Regulation and control of nitric oxide (NO) in macrophages: Protecting the "professional killer cell" from its own cytotoxic arsenal via MRP1 and GSTP1
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Regulation and control of nitric oxide (NO) in macrophages : Protecting the "professional killer cell" from its own cytotoxic arsenal via MRP1 and GSTP1. / Kovacevic, Zaklina; Sahni, Sumit; Lok, K.H.; Davies, M J; Wink, D A; Richardson, Des R.
In: B B A - Reviews on Cancer, Vol. 1861, No. 5 Pt A, 05.2017, p. 995-999.Research output: Contribution to journal › Review › Research › peer-review
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TY - JOUR
T1 - Regulation and control of nitric oxide (NO) in macrophages
T2 - Protecting the "professional killer cell" from its own cytotoxic arsenal via MRP1 and GSTP1
AU - Kovacevic, Zaklina
AU - Sahni, Sumit
AU - Lok, K.H.
AU - Davies, M J
AU - Wink, D A
AU - Richardson, Des R
N1 - Copyright © 2017 Elsevier B.V. All rights reserved.
PY - 2017/5
Y1 - 2017/5
N2 - We recently demonstrated that a novel storage and transport mechanism for nitric oxide (NO) mediated by glutathione-S-transferase P1 (GSTP1) and multidrug resistance protein 1 (MRP1/ABCC1), protects M1-macrophage (M1-MØ) models from large quantities of endogenous NO. This system stores and transports NO as dinitrosyl-dithiol-iron complexes (DNICs) composed of iron, NO and glutathione (GSH). Hence, this gas with contrasting anti- and pro-tumor effects, which has been assumed to be freely diffusible, is a tightly-regulated species in M1-MØs. These control systems prevent NO cytotoxicity and may be responsible for delivering cytotoxic NO as DNICs via MRP1 from M1-MØs, to tumor cell targets.
AB - We recently demonstrated that a novel storage and transport mechanism for nitric oxide (NO) mediated by glutathione-S-transferase P1 (GSTP1) and multidrug resistance protein 1 (MRP1/ABCC1), protects M1-macrophage (M1-MØ) models from large quantities of endogenous NO. This system stores and transports NO as dinitrosyl-dithiol-iron complexes (DNICs) composed of iron, NO and glutathione (GSH). Hence, this gas with contrasting anti- and pro-tumor effects, which has been assumed to be freely diffusible, is a tightly-regulated species in M1-MØs. These control systems prevent NO cytotoxicity and may be responsible for delivering cytotoxic NO as DNICs via MRP1 from M1-MØs, to tumor cell targets.
KW - Journal Article
KW - Review
U2 - 10.1016/j.bbagen.2017.02.021
DO - 10.1016/j.bbagen.2017.02.021
M3 - Review
C2 - 28219722
VL - 1861
SP - 995
EP - 999
JO - Biochimica et Biophysica Acta - Reviews on Cancer
JF - Biochimica et Biophysica Acta - Reviews on Cancer
SN - 0304-419X
IS - 5 Pt A
ER -
ID: 182331125