We are analyzing https://link.springer.com/article/10.1007/s00281-005-0004-1.

Title:
Emission of membrane vesicles: roles in complement resistance, immunity and cancer | Seminars in Immunopathology
Description:
Complement-mediated cell death is caused by C5b-9, the membrane attack complex (MAC) composed of the five complement proteins C5b, C6, C7, C8, and C9. Assembly of the C5b-9 complex initiates oligomerization of C9 and production of a transmembrane protein channel that inflicts damage to target cells. For protection, cells eliminate the MAC from their surface either by ectocytosis (direct emission of membrane vesicles) or by endocytosis (internalization). The process of ectosome release is rapid and involves cytosolic Ca2+ and activation of protein kinases, such as protein kinase C (PKC) and extracellular signal-regulated protein kinase (ERK). Recently, the involvement of mortalin (also known as GRP75 and mitochondrial hsp70) in MAC elimination has been suggested. Extracellular application of antibodies directed to mortalin increases cell sensitivity to MAC-mediated lysis. Release of membrane vesicles is ubiquitous and enhanced in apoptotic or tumor cells and upon cell activation. Composition of the ectosomes (also often referred to as microparticles) membrane proteins and lipids appears to be different from those of the original plasma membrane, indicating involvement of a selective sorting process during ectosome formation. Exosomes (unlike ectosomes) are membrane vesicles generated by endocytosis, endosome sorting into perinuclear multivesicular bodies (MVB) and exocytosis of MVBs. Exosomes appear to be different in size and composition from ectosomes. Exosome-associated MAC has also been described. Although research on ectosomes and exosomes is still limited, physiological roles in coagulation, vascular functions, angiogenesis, wound healing and development have been attributed to these shed membrane vesicles. On the other hand, there are indications that elevated levels of ectosomes and exosomes may predispose to morbidity. Membrane vesicles released by cells exposed to complement MAC may play roles in health and disease beyond protection from cell death.
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Keywords {🔍}

google, scholar, pubmed, cas, article, complement, membrane, immunol, cell, cells, vesicles, protein, attack, human, complex, cancer, exosomes, fishelson, kinase, lysis, microparticles, biol, terminal, res, complementmediated, activation, extracellular, blood, morgan, resistance, proteins, release, ectosomes, shin, exp, sublytic, function, protection, springer, gasser, death, mac, hsp, elimination, tumor, plasma, shed, released, access, cellular,

Topics {✒️}

formyl-methionyl-leucyl-phenylalanine gpi month download article/chapter glomerular epithelial cells rigid plasma-membrane-derived vesicles anti-hsp90 ribozyme reveals phosphatidylinositol 3-kinase/akt pathway t-cell signalling defects muller-eberhard hj terminal complement complex article springer seminars glycosyl-phosphatidylinositol-anchored proteins endogenous plasma-membrane proteins dendritic cell-derived exosomes mortalin/mthsp70/pbp74/grp75 antigen-presenting cell exosomes membrane attack complex complement c5b-9-induced shedding terminal complement complexes terminal complement intermediates full article pdf express prothrombinase activity mortalin/grp75 promotes release sublytic complement attack hsp90-dependent events membrane cofactor protein complement membrane attack heat shock proteins privacy choices/manage cookies complement-mediated lysis membrane-derived microparticles related subjects cleave human c3 cell-derived exosomes decay accelerating factor ecto-protein kinase complement-mediated killing sublytic c5b-9 complexes complement proteins c5b complement proteins c5b-9 protects cells predominantly de marco mc glycosyl-phosphatidylinositol grp75 plasma membrane injury humoral immune attack original plasma membrane intracellular free calcium transmembrane protein channel peptide binding protein protein import motor bohana-kashtan

Questions {❓}

Ahn YS, Jy W, Jimenez JJ et al (2004) More on: cellular microparticles: what are they bad or good for?
Freyssinet JM (2003) Cellular microparticles: what are they bad or good for?
Wadhwa R, Taira K, Kaul SC (2002) An Hsp70 family chaperone, mortalin/mthsp70/PBP74/Grp75: what, when, and where?

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         headline:Emission of membrane vesicles: roles in complement resistance, immunity and cancer
         description:Complement-mediated cell death is caused by C5b-9, the membrane attack complex (MAC) composed of the five complement proteins C5b, C6, C7, C8, and C9. Assembly of the C5b-9 complex initiates oligomerization of C9 and production of a transmembrane protein channel that inflicts damage to target cells. For protection, cells eliminate the MAC from their surface either by ectocytosis (direct emission of membrane vesicles) or by endocytosis (internalization). The process of ectosome release is rapid and involves cytosolic Ca2+ and activation of protein kinases, such as protein kinase C (PKC) and extracellular signal-regulated protein kinase (ERK). Recently, the involvement of mortalin (also known as GRP75 and mitochondrial hsp70) in MAC elimination has been suggested. Extracellular application of antibodies directed to mortalin increases cell sensitivity to MAC-mediated lysis. Release of membrane vesicles is ubiquitous and enhanced in apoptotic or tumor cells and upon cell activation. Composition of the ectosomes (also often referred to as microparticles) membrane proteins and lipids appears to be different from those of the original plasma membrane, indicating involvement of a selective sorting process during ectosome formation. Exosomes (unlike ectosomes) are membrane vesicles generated by endocytosis, endosome sorting into perinuclear multivesicular bodies (MVB) and exocytosis of MVBs. Exosomes appear to be different in size and composition from ectosomes. Exosome-associated MAC has also been described. Although research on ectosomes and exosomes is still limited, physiological roles in coagulation, vascular functions, angiogenesis, wound healing and development have been attributed to these shed membrane vesicles. On the other hand, there are indications that elevated levels of ectosomes and exosomes may predispose to morbidity. Membrane vesicles released by cells exposed to complement MAC may play roles in health and disease beyond protection from cell death.
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      description:Complement-mediated cell death is caused by C5b-9, the membrane attack complex (MAC) composed of the five complement proteins C5b, C6, C7, C8, and C9. Assembly of the C5b-9 complex initiates oligomerization of C9 and production of a transmembrane protein channel that inflicts damage to target cells. For protection, cells eliminate the MAC from their surface either by ectocytosis (direct emission of membrane vesicles) or by endocytosis (internalization). The process of ectosome release is rapid and involves cytosolic Ca2+ and activation of protein kinases, such as protein kinase C (PKC) and extracellular signal-regulated protein kinase (ERK). Recently, the involvement of mortalin (also known as GRP75 and mitochondrial hsp70) in MAC elimination has been suggested. Extracellular application of antibodies directed to mortalin increases cell sensitivity to MAC-mediated lysis. Release of membrane vesicles is ubiquitous and enhanced in apoptotic or tumor cells and upon cell activation. Composition of the ectosomes (also often referred to as microparticles) membrane proteins and lipids appears to be different from those of the original plasma membrane, indicating involvement of a selective sorting process during ectosome formation. Exosomes (unlike ectosomes) are membrane vesicles generated by endocytosis, endosome sorting into perinuclear multivesicular bodies (MVB) and exocytosis of MVBs. Exosomes appear to be different in size and composition from ectosomes. Exosome-associated MAC has also been described. Although research on ectosomes and exosomes is still limited, physiological roles in coagulation, vascular functions, angiogenesis, wound healing and development have been attributed to these shed membrane vesicles. On the other hand, there are indications that elevated levels of ectosomes and exosomes may predispose to morbidity. Membrane vesicles released by cells exposed to complement MAC may play roles in health and disease beyond protection from cell death.
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