HIV‐1 Tat potentiates TNF‐induced NF‐kappa B activation and cytotoxicity by altering the cellular redox state.

Abstract This study demonstrates that human immunodeficiency virus type 1 (HIV‐1) Tat protein amplifies the activity of tumor necrosis factor (TNF), a cytokine that stimulates HIV‐1 replication through activation of NF‐kappa B. In HeLa cells stably transfected with the HIV‐1 tat gene (HeLa‐tat cells...
Ausführliche Beschreibung

Gespeichert in:

Autor*in:	Westendorp, M.O. [verfasserIn] Shatrov, V.A. [verfasserIn] Schulze‐Osthoff, K. [verfasserIn] Frank, R. [verfasserIn] Kraft, M. [verfasserIn] Los, M. [verfasserIn] Krammer, P.H. [verfasserIn] Dröge, W. [verfasserIn] Lehmann, V. [verfasserIn]

Format:	E-Artikel
Sprache:	Englisch

Erschienen:	1995

Anmerkung:	© European Molecular Biology Organization 1995

Übergeordnetes Werk:	Enthalten in: The EMBO Journal - Nature Publishing Group UK, 2023, 14(1995), 3 vom: 01. Feb., Seite 546-554
Übergeordnetes Werk:	volume:14 ; year:1995 ; number:3 ; day:01 ; month:02 ; pages:546-554

Links:	Volltext

DOI / URN:	10.1002/j.1460-2075.1995.tb07030.x

Katalog-ID:	SPR05761122X

Internformat


LEADER	01000naa a22002652 4500
001	SPR05761122X
003	DE-627
005	20241001065502.0
007	cr uuu---uuuuu
008	241001s1995 xx \|\|\|\|\|o 00\| \|\|eng c
024	7		\|a 10.1002/j.1460-2075.1995.tb07030.x \|2 doi
035			\|a (DE-627)SPR05761122X
035			\|a (SPR)j.1460-2075.1995.tb07030.x-e
040			\|a DE-627 \|b ger \|c DE-627 \|e rakwb
041			\|a eng
100	1		\|a Westendorp, M.O. \|e verfasserin \|4 aut
245	1	0	\|a HIV‐1 Tat potentiates TNF‐induced NF‐kappa B activation and cytotoxicity by altering the cellular redox state.
264		1	\|c 1995
336			\|a Text \|b txt \|2 rdacontent
337			\|a Computermedien \|b c \|2 rdamedia
338			\|a Online-Ressource \|b cr \|2 rdacarrier
500			\|a © European Molecular Biology Organization 1995
520			\|a Abstract This study demonstrates that human immunodeficiency virus type 1 (HIV‐1) Tat protein amplifies the activity of tumor necrosis factor (TNF), a cytokine that stimulates HIV‐1 replication through activation of NF‐kappa B. In HeLa cells stably transfected with the HIV‐1 tat gene (HeLa‐tat cells), expression of the Tat protein enhanced both TNF‐induced activation of NF‐kappa B and TNF‐mediated cytotoxicity. A similar potentiation of TNF effects was observed in Jurkat T cells and HeLa cells treated with soluble Tat protein. TNF‐mediated activation of NF‐kappa B and cytotoxicity involves the intracellular formation of reactive oxygen intermediates. Therefore, Tat‐mediated effects on the cellular redox state were analyzed. In both T cells and HeLa cells HIV‐1 Tat suppressed the expression of Mn‐dependent superoxide dismutase (Mn‐SOD), a mitochondrial enzyme that is part of the cellular defense system against oxidative stress. Thus, Mn‐SOD RNA protein levels and activity were markedly reduced in the presence of Tat. Decreased Mn‐SOD expression was associated with decreased levels of glutathione and a lower ratio of reduced:oxidized glutathione. A truncated Tat protein (Tat1‐72), known to transactivate the HIV‐1 long terminal repeat (LTR), no longer affected Mn‐SOD expression, the cellular redox state or TNF‐mediated cytotoxicity. Thus, our experiments demonstrate that the C‐terminal region of HIV‐1 Tat is required to suppress Mn‐SOD expression and to induce pro‐oxidative conditions reflected by a drop in reduced glutathione (GSH) and the GSH:oxidized GSH (GSSG) ratio.(ABSTRACT TRUNCATED AT 250 WORDS)
700	1		\|a Shatrov, V.A. \|e verfasserin \|4 aut
700	1		\|a Schulze‐Osthoff, K. \|e verfasserin \|4 aut
700	1		\|a Frank, R. \|e verfasserin \|4 aut
700	1		\|a Kraft, M. \|e verfasserin \|4 aut
700	1		\|a Los, M. \|e verfasserin \|4 aut
700	1		\|a Krammer, P.H. \|e verfasserin \|4 aut
700	1		\|a Dröge, W. \|e verfasserin \|4 aut
700	1		\|a Lehmann, V. \|e verfasserin \|4 aut
773	0	8	\|i Enthalten in \|t The EMBO Journal \|d Nature Publishing Group UK, 2023 \|g 14(1995), 3 vom: 01. Feb., Seite 546-554 \|w (DE-627)266022529 \|w (DE-600)1467419-1 \|x 1460-2075 \|7 nnns
773	1	8	\|g volume:14 \|g year:1995 \|g number:3 \|g day:01 \|g month:02 \|g pages:546-554
856	4	0	\|u https://dx.doi.org/10.1002/j.1460-2075.1995.tb07030.x \|m X:SPRINGER \|x Resolving-System \|z lizenzpflichtig \|3 Volltext
912			\|a SYSFLAG_0
912			\|a GBV_SPRINGER
912			\|a GBV_ILN_20
912			\|a GBV_ILN_22
912			\|a GBV_ILN_23
912			\|a GBV_ILN_24
912			\|a GBV_ILN_31
912			\|a GBV_ILN_39
912			\|a GBV_ILN_40
912			\|a GBV_ILN_62
912			\|a GBV_ILN_63
912			\|a GBV_ILN_65
912			\|a GBV_ILN_69
912			\|a GBV_ILN_70
912			\|a GBV_ILN_72
912			\|a GBV_ILN_73
912			\|a GBV_ILN_74
912			\|a GBV_ILN_95
912			\|a GBV_ILN_105
912			\|a GBV_ILN_110
912			\|a GBV_ILN_151
912			\|a GBV_ILN_161
912			\|a GBV_ILN_170
912			\|a GBV_ILN_213
912			\|a GBV_ILN_230
912			\|a GBV_ILN_252
912			\|a GBV_ILN_285
912			\|a GBV_ILN_293
912			\|a GBV_ILN_602
912			\|a GBV_ILN_2014
912			\|a GBV_ILN_2021
912			\|a GBV_ILN_2050
912			\|a GBV_ILN_4012
912			\|a GBV_ILN_4037
912			\|a GBV_ILN_4112
912			\|a GBV_ILN_4125
912			\|a GBV_ILN_4126
912			\|a GBV_ILN_4249
912			\|a GBV_ILN_4305
912			\|a GBV_ILN_4306
912			\|a GBV_ILN_4307
912			\|a GBV_ILN_4313
912			\|a GBV_ILN_4322
912			\|a GBV_ILN_4323
912			\|a GBV_ILN_4324
912			\|a GBV_ILN_4325
912			\|a GBV_ILN_4338
912			\|a GBV_ILN_4367
912			\|a GBV_ILN_4700
951			\|a AR
952			\|d 14 \|j 1995 \|e 3 \|b 01 \|c 02 \|h 546-554

