THE INHIBITION OF PLASMIN, PLASMA KALLIKREIN, PLASMA PERMEABILITY FACTOR, AND THE C'1r SUBCOMPONENT OF THE FIRST COMPONENT OF COMPLEMENT BY SERUM C'1 ESTERASE INHIBITOR

Ratnoff, Oscar D.; Pensky, Jack; Ogston, D.; Naff, George B.

doi:10.1084/jem.129.2.315

Cited by 318 publications

(106 citation statements)

References 29 publications

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“…No enzymatic activity has been detected in Clq. I n contrast, Clr and Clq, Clr, AND C l s IN NORMAL AND PATHOLOGIC SERA Cls have enzymatic activities that can be inhibited by the same normal serum inhibitor (36) suggesting a similarity between these two proteins. It is possible that the synthesis and catabolism of Clr and CIS are closely related, as was pointed out by Pickering et a1 (31).…”

Section: Discussionmentioning

confidence: 99%

Serum levels of C1q, C1r and C1s in normal and pathologic sera

Bracco

Manni

1974

Arthritis & Rheumatism

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C1q, C1r and C1s protein concentrations were simultaneously assayed in sera of patients with systemic lupus erythematosus (SLE), rheumatoid arthritis, autoimmune hemolytic anemia, and viral hemorrhagic fever as well as in healthy adult control subjects. Correlation coefficients between the three subunits of C1 were calculated and the sequential evolution of C1q, C1r, and C1s levels was studied in patients with SLE. In the majority of cases there was a good correlation between C1q, C1r, and C1s; subunit levels increased or decreased in a coordinated fashion. A marked discrepancy between C1q, C1r, and C1s serum concentration was observed in 3 instances. Low C1q coexisted with extremely high C1r and C1s values. It appears that C1r and C1s are closely linked while C1q may vary in a more independent way.

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Section: Discussionmentioning

confidence: 99%

Serum levels of C1q, C1r and C1s in normal and pathologic sera

Bracco

Manni

1974

Arthritis & Rheumatism

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“…C1Inh is the major inhibitor of various kinin-generating protein cascade systems. 47 Its secretion into the tumor cell environment may thereby provide protection beyond the complement system.…”

Section: Discussionmentioning

confidence: 99%

K562 erythroleukemic cells are equipped with multiple mechanisms of resistance to lysis by complement

et al. 2001

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Resistance of tumor cells to lysis by complement is generally attributed to several protective mechanisms. The relative impact of these mechanisms in the same tumor cell, however, has not been assessed yet. We have analyzed the interaction of the human erythroleukemia tumor cell line K562 with human complement. K562 cells express the membrane complement regulatory proteins CD59, CD55 and CD46. As shown here for the first time, K562 also spontaneously release the soluble regulators C1 inhibitor, factor H, and soluble CD59. Complement resistance of K562 cells is augmented upon treatment with PMA, TNF or even with sublytic complement. Unlike TNF and sublytic complement, PMA enhanced the expression of membrane-bound CD55 and CD59 and led to increased secretion of soluble CD59. In addition, we show that complement-resistant K562 cells express a membrane-associated proteolytic activity, higher than the complement-sensitive K562/S cells. Treatment of complement-resistant K562 cells with serine protease inhibitors enhance their sensitivity to complement-mediated lysis. Inhibitors of protein kinase C (PKC) also sensitize K562 cells to complement lysis, implicating PKC-mediated signaling in cell resistance to complement. Neutralization of the CD55 and CD59 but not of CD46 regulatory activity with specific antibodies significantly increases complement-mediated K562 cell lysis. Treatment of K562 cells with a mixture of inhibitory reagents results in a significant additive enhancing effect on complement-mediated lysis of K562. In conclusion, K562 cells resist a complement attack by concomitantly using multiple molecular evasion strategies. Future attempts in antibody-based tumor therapy should include strategies to interfere with those resistance mechanisms.

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“…The in situ hybridisation results revealed strongest expression in stromal cells. The upregulation of the mRNAs coding for the complement components C1R and C4A and the C1 inhibitor SERPING1 (Ratnoff et al 1969) reflects the regulation of the complement cascade. Co-localisation of C1R, C1S and SERPING1 mRNA in the endometrium of day 18 pregnant cows was previously shown (Klein et al 2006).…”

Section: Modulation Of the Maternal Immune Systemmentioning

confidence: 99%

Embryo-induced transcriptome changes in bovine endometrium reveal species-specific and common molecular markers of uterine receptivity

Bauersachs¹,

Ulbrich²,

Groß³

et al. 2006

Reproduction

194

132

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The endometrium plays a central role among the reproductive tissues in the context of early embryo-maternal communication and pregnancy. This study investigated transcriptome profiles of endometrium samples from day 18 pregnant vs non-pregnant heifers to get insight into the molecular mechanisms involved in conditioning the endometrium for embryo attachment and implantation. Using a combination of subtracted cDNA libraries and cDNA array hybridisation, 109 mRNAs with at least twofold higher abundance in endometrium of pregnant animals and 70 mRNAs with higher levels in the control group were identified. Among the mRNAs with higher abundance in pregnant animals, at least 41 are already described as induced by interferons. In addition, transcript levels of many new candidate genes involved in the regulation of transcription, cell adhesion, modulation of the maternal immune system and endometrial remodelling were found to be increased. The different expression level was confirmed with real-time PCR for nine genes. Localisation of mRNA expression in the endometrium was shown by in situ hybridisation for AGRN, LGALS3BP, LGALS9, USP18, PARP12 and BST2. A comparison with similar studies in humans, mice, and revealed species-specific and common molecular markers of uterine receptivity.

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THE INHIBITION OF PLASMIN, PLASMA KALLIKREIN, PLASMA PERMEABILITY FACTOR, AND THE C'1r SUBCOMPONENT OF THE FIRST COMPONENT OF COMPLEMENT BY SERUM C'1 ESTERASE INHIBITOR

Cited by 318 publications

References 29 publications

Serum levels of C1q, C1r and C1s in normal and pathologic sera

Serum levels of C1q, C1r and C1s in normal and pathologic sera

K562 erythroleukemic cells are equipped with multiple mechanisms of resistance to lysis by complement

Embryo-induced transcriptome changes in bovine endometrium reveal species-specific and common molecular markers of uterine receptivity

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