Copines: a ubiquitous family of Ca 2+ -dependent phospholipid-binding proteins

2002 ◽  
Vol 59 (9) ◽  
pp. 1467-1477 ◽  
Author(s):  
J. L. Tomsig ◽  
C. E. Creutz
Keyword(s):  
Binding Proteins ◽  
Phospholipid Binding

scholarly journals A calcyclin-associated protein is a newly identified member of the Ca2+/phospholipid-binding proteins, annexin family.

1992 ◽  
Vol 267 (13) ◽  
pp. 8919-8924
Author(s):  
H Tokumitsu ◽  
A Mizutani ◽  
H Minami ◽  
R Kobayashi ◽  
H Hidaka
Keyword(s):  
Binding Proteins ◽  
Phospholipid Binding

Cutaneous manifestations of antiphospholipid syndrome

Lupus ◽  
2021 ◽  
pp. 096120332199010
Author(s):  
Minerva Gomez-Flores ◽  
Genesis Herrera-Argaez ◽  
Osvaldo Vazquez-Martinez ◽  
Maira Herz-Ruelas ◽  
Jorge Ocampo-Candiani ◽  
...  
Keyword(s):  
Antiphospholipid Syndrome ◽  
Binding Proteins ◽  
Cutaneous Manifestations ◽  
Phospholipid Binding

Antiphospholipid syndrome (APS) is an acquired thrombophilic disorder in which autoantibodies are produced against a variety of phospholipids and phospholipid-binding proteins. The purpose of this article is to review cutaneous findings in patients with APS diagnosis. An overview regarding prevalence, description, pathogenesis and histopathology, are described for cutaneous manifestations of APS.

scholarly journals Annexins--multifunctional, calcium-dependent, phospholipid-binding proteins.

1993 ◽  
Vol 40 (3) ◽  
pp. 281-293 ◽  
Author(s):  
J Bandorowicz ◽  
S Pikuła
Keyword(s):  
Binding Proteins ◽  
Phospholipid Binding ◽  
Calcium Dependent

Pregnancy loss and autoantibodies against phospholipid-binding proteins

1997 ◽  
Vol 89 (6) ◽  
pp. 975-980 ◽  
Author(s):  
C FALCON ◽  
M MARTINUZZO ◽  
R FORASTIERO ◽  
G CERRATO ◽  
L CARRERAS
Keyword(s):  
Pregnancy Loss ◽  
Binding Proteins ◽  
Phospholipid Binding

Annexin 1 and neutrophil apoptosis

2004 ◽  
Vol 32 (3) ◽  
pp. 507-510 ◽  
Author(s):  
M. Perretti ◽  
E. Solito
Keyword(s):  
Inflammatory Response ◽  
Binding Proteins ◽  
Neutrophil Apoptosis ◽  
The Novel ◽  
Inhibitory Effects ◽  
Phospholipid Binding ◽  
Annexin 1 ◽  
Anti Inflammatory ◽  
Leucocyte Recruitment ◽  
Host Inflammatory Response

ANXA1 (annexin 1), a member of the ‘annexin’ family of calcium- and phospholipid-binding proteins, was originally identified as an endogenous mediator of the anti-inflammatory actions of glucocorticoids. However, this protein exerts multiple inhibitory effects on the host inflammatory response, including a preferential regulation of the adhesion step of blood-borne neutrophil within the microenvironment of an inflamed vasculature. It is now emerging that ANXA1 is endowed with other roles, since the protein is abundant in inflammatory exudates as it is produced and released by the extravasated neutrophil. In the present paper, we review the novel proapoptotic effect of ANXA1 and discuss its potential with respect to the pathophysiology of inflammation and leucocyte recruitment.

The Antiphospholipid Syndrome

Hematology ◽  
2007 ◽  
Vol 2007 (1) ◽  
pp. 136-142 ◽  
Author(s):  
Jacob H. Rand
Keyword(s):  
Antiphospholipid Syndrome ◽  
Pregnancy Complications ◽  
Binding Proteins ◽  
Clinical Manifestations ◽  
Therapeutic Approaches ◽  
Vascular Thrombosis ◽  
Phospholipid Binding ◽  
Thrombophilic Condition

Abstract The antiphospholipid syndrome (APS) is an autoimmune thrombophilic condition that is marked by the presence of antibodies that recognize phospholipid-binding proteins. The clinical manifestations of APS include vascular thrombosis and pregnancy complications, especially recurrent spontaneous miscarriages. This article provides an update on diagnostic and therapeutic approaches to this disorder.

scholarly journals Isolation and characterization of two novel calcium-dependent phospholipid-binding proteins from bovine lung

FEBS Letters ◽  
1988 ◽  
Vol 233 (2) ◽  
pp. 233-238 ◽  
Author(s):  
Catherine M. Boustead ◽  
John H. Walker ◽  
Michael J. Geisow
Keyword(s):  
Binding Proteins ◽  
Phospholipid Binding ◽  
Calcium Dependent ◽  
Isolation And Characterization

scholarly journals Pathophysiology of the Antiphospholipid Antibody Syndrome

2021 ◽  
Author(s):  
David Green
Keyword(s):  
Antiphospholipid Syndrome ◽  
Binding Proteins ◽  
Membrane Receptors ◽  
Antiphospholipid Antibody ◽  
Antiphospholipid Antibody Syndrome ◽  
Clotting Factors ◽  
Anionic Phospholipid ◽  
Autoantibody Production ◽  
Phospholipid Binding ◽  
Glycoprotein I

The antiphospholipid syndrome is characterized by antibodies directed against phospholipid-binding proteins and phospholipids attached to cell membrane receptors, mitochondria, oxidized lipoproteins, and activated complement components. When antibodies bind to these complex antigens, cells are activated and the coagulation and complement cascades are triggered, culminating in thrombotic events and pregnancy morbidity that further define the syndrome. The phospholipid-binding proteins most often involved are annexins II and V, β2-glycoprotein I, prothrombin, and cardiolipin. A distinguishing feature of the antiphospholipid syndrome is the “lupus anticoagulant”. This is not a single entity but rather a family of antibodies directed against complex antigens consisting of β2-glycoprotein I and/or prothrombin bound to an anionic phospholipid. Although these antibodies prolong in vitro clotting times by competing with clotting factors for phospholipid binding sites, they are not associated with clinical bleeding. Rather, they are thrombogenic because they augment thrombin production in vivo by concentrating prothrombin on phospholipid surfaces. Other antiphospholipid antibodies decrease the clot-inhibitory properties of the endothelium and enhance platelet adherence and aggregation. Some are atherogenic because they increase lipid peroxidation by reducing paraoxonase activity, and others impair fetal nutrition by diminishing placental antithrombotic and fibrinolytic activity. This plethora of destructive autoantibodies is currently managed with immunomodulatory agents, but new approaches to treatment might include vaccines against specific autoantigens, blocking the antibodies generated by exposure to cytoplasmic DNA, and selective targeting of aberrant B-cells to reduce or eliminate autoantibody production.

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