Indexfelder

author_variant	m w mw v s vs k s ks r f rf m k mk m l ml p k pk w d wd v l vl
matchkey_str	article:14602075:1995----::i1aptnitsnidcdfapbciainncttxctbatr
hierarchy_sort_str	1995
publishDate	1995
allfields	10.1002/j.1460-2075.1995.tb07030.x doi (DE-627)SPR05761122X (SPR)j.1460-2075.1995.tb07030.x-e DE-627 ger DE-627 rakwb eng Westendorp, M.O. verfasserin aut HIV‐1 Tat potentiates TNF‐induced NF‐kappa B activation and cytotoxicity by altering the cellular redox state. 1995 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier © European Molecular Biology Organization 1995 Abstract This study demonstrates that human immunodeficiency virus type 1 (HIV‐1) Tat protein amplifies the activity of tumor necrosis factor (TNF), a cytokine that stimulates HIV‐1 replication through activation of NF‐kappa B. In HeLa cells stably transfected with the HIV‐1 tat gene (HeLa‐tat cells), expression of the Tat protein enhanced both TNF‐induced activation of NF‐kappa B and TNF‐mediated cytotoxicity. A similar potentiation of TNF effects was observed in Jurkat T cells and HeLa cells treated with soluble Tat protein. TNF‐mediated activation of NF‐kappa B and cytotoxicity involves the intracellular formation of reactive oxygen intermediates. Therefore, Tat‐mediated effects on the cellular redox state were analyzed. In both T cells and HeLa cells HIV‐1 Tat suppressed the expression of Mn‐dependent superoxide dismutase (Mn‐SOD), a mitochondrial enzyme that is part of the cellular defense system against oxidative stress. Thus, Mn‐SOD RNA protein levels and activity were markedly reduced in the presence of Tat. Decreased Mn‐SOD expression was associated with decreased levels of glutathione and a lower ratio of reduced:oxidized glutathione. A truncated Tat protein (Tat1‐72), known to transactivate the HIV‐1 long terminal repeat (LTR), no longer affected Mn‐SOD expression, the cellular redox state or TNF‐mediated cytotoxicity. Thus, our experiments demonstrate that the C‐terminal region of HIV‐1 Tat is required to suppress Mn‐SOD expression and to induce pro‐oxidative conditions reflected by a drop in reduced glutathione (GSH) and the GSH:oxidized GSH (GSSG) ratio.(ABSTRACT TRUNCATED AT 250 WORDS) Shatrov, V.A. verfasserin aut Schulze‐Osthoff, K. verfasserin aut Frank, R. verfasserin aut Kraft, M. verfasserin aut Los, M. verfasserin aut Krammer, P.H. verfasserin aut Dröge, W. verfasserin aut Lehmann, V. verfasserin aut Enthalten in The EMBO Journal Nature Publishing Group UK, 2023 14(1995), 3 vom: 01. Feb., Seite 546-554 (DE-627)266022529 (DE-600)1467419-1 1460-2075 nnns volume:14 year:1995 number:3 day:01 month:02 pages:546-554 https://dx.doi.org/10.1002/j.1460-2075.1995.tb07030.x X:SPRINGER Resolving-System lizenzpflichtig Volltext SYSFLAG_0 GBV_SPRINGER GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_39 GBV_ILN_40 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_70 GBV_ILN_72 GBV_ILN_73 GBV_ILN_74 GBV_ILN_95 GBV_ILN_105 GBV_ILN_110 GBV_ILN_151 GBV_ILN_161 GBV_ILN_170 GBV_ILN_213 GBV_ILN_230 GBV_ILN_252 GBV_ILN_285 GBV_ILN_293 GBV_ILN_602 GBV_ILN_2014 GBV_ILN_2021 GBV_ILN_2050 GBV_ILN_4012 GBV_ILN_4037 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4249 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4338 GBV_ILN_4367 GBV_ILN_4700 AR 14 1995 3 01 02 546-554
spelling	10.1002/j.1460-2075.1995.tb07030.x doi (DE-627)SPR05761122X (SPR)j.1460-2075.1995.tb07030.x-e DE-627 ger DE-627 rakwb eng Westendorp, M.O. verfasserin aut HIV‐1 Tat potentiates TNF‐induced NF‐kappa B activation and cytotoxicity by altering the cellular redox state. 1995 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier © European Molecular Biology Organization 1995 Abstract This study demonstrates that human immunodeficiency virus type 1 (HIV‐1) Tat protein amplifies the activity of tumor necrosis factor (TNF), a cytokine that stimulates HIV‐1 replication through activation of NF‐kappa B. In HeLa cells stably transfected with the HIV‐1 tat gene (HeLa‐tat cells), expression of the Tat protein enhanced both TNF‐induced activation of NF‐kappa B and TNF‐mediated cytotoxicity. A similar potentiation of TNF effects was observed in Jurkat T cells and HeLa cells treated with soluble Tat protein. TNF‐mediated activation of NF‐kappa B and cytotoxicity involves the intracellular formation of reactive oxygen intermediates. Therefore, Tat‐mediated effects on the cellular redox state were analyzed. In both T cells and HeLa cells HIV‐1 Tat suppressed the expression of Mn‐dependent superoxide dismutase (Mn‐SOD), a mitochondrial enzyme that is part of the cellular defense system against oxidative stress. Thus, Mn‐SOD RNA protein levels and activity were markedly reduced in the presence of Tat. Decreased Mn‐SOD expression was associated with decreased levels of glutathione and a lower ratio of reduced:oxidized glutathione. A truncated Tat protein (Tat1‐72), known to transactivate the HIV‐1 long terminal repeat (LTR), no longer affected Mn‐SOD expression, the cellular redox state or TNF‐mediated cytotoxicity. Thus, our experiments demonstrate that the C‐terminal region of HIV‐1 Tat is required to suppress Mn‐SOD expression and to induce pro‐oxidative conditions reflected by a drop in reduced glutathione (GSH) and the GSH:oxidized GSH (GSSG) ratio.(ABSTRACT TRUNCATED AT 250 WORDS) Shatrov, V.A. verfasserin aut Schulze‐Osthoff, K. verfasserin aut Frank, R. verfasserin aut Kraft, M. verfasserin aut Los, M. verfasserin aut Krammer, P.H. verfasserin aut Dröge, W. verfasserin aut Lehmann, V. verfasserin aut Enthalten in The EMBO Journal Nature Publishing Group UK, 2023 14(1995), 3 vom: 01. Feb., Seite 546-554 (DE-627)266022529 (DE-600)1467419-1 1460-2075 nnns volume:14 year:1995 number:3 day:01 month:02 pages:546-554 https://dx.doi.org/10.1002/j.1460-2075.1995.tb07030.x X:SPRINGER Resolving-System lizenzpflichtig Volltext SYSFLAG_0 GBV_SPRINGER GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_39 GBV_ILN_40 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_70 GBV_ILN_72 GBV_ILN_73 GBV_ILN_74 GBV_ILN_95 GBV_ILN_105 GBV_ILN_110 GBV_ILN_151 GBV_ILN_161 GBV_ILN_170 GBV_ILN_213 GBV_ILN_230 GBV_ILN_252 GBV_ILN_285 GBV_ILN_293 GBV_ILN_602 GBV_ILN_2014 GBV_ILN_2021 GBV_ILN_2050 GBV_ILN_4012 GBV_ILN_4037 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4249 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4338 GBV_ILN_4367 GBV_ILN_4700 AR 14 1995 3 01 02 546-554
