Protein phosphorylation as a mechanism of resistance against complement damage

Z Fishelson; E Kopf; Y Paas; L Ross; Y Reiter

Protein phosphorylation as a mechanism of resistance against complement damage

Z Fishelson, E Kopf, Y Paas, L Ross, Y Reiter

The Mina and Everard Goodman Faculty of Life Sciences

Research output: Chapter in Book/Report/Conference proceeding › Chapter › peer-review

Abstract

Complement inflicts cell damage by insertion of a membrane attack complex (MAC) comprised of the C5b, C6, C7, C8 and C9 proteins into the plasma membrane of target cells (Muller-Eberhard 1986). Nucleated cells vary in their sensitivity to complement-mediated lysis, however, generally, they are more resistant to immune damage than erythrocytes (Koski et al. 1983). It has been suggested that this resistance of nucleated cells is due to a postulated capacity of the cells to actively resist and repair complement damage (Ohanian and Schlager 1981). Recently, a Ca2+-dependent process of rapid MAC removal from the surface of nucleated cells has been suggested to be involved (Carney et al. 1986; Morgan et al. 1987). Yet, the cellular regulatory mechanisms which support these and other postulated resistance/repair processes are poorly characterized.

Original language	American English
Title of host publication	Progress in Immunology
Editors	Fritz Melchers, E. D. Albert, H. von Boehmer, M. P. Dierich, L. Du Pasquier, K. Eichmann, D. Gemsa, O. Götze, J. R. Kalden, S. H. E. Kaufmann, H. Kirchner, K. Resch, G. Riethmüller, A. Schimpl, C. Sorg, M. Steinmetz, H. Wagner, H. G. Zachau
Publisher	Springer Berlin Heidelberg
Pages	205-208
ISBN (Print)	978-3-642-83755-5
State	Published - 1989

Cite this

Fishelson, Z., Kopf, E., Paas, Y., Ross, L., & Reiter, Y. (1989). Protein phosphorylation as a mechanism of resistance against complement damage. In F. Melchers, E. D. Albert, H. von Boehmer, M. P. Dierich, L. Du Pasquier, K. Eichmann, D. Gemsa, O. Götze, J. R. Kalden, S. H. E. Kaufmann, H. Kirchner, K. Resch, G. Riethmüller, A. Schimpl, C. Sorg, M. Steinmetz, H. Wagner, & H. G. Zachau (Eds.), Progress in Immunology (pp. 205-208). Springer Berlin Heidelberg.

Fishelson, Z ; Kopf, E ; Paas, Y et al. / Protein phosphorylation as a mechanism of resistance against complement damage. Progress in Immunology. editor / Fritz Melchers ; E. D. Albert ; H. von Boehmer ; M. P. Dierich ; L. Du Pasquier ; K. Eichmann ; D. Gemsa ; O. Götze ; J. R. Kalden ; S. H. E. Kaufmann ; H. Kirchner ; K. Resch ; G. Riethmüller ; A. Schimpl ; C. Sorg ; M. Steinmetz ; H. Wagner ; H. G. Zachau. Springer Berlin Heidelberg, 1989. pp. 205-208

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abstract = "Complement inflicts cell damage by insertion of a membrane attack complex (MAC) comprised of the C5b, C6, C7, C8 and C9 proteins into the plasma membrane of target cells (Muller-Eberhard 1986). Nucleated cells vary in their sensitivity to complement-mediated lysis, however, generally, they are more resistant to immune damage than erythrocytes (Koski et al. 1983). It has been suggested that this resistance of nucleated cells is due to a postulated capacity of the cells to actively resist and repair complement damage (Ohanian and Schlager 1981). Recently, a Ca2+-dependent process of rapid MAC removal from the surface of nucleated cells has been suggested to be involved (Carney et al. 1986; Morgan et al. 1987). Yet, the cellular regulatory mechanisms which support these and other postulated resistance/repair processes are poorly characterized.",

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editor = "Fritz Melchers and {D. Albert}, E. and {von Boehmer}, H. and {P. Dierich}, M. and {Du Pasquier}, L. and K. Eichmann and D. Gemsa and O. G{\"o}tze and {R. Kalden}, J. and {H. E. Kaufmann}, S. and H. Kirchner and K. Resch and G. Riethm{\"u}ller and A. Schimpl and C. Sorg and M. Steinmetz and H. Wagner and {G. Zachau}, H.",

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Fishelson, Z, Kopf, E, Paas, Y, Ross, L & Reiter, Y 1989, Protein phosphorylation as a mechanism of resistance against complement damage. in F Melchers, E D. Albert, H von Boehmer, M P. Dierich, L Du Pasquier, K Eichmann, D Gemsa, O Götze, J R. Kalden, S H. E. Kaufmann, H Kirchner, K Resch, G Riethmüller, A Schimpl, C Sorg, M Steinmetz, H Wagner & H G. Zachau (eds), Progress in Immunology. Springer Berlin Heidelberg, pp. 205-208.

