebeni, Janos, Helmut Spielberg, Richard O. Cliff, Nabila M. Wassef, Alan S. Rudolph, and Carl R. Alving. "Complement Activation and Thromboxane Secretion by Liposome-Encapsulated Hemoglobin in Rats in Vivo: Inhibition by Soluble Complement Receptor Type 1." Artificial Cells, Blood Substitutes, and Biotechnology 25, no. 4 (January 1997): 347–55. http://dx.doi.org/10.3109/10731199709118925.

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