allfields_unstemmed	10.1002/j.1460-2075.1995.tb07030.x doi (DE-627)SPR05761122X (SPR)j.1460-2075.1995.tb07030.x-e DE-627 ger DE-627 rakwb eng Westendorp, M.O. verfasserin aut HIV‐1 Tat potentiates TNF‐induced NF‐kappa B activation and cytotoxicity by altering the cellular redox state. 1995 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier © European Molecular Biology Organization 1995 Abstract This study demonstrates that human immunodeficiency virus type 1 (HIV‐1) Tat protein amplifies the activity of tumor necrosis factor (TNF), a cytokine that stimulates HIV‐1 replication through activation of NF‐kappa B. In HeLa cells stably transfected with the HIV‐1 tat gene (HeLa‐tat cells), expression of the Tat protein enhanced both TNF‐induced activation of NF‐kappa B and TNF‐mediated cytotoxicity. A similar potentiation of TNF effects was observed in Jurkat T cells and HeLa cells treated with soluble Tat protein. TNF‐mediated activation of NF‐kappa B and cytotoxicity involves the intracellular formation of reactive oxygen intermediates. Therefore, Tat‐mediated effects on the cellular redox state were analyzed. In both T cells and HeLa cells HIV‐1 Tat suppressed the expression of Mn‐dependent superoxide dismutase (Mn‐SOD), a mitochondrial enzyme that is part of the cellular defense system against oxidative stress. Thus, Mn‐SOD RNA protein levels and activity were markedly reduced in the presence of Tat. Decreased Mn‐SOD expression was associated with decreased levels of glutathione and a lower ratio of reduced:oxidized glutathione. A truncated Tat protein (Tat1‐72), known to transactivate the HIV‐1 long terminal repeat (LTR), no longer affected Mn‐SOD expression, the cellular redox state or TNF‐mediated cytotoxicity. Thus, our experiments demonstrate that the C‐terminal region of HIV‐1 Tat is required to suppress Mn‐SOD expression and to induce pro‐oxidative conditions reflected by a drop in reduced glutathione (GSH) and the GSH:oxidized GSH (GSSG) ratio.(ABSTRACT TRUNCATED AT 250 WORDS) Shatrov, V.A. verfasserin aut Schulze‐Osthoff, K. verfasserin aut Frank, R. verfasserin aut Kraft, M. verfasserin aut Los, M. verfasserin aut Krammer, P.H. verfasserin aut Dröge, W. verfasserin aut Lehmann, V. verfasserin aut Enthalten in The EMBO Journal Nature Publishing Group UK, 2023 14(1995), 3 vom: 01. Feb., Seite 546-554 (DE-627)266022529 (DE-600)1467419-1 1460-2075 nnns volume:14 year:1995 number:3 day:01 month:02 pages:546-554 https://dx.doi.org/10.1002/j.1460-2075.1995.tb07030.x X:SPRINGER Resolving-System lizenzpflichtig Volltext SYSFLAG_0 GBV_SPRINGER GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_39 GBV_ILN_40 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_70 GBV_ILN_72 GBV_ILN_73 GBV_ILN_74 GBV_ILN_95 GBV_ILN_105 GBV_ILN_110 GBV_ILN_151 GBV_ILN_161 GBV_ILN_170 GBV_ILN_213 GBV_ILN_230 GBV_ILN_252 GBV_ILN_285 GBV_ILN_293 GBV_ILN_602 GBV_ILN_2014 GBV_ILN_2021 GBV_ILN_2050 GBV_ILN_4012 GBV_ILN_4037 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4249 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4338 GBV_ILN_4367 GBV_ILN_4700 AR 14 1995 3 01 02 546-554
allfieldsGer	10.1002/j.1460-2075.1995.tb07030.x doi (DE-627)SPR05761122X (SPR)j.1460-2075.1995.tb07030.x-e DE-627 ger DE-627 rakwb eng Westendorp, M.O. verfasserin aut HIV‐1 Tat potentiates TNF‐induced NF‐kappa B activation and cytotoxicity by altering the cellular redox state. 1995 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier © European Molecular Biology Organization 1995 Abstract This study demonstrates that human immunodeficiency virus type 1 (HIV‐1) Tat protein amplifies the activity of tumor necrosis factor (TNF), a cytokine that stimulates HIV‐1 replication through activation of NF‐kappa B. In HeLa cells stably transfected with the HIV‐1 tat gene (HeLa‐tat cells), expression of the Tat protein enhanced both TNF‐induced activation of NF‐kappa B and TNF‐mediated cytotoxicity. A similar potentiation of TNF effects was observed in Jurkat T cells and HeLa cells treated with soluble Tat protein. TNF‐mediated activation of NF‐kappa B and cytotoxicity involves the intracellular formation of reactive oxygen intermediates. Therefore, Tat‐mediated effects on the cellular redox state were analyzed. In both T cells and HeLa cells HIV‐1 Tat suppressed the expression of Mn‐dependent superoxide dismutase (Mn‐SOD), a mitochondrial enzyme that is part of the cellular defense system against oxidative stress. Thus, Mn‐SOD RNA protein levels and activity were markedly reduced in the presence of Tat. Decreased Mn‐SOD expression was associated with decreased levels of glutathione and a lower ratio of reduced:oxidized glutathione. A truncated Tat protein (Tat1‐72), known to transactivate the HIV‐1 long terminal repeat (LTR), no longer affected Mn‐SOD expression, the cellular redox state or TNF‐mediated cytotoxicity. Thus, our experiments demonstrate that the C‐terminal region of HIV‐1 Tat is required to suppress Mn‐SOD expression and to induce pro‐oxidative conditions reflected by a drop in reduced glutathione (GSH) and the GSH:oxidized GSH (GSSG) ratio.(ABSTRACT TRUNCATED AT 250 WORDS) Shatrov, V.A. verfasserin aut Schulze‐Osthoff, K. verfasserin aut Frank, R. verfasserin aut Kraft, M. verfasserin aut Los, M. verfasserin aut Krammer, P.H. verfasserin aut Dröge, W. verfasserin aut Lehmann, V. verfasserin aut Enthalten in The EMBO Journal Nature Publishing Group UK, 2023 14(1995), 3 vom: 01. Feb., Seite 546-554 (DE-627)266022529 (DE-600)1467419-1 1460-2075 nnns volume:14 year:1995 number:3 day:01 month:02 pages:546-554 https://dx.doi.org/10.1002/j.1460-2075.1995.tb07030.x X:SPRINGER Resolving-System lizenzpflichtig Volltext SYSFLAG_0 GBV_SPRINGER GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_39 GBV_ILN_40 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_70 GBV_ILN_72 GBV_ILN_73 GBV_ILN_74 GBV_ILN_95 GBV_ILN_105 GBV_ILN_110 GBV_ILN_151 GBV_ILN_161 GBV_ILN_170 GBV_ILN_213 GBV_ILN_230 GBV_ILN_252 GBV_ILN_285 GBV_ILN_293 GBV_ILN_602 GBV_ILN_2014 GBV_ILN_2021 GBV_ILN_2050 GBV_ILN_4012 GBV_ILN_4037 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4249 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4338 GBV_ILN_4367 GBV_ILN_4700 AR 14 1995 3 01 02 546-554