Protein phosphorylation as a mechanism of resistance against complement damage. / Fishelson, Z; Kopf, E; Paas, Y et al.
Progress in Immunology. ed. / Fritz Melchers; E. D. Albert; H. von Boehmer; M. P. Dierich; L. Du Pasquier; K. Eichmann; D. Gemsa; O. Götze; J. R. Kalden; S. H. E. Kaufmann; H. Kirchner; K. Resch; G. Riethmüller; A. Schimpl; C. Sorg; M. Steinmetz; H. Wagner; H. G. Zachau. Springer Berlin Heidelberg, 1989. p. 205-208.

Research output: Chapter in Book/Report/Conference proceeding › Chapter › peer-review

TY - CHAP

T1 - Protein phosphorylation as a mechanism of resistance against complement damage

AU - Fishelson, Z

AU - Kopf, E

AU - Paas, Y

AU - Ross, L

AU - Reiter, Y

PY - 1989

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N2 - Complement inflicts cell damage by insertion of a membrane attack complex (MAC) comprised of the C5b, C6, C7, C8 and C9 proteins into the plasma membrane of target cells (Muller-Eberhard 1986). Nucleated cells vary in their sensitivity to complement-mediated lysis, however, generally, they are more resistant to immune damage than erythrocytes (Koski et al. 1983). It has been suggested that this resistance of nucleated cells is due to a postulated capacity of the cells to actively resist and repair complement damage (Ohanian and Schlager 1981). Recently, a Ca2+-dependent process of rapid MAC removal from the surface of nucleated cells has been suggested to be involved (Carney et al. 1986; Morgan et al. 1987). Yet, the cellular regulatory mechanisms which support these and other postulated resistance/repair processes are poorly characterized.

AB - Complement inflicts cell damage by insertion of a membrane attack complex (MAC) comprised of the C5b, C6, C7, C8 and C9 proteins into the plasma membrane of target cells (Muller-Eberhard 1986). Nucleated cells vary in their sensitivity to complement-mediated lysis, however, generally, they are more resistant to immune damage than erythrocytes (Koski et al. 1983). It has been suggested that this resistance of nucleated cells is due to a postulated capacity of the cells to actively resist and repair complement damage (Ohanian and Schlager 1981). Recently, a Ca2+-dependent process of rapid MAC removal from the surface of nucleated cells has been suggested to be involved (Carney et al. 1986; Morgan et al. 1987). Yet, the cellular regulatory mechanisms which support these and other postulated resistance/repair processes are poorly characterized.

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M3 - Chapter

SN - 978-3-642-83755-5

SP - 205

EP - 208

BT - Progress in Immunology

A2 - Melchers, Fritz

A2 - D. Albert, E.

A2 - von Boehmer, H.

A2 - P. Dierich, M.

A2 - Du Pasquier, L.

A2 - Eichmann, K.

A2 - Gemsa, D.

A2 - Götze, O.

A2 - R. Kalden, J.

A2 - H. E. Kaufmann, S.

A2 - Kirchner, H.

A2 - Resch, K.

A2 - Riethmüller, G.

A2 - Schimpl, A.

A2 - Sorg, C.

A2 - Steinmetz, M.

A2 - Wagner, H.

A2 - G. Zachau, H.

PB - Springer Berlin Heidelberg

ER -

Fishelson Z, Kopf E, Paas Y, Ross L, Reiter Y. Protein phosphorylation as a mechanism of resistance against complement damage. In Melchers F, D. Albert E, von Boehmer H, P. Dierich M, Du Pasquier L, Eichmann K, Gemsa D, Götze O, R. Kalden J, H. E. Kaufmann S, Kirchner H, Resch K, Riethmüller G, Schimpl A, Sorg C, Steinmetz M, Wagner H, G. Zachau H, editors, Progress in Immunology. Springer Berlin Heidelberg. 1989. p. 205-208

Protein phosphorylation as a mechanism of resistance against complement damage

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