allfieldsSound	10.1002/j.1460-2075.1995.tb07030.x doi (DE-627)SPR05761122X (SPR)j.1460-2075.1995.tb07030.x-e DE-627 ger DE-627 rakwb eng Westendorp, M.O. verfasserin aut HIV‐1 Tat potentiates TNF‐induced NF‐kappa B activation and cytotoxicity by altering the cellular redox state. 1995 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier © European Molecular Biology Organization 1995 Abstract This study demonstrates that human immunodeficiency virus type 1 (HIV‐1) Tat protein amplifies the activity of tumor necrosis factor (TNF), a cytokine that stimulates HIV‐1 replication through activation of NF‐kappa B. In HeLa cells stably transfected with the HIV‐1 tat gene (HeLa‐tat cells), expression of the Tat protein enhanced both TNF‐induced activation of NF‐kappa B and TNF‐mediated cytotoxicity. A similar potentiation of TNF effects was observed in Jurkat T cells and HeLa cells treated with soluble Tat protein. TNF‐mediated activation of NF‐kappa B and cytotoxicity involves the intracellular formation of reactive oxygen intermediates. Therefore, Tat‐mediated effects on the cellular redox state were analyzed. In both T cells and HeLa cells HIV‐1 Tat suppressed the expression of Mn‐dependent superoxide dismutase (Mn‐SOD), a mitochondrial enzyme that is part of the cellular defense system against oxidative stress. Thus, Mn‐SOD RNA protein levels and activity were markedly reduced in the presence of Tat. Decreased Mn‐SOD expression was associated with decreased levels of glutathione and a lower ratio of reduced:oxidized glutathione. A truncated Tat protein (Tat1‐72), known to transactivate the HIV‐1 long terminal repeat (LTR), no longer affected Mn‐SOD expression, the cellular redox state or TNF‐mediated cytotoxicity. Thus, our experiments demonstrate that the C‐terminal region of HIV‐1 Tat is required to suppress Mn‐SOD expression and to induce pro‐oxidative conditions reflected by a drop in reduced glutathione (GSH) and the GSH:oxidized GSH (GSSG) ratio.(ABSTRACT TRUNCATED AT 250 WORDS) Shatrov, V.A. verfasserin aut Schulze‐Osthoff, K. verfasserin aut Frank, R. verfasserin aut Kraft, M. verfasserin aut Los, M. verfasserin aut Krammer, P.H. verfasserin aut Dröge, W. verfasserin aut Lehmann, V. verfasserin aut Enthalten in The EMBO Journal Nature Publishing Group UK, 2023 14(1995), 3 vom: 01. Feb., Seite 546-554 (DE-627)266022529 (DE-600)1467419-1 1460-2075 nnns volume:14 year:1995 number:3 day:01 month:02 pages:546-554 https://dx.doi.org/10.1002/j.1460-2075.1995.tb07030.x X:SPRINGER Resolving-System lizenzpflichtig Volltext SYSFLAG_0 GBV_SPRINGER GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_39 GBV_ILN_40 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_70 GBV_ILN_72 GBV_ILN_73 GBV_ILN_74 GBV_ILN_95 GBV_ILN_105 GBV_ILN_110 GBV_ILN_151 GBV_ILN_161 GBV_ILN_170 GBV_ILN_213 GBV_ILN_230 GBV_ILN_252 GBV_ILN_285 GBV_ILN_293 GBV_ILN_602 GBV_ILN_2014 GBV_ILN_2021 GBV_ILN_2050 GBV_ILN_4012 GBV_ILN_4037 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4249 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4338 GBV_ILN_4367 GBV_ILN_4700 AR 14 1995 3 01 02 546-554
language	English
source	Enthalten in The EMBO Journal 14(1995), 3 vom: 01. Feb., Seite 546-554 volume:14 year:1995 number:3 day:01 month:02 pages:546-554
sourceStr	Enthalten in The EMBO Journal 14(1995), 3 vom: 01. Feb., Seite 546-554 volume:14 year:1995 number:3 day:01 month:02 pages:546-554
format_phy_str_mv	Article
institution	findex.gbv.de
isfreeaccess_bool	false
container_title	The EMBO Journal
authorswithroles_txt_mv	Westendorp, M.O. @@aut@@ Shatrov, V.A. @@aut@@ Schulze‐Osthoff, K. @@aut@@ Frank, R. @@aut@@ Kraft, M. @@aut@@ Los, M. @@aut@@ Krammer, P.H. @@aut@@ Dröge, W. @@aut@@ Lehmann, V. @@aut@@
publishDateDaySort_date	1995-02-01T00:00:00Z
hierarchy_top_id	266022529
id	SPR05761122X
language_de	englisch
fullrecord	<?xml version="1.0" encoding="UTF-8"?><collection xmlns="http://www.loc.gov/MARC21/slim"><record><leader>01000naa a22002652 4500</leader><controlfield tag="001">SPR05761122X</controlfield><controlfield tag="003">DE-627</controlfield><controlfield tag="005">20241001065502.0</controlfield><controlfield tag="007">cr uuu---uuuuu</controlfield><controlfield tag="008">241001s1995 xx \|\|\|\|\|o 00\| \|\|eng c</controlfield><datafield tag="024" ind1="7" ind2=" "><subfield code="a">10.1002/j.1460-2075.1995.tb07030.x</subfield><subfield code="2">doi</subfield></datafield><datafield tag="035" ind1=" " ind2=" "><subfield code="a">(DE-627)SPR05761122X</subfield></datafield><datafield tag="035" ind1=" " ind2=" "><subfield code="a">(SPR)j.1460-2075.1995.tb07030.x-e</subfield></datafield><datafield tag="040" ind1=" " ind2=" "><subfield code="a">DE-627</subfield><subfield code="b">ger</subfield><subfield code="c">DE-627</subfield><subfield code="e">rakwb</subfield></datafield><datafield tag="041" ind1=" " ind2=" "><subfield code="a">eng</subfield></datafield><datafield tag="100" ind1="1" ind2=" "><subfield code="a">Westendorp, M.O.</subfield><subfield code="e">verfasserin</subfield><subfield code="4">aut</subfield></datafield><datafield tag="245" ind1="1" ind2="0"><subfield code="a">HIV‐1 Tat potentiates TNF‐induced NF‐kappa B activation and cytotoxicity by altering the cellular redox state.</subfield></datafield><datafield tag="264" ind1=" " ind2="1"><subfield code="c">1995</subfield></datafield><datafield tag="336" ind1=" " ind2=" "><subfield code="a">Text</subfield><subfield code="b">txt</subfield><subfield code="2">rdacontent</subfield></datafield><datafield tag="337" ind1=" " ind2=" "><subfield code="a">Computermedien</subfield><subfield code="b">c</subfield><subfield code="2">rdamedia</subfield></datafield><datafield tag="338" ind1=" " ind2=" "><subfield code="a">Online-Ressource</subfield><subfield code="b">cr</subfield><subfield code="2">rdacarrier</subfield></datafield><datafield tag="500" ind1=" " ind2=" "><subfield code="a">© European Molecular Biology Organization 1995</subfield></datafield><datafield tag="520" ind1=" " ind2=" "><subfield code="a">Abstract This study demonstrates that human immunodeficiency virus type 1 (HIV‐1) Tat protein amplifies the activity of tumor necrosis factor (TNF), a cytokine that stimulates HIV‐1 replication through activation of NF‐kappa B. In HeLa cells stably transfected with the HIV‐1 tat gene (HeLa‐tat cells), expression of the Tat protein enhanced both TNF‐induced activation of NF‐kappa B and TNF‐mediated cytotoxicity. A similar potentiation of TNF effects was observed in Jurkat T cells and HeLa cells treated with soluble Tat protein. TNF‐mediated activation of NF‐kappa B and cytotoxicity involves the intracellular formation of reactive oxygen intermediates. Therefore, Tat‐mediated effects on the cellular redox state were analyzed. In both T cells and HeLa cells HIV‐1 Tat suppressed the expression of Mn‐dependent superoxide dismutase (Mn‐SOD), a mitochondrial enzyme that is part of the cellular defense system against oxidative stress. Thus, Mn‐SOD RNA protein levels and activity were markedly reduced in the presence of Tat. Decreased Mn‐SOD expression was associated with decreased levels of glutathione and a lower ratio of reduced:oxidized glutathione. A truncated Tat protein (Tat1‐72), known to transactivate the HIV‐1 long terminal repeat (LTR), no longer affected Mn‐SOD expression, the cellular redox state or TNF‐mediated cytotoxicity. Thus, our experiments demonstrate that the C‐terminal region of HIV‐1 Tat is required to suppress Mn‐SOD expression and to induce pro‐oxidative conditions reflected by a drop in reduced glutathione (GSH) and the GSH:oxidized GSH (GSSG) ratio.(ABSTRACT TRUNCATED AT 250 WORDS)</subfield></datafield><datafield tag="700" ind1="1" ind2=" "><subfield code="a">Shatrov, V.A.</subfield><subfield code="e">verfasserin</subfield><subfield code="4">aut</subfield></datafield><datafield tag="700" ind1="1" ind2=" "><subfield code="a">Schulze‐Osthoff, K.</subfield><subfield code="e">verfasserin</subfield><subfield code="4">aut</subfield></datafield><datafield tag="700" ind1="1" ind2=" "><subfield code="a">Frank, R.</subfield><subfield code="e">verfasserin</subfield><subfield code="4">aut</subfield></datafield><datafield tag="700" ind1="1" ind2=" "><subfield code="a">Kraft, M.</subfield><subfield code="e">verfasserin</subfield><subfield code="4">aut</subfield></datafield><datafield tag="700" ind1="1" ind2=" "><subfield code="a">Los, M.</subfield><subfield code="e">verfasserin</subfield><subfield code="4">aut</subfield></datafield><datafield tag="700" ind1="1" ind2=" "><subfield code="a">Krammer, P.H.</subfield><subfield code="e">verfasserin</subfield><subfield code="4">aut</subfield></datafield><datafield tag="700" ind1="1" ind2=" "><subfield code="a">Dröge, W.</subfield><subfield code="e">verfasserin</subfield><subfield code="4">aut</subfield></datafield><datafield tag="700" ind1="1" ind2=" "><subfield code="a">Lehmann, V.</subfield><subfield code="e">verfasserin</subfield><subfield code="4">aut</subfield></datafield><datafield tag="773" ind1="0" ind2="8"><subfield code="i">Enthalten in</subfield><subfield code="t">The EMBO Journal</subfield><subfield code="d">Nature Publishing Group UK, 2023</subfield><subfield code="g">14(1995), 3 vom: 01. Feb., Seite 546-554</subfield><subfield code="w">(DE-627)266022529</subfield><subfield code="w">(DE-600)1467419-1</subfield><subfield code="x">1460-2075</subfield><subfield code="7">nnns</subfield></datafield><datafield tag="773" ind1="1" ind2="8"><subfield code="g">volume:14</subfield><subfield code="g">year:1995</subfield><subfield code="g">number:3</subfield><subfield code="g">day:01</subfield><subfield code="g">month:02</subfield><subfield code="g">pages:546-554</subfield></datafield><datafield tag="856" ind1="4" ind2="0"><subfield code="u">https://dx.doi.org/10.1002/j.1460-2075.1995.tb07030.x</subfield><subfield code="m">X:SPRINGER</subfield><subfield code="x">Resolving-System</subfield><subfield code="z">lizenzpflichtig</subfield><subfield code="3">Volltext</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">SYSFLAG_0</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_SPRINGER</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_ILN_20</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_ILN_22</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_ILN_23</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_ILN_24</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_ILN_31</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_ILN_39</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_ILN_40</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_ILN_62</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_ILN_63</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_ILN_65</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_ILN_69</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_ILN_70</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_ILN_72</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_ILN_73</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_ILN_74</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_ILN_95</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_ILN_105</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_ILN_110</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_ILN_151</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_ILN_161</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_ILN_170</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_ILN_213</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_ILN_230</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_ILN_252</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_ILN_285</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_ILN_293</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_ILN_602</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_ILN_2014</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_ILN_2021</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_ILN_2050</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_ILN_4012</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_ILN_4037</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_ILN_4112</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_ILN_4125</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_ILN_4126</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_ILN_4249</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_ILN_4305</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_ILN_4306</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_ILN_4307</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_ILN_4313</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_ILN_4322</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_ILN_4323</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_ILN_4324</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_ILN_4325</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_ILN_4338</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_ILN_4367</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_ILN_4700</subfield></datafield><datafield tag="951" ind1=" " ind2=" "><subfield code="a">AR</subfield></datafield><datafield tag="952" ind1=" " ind2=" "><subfield code="d">14</subfield><subfield code="j">1995</subfield><subfield code="e">3</subfield><subfield code="b">01</subfield><subfield code="c">02</subfield><subfield code="h">546-554</subfield></datafield></record></collection>
author	Westendorp, M.O.
spellingShingle	Westendorp, M.O. HIV‐1 Tat potentiates TNF‐induced NF‐kappa B activation and cytotoxicity by altering the cellular redox state.
authorStr	Westendorp, M.O.
ppnlink_with_tag_str_mv	@@773@@(DE-627)266022529
format	electronic Article
delete_txt_mv	keep
author_role	aut aut aut aut aut aut aut aut aut
collection	springer
remote_str	true
illustrated	Not Illustrated
issn	1460-2075
topic_title	HIV‐1 Tat potentiates TNF‐induced NF‐kappa B activation and cytotoxicity by altering the cellular redox state
format_facet	Elektronische Aufsätze Aufsätze Elektronische Ressource
format_main_str_mv	Text Zeitschrift/Artikel
carriertype_str_mv	cr
hierarchy_parent_title	The EMBO Journal
hierarchy_parent_id	266022529
hierarchy_top_title	The EMBO Journal
isfreeaccess_txt	false
familylinks_str_mv	(DE-627)266022529 (DE-600)1467419-1
title	HIV‐1 Tat potentiates TNF‐induced NF‐kappa B activation and cytotoxicity by altering the cellular redox state.
ctrlnum	(DE-627)SPR05761122X (SPR)j.1460-2075.1995.tb07030.x-e
title_full	HIV‐1 Tat potentiates TNF‐induced NF‐kappa B activation and cytotoxicity by altering the cellular redox state
author_sort	Westendorp, M.O.
journal	The EMBO Journal
journalStr	The EMBO Journal
lang_code	eng
isOA_bool	false
recordtype	marc
publishDateSort	1995
contenttype_str_mv	txt
container_start_page	546
author_browse	Westendorp, M.O. Shatrov, V.A. Schulze‐Osthoff, K. Frank, R. Kraft, M. Los, M. Krammer, P.H. Dröge, W. Lehmann, V.
container_volume	14
format_se	Elektronische Aufsätze
author-letter	Westendorp, M.O.
doi_str_mv	10.1002/j.1460-2075.1995.tb07030.x
author2-role	verfasserin
title_sort	hiv‐1 tat potentiates tnf‐induced nf‐kappa b activation and cytotoxicity by altering the cellular redox state
title_auth	HIV‐1 Tat potentiates TNF‐induced NF‐kappa B activation and cytotoxicity by altering the cellular redox state.
abstract	Abstract This study demonstrates that human immunodeficiency virus type 1 (HIV‐1) Tat protein amplifies the activity of tumor necrosis factor (TNF), a cytokine that stimulates HIV‐1 replication through activation of NF‐kappa B. In HeLa cells stably transfected with the HIV‐1 tat gene (HeLa‐tat cells), expression of the Tat protein enhanced both TNF‐induced activation of NF‐kappa B and TNF‐mediated cytotoxicity. A similar potentiation of TNF effects was observed in Jurkat T cells and HeLa cells treated with soluble Tat protein. TNF‐mediated activation of NF‐kappa B and cytotoxicity involves the intracellular formation of reactive oxygen intermediates. Therefore, Tat‐mediated effects on the cellular redox state were analyzed. In both T cells and HeLa cells HIV‐1 Tat suppressed the expression of Mn‐dependent superoxide dismutase (Mn‐SOD), a mitochondrial enzyme that is part of the cellular defense system against oxidative stress. Thus, Mn‐SOD RNA protein levels and activity were markedly reduced in the presence of Tat. Decreased Mn‐SOD expression was associated with decreased levels of glutathione and a lower ratio of reduced:oxidized glutathione. A truncated Tat protein (Tat1‐72), known to transactivate the HIV‐1 long terminal repeat (LTR), no longer affected Mn‐SOD expression, the cellular redox state or TNF‐mediated cytotoxicity. Thus, our experiments demonstrate that the C‐terminal region of HIV‐1 Tat is required to suppress Mn‐SOD expression and to induce pro‐oxidative conditions reflected by a drop in reduced glutathione (GSH) and the GSH:oxidized GSH (GSSG) ratio.(ABSTRACT TRUNCATED AT 250 WORDS) © European Molecular Biology Organization 1995
abstractGer	Abstract This study demonstrates that human immunodeficiency virus type 1 (HIV‐1) Tat protein amplifies the activity of tumor necrosis factor (TNF), a cytokine that stimulates HIV‐1 replication through activation of NF‐kappa B. In HeLa cells stably transfected with the HIV‐1 tat gene (HeLa‐tat cells), expression of the Tat protein enhanced both TNF‐induced activation of NF‐kappa B and TNF‐mediated cytotoxicity. A similar potentiation of TNF effects was observed in Jurkat T cells and HeLa cells treated with soluble Tat protein. TNF‐mediated activation of NF‐kappa B and cytotoxicity involves the intracellular formation of reactive oxygen intermediates. Therefore, Tat‐mediated effects on the cellular redox state were analyzed. In both T cells and HeLa cells HIV‐1 Tat suppressed the expression of Mn‐dependent superoxide dismutase (Mn‐SOD), a mitochondrial enzyme that is part of the cellular defense system against oxidative stress. Thus, Mn‐SOD RNA protein levels and activity were markedly reduced in the presence of Tat. Decreased Mn‐SOD expression was associated with decreased levels of glutathione and a lower ratio of reduced:oxidized glutathione. A truncated Tat protein (Tat1‐72), known to transactivate the HIV‐1 long terminal repeat (LTR), no longer affected Mn‐SOD expression, the cellular redox state or TNF‐mediated cytotoxicity. Thus, our experiments demonstrate that the C‐terminal region of HIV‐1 Tat is required to suppress Mn‐SOD expression and to induce pro‐oxidative conditions reflected by a drop in reduced glutathione (GSH) and the GSH:oxidized GSH (GSSG) ratio.(ABSTRACT TRUNCATED AT 250 WORDS) © European Molecular Biology Organization 1995
abstract_unstemmed	Abstract This study demonstrates that human immunodeficiency virus type 1 (HIV‐1) Tat protein amplifies the activity of tumor necrosis factor (TNF), a cytokine that stimulates HIV‐1 replication through activation of NF‐kappa B. In HeLa cells stably transfected with the HIV‐1 tat gene (HeLa‐tat cells), expression of the Tat protein enhanced both TNF‐induced activation of NF‐kappa B and TNF‐mediated cytotoxicity. A similar potentiation of TNF effects was observed in Jurkat T cells and HeLa cells treated with soluble Tat protein. TNF‐mediated activation of NF‐kappa B and cytotoxicity involves the intracellular formation of reactive oxygen intermediates. Therefore, Tat‐mediated effects on the cellular redox state were analyzed. In both T cells and HeLa cells HIV‐1 Tat suppressed the expression of Mn‐dependent superoxide dismutase (Mn‐SOD), a mitochondrial enzyme that is part of the cellular defense system against oxidative stress. Thus, Mn‐SOD RNA protein levels and activity were markedly reduced in the presence of Tat. Decreased Mn‐SOD expression was associated with decreased levels of glutathione and a lower ratio of reduced:oxidized glutathione. A truncated Tat protein (Tat1‐72), known to transactivate the HIV‐1 long terminal repeat (LTR), no longer affected Mn‐SOD expression, the cellular redox state or TNF‐mediated cytotoxicity. Thus, our experiments demonstrate that the C‐terminal region of HIV‐1 Tat is required to suppress Mn‐SOD expression and to induce pro‐oxidative conditions reflected by a drop in reduced glutathione (GSH) and the GSH:oxidized GSH (GSSG) ratio.(ABSTRACT TRUNCATED AT 250 WORDS) © European Molecular Biology Organization 1995
collection_details	SYSFLAG_0 GBV_SPRINGER GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_39 GBV_ILN_40 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_70 GBV_ILN_72 GBV_ILN_73 GBV_ILN_74 GBV_ILN_95 GBV_ILN_105 GBV_ILN_110 GBV_ILN_151 GBV_ILN_161 GBV_ILN_170 GBV_ILN_213 GBV_ILN_230 GBV_ILN_252 GBV_ILN_285 GBV_ILN_293 GBV_ILN_602 GBV_ILN_2014 GBV_ILN_2021 GBV_ILN_2050 GBV_ILN_4012 GBV_ILN_4037 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4249 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4338 GBV_ILN_4367 GBV_ILN_4700
container_issue	3
title_short	HIV‐1 Tat potentiates TNF‐induced NF‐kappa B activation and cytotoxicity by altering the cellular redox state.
url	https://dx.doi.org/10.1002/j.1460-2075.1995.tb07030.x
remote_bool	true
author2	Shatrov, V.A. Schulze‐Osthoff, K. Frank, R. Kraft, M. Los, M. Krammer, P.H. Dröge, W. Lehmann, V.
author2Str	Shatrov, V.A. Schulze‐Osthoff, K. Frank, R. Kraft, M. Los, M. Krammer, P.H. Dröge, W. Lehmann, V.
ppnlink	266022529
mediatype_str_mv	c
isOA_txt	false
hochschulschrift_bool	false
doi_str	10.1002/j.1460-2075.1995.tb07030.x
up_date	2024-10-01T04:59:02.741Z
_version_	1811686351430483968
fullrecord_marcxml	<?xml version="1.0" encoding="UTF-8"?><collection xmlns="http://www.loc.gov/MARC21/slim"><record><leader>01000naa a22002652 4500</leader><controlfield tag="001">SPR05761122X</controlfield><controlfield tag="003">DE-627</controlfield><controlfield tag="005">20241001065502.0</controlfield><controlfield tag="007">cr uuu---uuuuu</controlfield><controlfield tag="008">241001s1995 xx \|\|\|\|\|o 00\| \|\|eng c</controlfield><datafield tag="024" ind1="7" ind2=" "><subfield code="a">10.1002/j.1460-2075.1995.tb07030.x</subfield><subfield code="2">doi</subfield></datafield><datafield tag="035" ind1=" " ind2=" "><subfield code="a">(DE-627)SPR05761122X</subfield></datafield><datafield tag="035" ind1=" " ind2=" "><subfield code="a">(SPR)j.1460-2075.1995.tb07030.x-e</subfield></datafield><datafield tag="040" ind1=" " ind2=" "><subfield code="a">DE-627</subfield><subfield code="b">ger</subfield><subfield code="c">DE-627</subfield><subfield code="e">rakwb</subfield></datafield><datafield tag="041" ind1=" " ind2=" "><subfield code="a">eng</subfield></datafield><datafield tag="100" ind1="1" ind2=" "><subfield code="a">Westendorp, M.O.</subfield><subfield code="e">verfasserin</subfield><subfield code="4">aut</subfield></datafield><datafield tag="245" ind1="1" ind2="0"><subfield code="a">HIV‐1 Tat potentiates TNF‐induced NF‐kappa B activation and cytotoxicity by altering the cellular redox state.</subfield></datafield><datafield tag="264" ind1=" " ind2="1"><subfield code="c">1995</subfield></datafield><datafield tag="336" ind1=" " ind2=" "><subfield code="a">Text</subfield><subfield code="b">txt</subfield><subfield code="2">rdacontent</subfield></datafield><datafield tag="337" ind1=" " ind2=" "><subfield code="a">Computermedien</subfield><subfield code="b">c</subfield><subfield code="2">rdamedia</subfield></datafield><datafield tag="338" ind1=" " ind2=" "><subfield code="a">Online-Ressource</subfield><subfield code="b">cr</subfield><subfield code="2">rdacarrier</subfield></datafield><datafield tag="500" ind1=" " ind2=" "><subfield code="a">© European Molecular Biology Organization 1995</subfield></datafield><datafield tag="520" ind1=" " ind2=" "><subfield code="a">Abstract This study demonstrates that human immunodeficiency virus type 1 (HIV‐1) Tat protein amplifies the activity of tumor necrosis factor (TNF), a cytokine that stimulates HIV‐1 replication through activation of NF‐kappa B. In HeLa cells stably transfected with the HIV‐1 tat gene (HeLa‐tat cells), expression of the Tat protein enhanced both TNF‐induced activation of NF‐kappa B and TNF‐mediated cytotoxicity. A similar potentiation of TNF effects was observed in Jurkat T cells and HeLa cells treated with soluble Tat protein. TNF‐mediated activation of NF‐kappa B and cytotoxicity involves the intracellular formation of reactive oxygen intermediates. Therefore, Tat‐mediated effects on the cellular redox state were analyzed. In both T cells and HeLa cells HIV‐1 Tat suppressed the expression of Mn‐dependent superoxide dismutase (Mn‐SOD), a mitochondrial enzyme that is part of the cellular defense system against oxidative stress. Thus, Mn‐SOD RNA protein levels and activity were markedly reduced in the presence of Tat. Decreased Mn‐SOD expression was associated with decreased levels of glutathione and a lower ratio of reduced:oxidized glutathione. A truncated Tat protein (Tat1‐72), known to transactivate the HIV‐1 long terminal repeat (LTR), no longer affected Mn‐SOD expression, the cellular redox state or TNF‐mediated cytotoxicity. Thus, our experiments demonstrate that the C‐terminal region of HIV‐1 Tat is required to suppress Mn‐SOD expression and to induce pro‐oxidative conditions reflected by a drop in reduced glutathione (GSH) and the GSH:oxidized GSH (GSSG) ratio.(ABSTRACT TRUNCATED AT 250 WORDS)</subfield></datafield><datafield tag="700" ind1="1" ind2=" "><subfield code="a">Shatrov, V.A.</subfield><subfield code="e">verfasserin</subfield><subfield code="4">aut</subfield></datafield><datafield tag="700" ind1="1" ind2=" "><subfield code="a">Schulze‐Osthoff, K.</subfield><subfield code="e">verfasserin</subfield><subfield code="4">aut</subfield></datafield><datafield tag="700" ind1="1" ind2=" "><subfield code="a">Frank, R.</subfield><subfield code="e">verfasserin</subfield><subfield code="4">aut</subfield></datafield><datafield tag="700" ind1="1" ind2=" "><subfield code="a">Kraft, M.</subfield><subfield code="e">verfasserin</subfield><subfield code="4">aut</subfield></datafield><datafield tag="700" ind1="1" ind2=" "><subfield code="a">Los, M.</subfield><subfield code="e">verfasserin</subfield><subfield code="4">aut</subfield></datafield><datafield tag="700" ind1="1" ind2=" "><subfield code="a">Krammer, P.H.</subfield><subfield code="e">verfasserin</subfield><subfield code="4">aut</subfield></datafield><datafield tag="700" ind1="1" ind2=" "><subfield code="a">Dröge, W.</subfield><subfield code="e">verfasserin</subfield><subfield code="4">aut</subfield></datafield><datafield tag="700" ind1="1" ind2=" "><subfield code="a">Lehmann, V.</subfield><subfield code="e">verfasserin</subfield><subfield code="4">aut</subfield></datafield><datafield tag="773" ind1="0" ind2="8"><subfield code="i">Enthalten in</subfield><subfield code="t">The EMBO Journal</subfield><subfield code="d">Nature Publishing Group UK, 2023</subfield><subfield code="g">14(1995), 3 vom: 01. Feb., Seite 546-554</subfield><subfield code="w">(DE-627)266022529</subfield><subfield code="w">(DE-600)1467419-1</subfield><subfield code="x">1460-2075</subfield><subfield code="7">nnns</subfield></datafield><datafield tag="773" ind1="1" ind2="8"><subfield code="g">volume:14</subfield><subfield code="g">year:1995</subfield><subfield code="g">number:3</subfield><subfield code="g">day:01</subfield><subfield code="g">month:02</subfield><subfield code="g">pages:546-554</subfield></datafield><datafield tag="856" ind1="4" ind2="0"><subfield code="u">https://dx.doi.org/10.1002/j.1460-2075.1995.tb07030.x</subfield><subfield code="m">X:SPRINGER</subfield><subfield code="x">Resolving-System</subfield><subfield code="z">lizenzpflichtig</subfield><subfield code="3">Volltext</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">SYSFLAG_0</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_SPRINGER</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_ILN_20</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_ILN_22</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_ILN_23</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_ILN_24</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_ILN_31</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_ILN_39</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_ILN_40</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_ILN_62</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_ILN_63</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_ILN_65</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_ILN_69</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_ILN_70</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_ILN_72</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_ILN_73</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_ILN_74</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_ILN_95</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_ILN_105</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_ILN_110</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_ILN_151</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_ILN_161</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_ILN_170</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_ILN_213</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_ILN_230</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_ILN_252</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_ILN_285</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_ILN_293</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_ILN_602</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_ILN_2014</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_ILN_2021</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_ILN_2050</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_ILN_4012</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_ILN_4037</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_ILN_4112</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_ILN_4125</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_ILN_4126</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_ILN_4249</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_ILN_4305</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_ILN_4306</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_ILN_4307</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_ILN_4313</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_ILN_4322</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_ILN_4323</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_ILN_4324</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_ILN_4325</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_ILN_4338</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_ILN_4367</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_ILN_4700</subfield></datafield><datafield tag="951" ind1=" " ind2=" "><subfield code="a">AR</subfield></datafield><datafield tag="952" ind1=" " ind2=" "><subfield code="d">14</subfield><subfield code="j">1995</subfield><subfield code="e">3</subfield><subfield code="b">01</subfield><subfield code="c">02</subfield><subfield code="h">546-554</subfield></datafield></record></collection>
score	7.3993464

Nicht das Richtige dabei?

Schreiben Sie uns!

HIV‐1 Tat potentiates TNF‐induced NF‐kappa B activation and cytotoxicity by altering the cellular redox state.

Nicht das Richtige dabei?

Zugang & Verfügbarkeit

Vorhandene Bände

Nicht das Richtige dabei?