Ethanol inhibits palmitoylation of G protein Gαs
Neurobiological actions of ethanol have been linked to perturbations in cyclic AMP (cAMP)-dependent signaling processes. Chronic ethanol exposure leads to desensitization of cAMP production in response to physiological ligands (heterologous desensitization). Ethanol-induced alterations in neuronal e...
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| Autor*in: |
Hallak, Hazem [verfasserIn] Rubin, Raphael [verfasserIn] |
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| Format: |
E-Artikel |
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| Erschienen: |
Oxford, UK: Blackwell Science Ltd ; 2004 |
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Online-Ressource |
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| Reproduktion: |
2004 ; Blackwell Publishing Journal Backfiles 1879-2005 |
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| Übergeordnetes Werk: |
In: Journal of neurochemistry - Oxford : Wiley-Blackwell, 1956, 89(2004), 4, Seite 0 |
| Übergeordnetes Werk: |
volume:89 ; year:2004 ; number:4 ; pages:0 |
| Links: |
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| DOI / URN: |
10.1046/j.1471-4159.2004.02364.x |
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| 520 | |a Neurobiological actions of ethanol have been linked to perturbations in cyclic AMP (cAMP)-dependent signaling processes. Chronic ethanol exposure leads to desensitization of cAMP production in response to physiological ligands (heterologous desensitization). Ethanol-induced alterations in neuronal expression of G proteins Gs and Gi have been invoked as a cause of heterologous desensitization. However, effects of ethanol on G protein expression vary considerably among different experimental protocols, various brain regions and diverse neuronal cell types. Dynamic palmitoylation of G protein α subunits is critical for membrane localization and protein–protein interactions, and represents a regulatory feature of G protein function. We studied the effect of ethanol on Gαs palmitoylation. In NG108-15 rat neuroblastoma × glioma hybrid cells, acute exposure to pharmacologically relevant concentrations of ethanol (25–100 mm) inhibited basal and prostaglandin E1-stimulated incorporation of palmitate into Gαs. Exposure of NG108-15 cells to ethanol for 72 h induced a shift in Gαs to its non-palmitoylated state, coincident with an inhibition of prostaglandin E1-induced cAMP production. Both parameters were restored following 24 h of ethanol withdrawal. Chronic ethanol exposure also induced the depalmitoylation of Gαs in human embryonic kidney (HEK)293 cells that overexpress wild-type Gαs and caused heterologous desensitization of adenylyl cyclase. By contrast, HEK293 cells that express a non-palmitoylated mutant of Gαs were insensitive to heterologous desensitization after chronic ethanol exposure. In summary, the findings identify a novel effect of ethanol on post-translational lipid modification of Gαs, and represent a mechanism by which ethanol might affect adenylyl cyclase activity. | ||
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10.1046/j.1471-4159.2004.02364.x doi (DE-627)NLEJ243121938 DE-627 ger DE-627 rakwb Hallak, Hazem verfasserin aut Ethanol inhibits palmitoylation of G protein Gαs Oxford, UK Blackwell Science Ltd 2004 Online-Ressource nicht spezifiziert zzz rdacontent nicht spezifiziert z rdamedia nicht spezifiziert zu rdacarrier Neurobiological actions of ethanol have been linked to perturbations in cyclic AMP (cAMP)-dependent signaling processes. Chronic ethanol exposure leads to desensitization of cAMP production in response to physiological ligands (heterologous desensitization). Ethanol-induced alterations in neuronal expression of G proteins Gs and Gi have been invoked as a cause of heterologous desensitization. However, effects of ethanol on G protein expression vary considerably among different experimental protocols, various brain regions and diverse neuronal cell types. Dynamic palmitoylation of G protein α subunits is critical for membrane localization and protein–protein interactions, and represents a regulatory feature of G protein function. We studied the effect of ethanol on Gαs palmitoylation. In NG108-15 rat neuroblastoma × glioma hybrid cells, acute exposure to pharmacologically relevant concentrations of ethanol (25–100 mm) inhibited basal and prostaglandin E1-stimulated incorporation of palmitate into Gαs. Exposure of NG108-15 cells to ethanol for 72 h induced a shift in Gαs to its non-palmitoylated state, coincident with an inhibition of prostaglandin E1-induced cAMP production. Both parameters were restored following 24 h of ethanol withdrawal. Chronic ethanol exposure also induced the depalmitoylation of Gαs in human embryonic kidney (HEK)293 cells that overexpress wild-type Gαs and caused heterologous desensitization of adenylyl cyclase. By contrast, HEK293 cells that express a non-palmitoylated mutant of Gαs were insensitive to heterologous desensitization after chronic ethanol exposure. In summary, the findings identify a novel effect of ethanol on post-translational lipid modification of Gαs, and represent a mechanism by which ethanol might affect adenylyl cyclase activity. 2004 Blackwell Publishing Journal Backfiles 1879-2005 |2004|||||||||| cyclic AMP Rubin, Raphael verfasserin aut In Journal of neurochemistry Oxford : Wiley-Blackwell, 1956 89(2004), 4, Seite 0 Online-Ressource (DE-627)NLEJ243927584 (DE-600)2020528-4 1471-4159 nnns volume:89 year:2004 number:4 pages:0 http://dx.doi.org/10.1046/j.1471-4159.2004.02364.x text/html Verlag Deutschlandweit zugänglich Volltext GBV_USEFLAG_U ZDB-1-DJB GBV_NL_ARTICLE AR 89 2004 4 0 |
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10.1046/j.1471-4159.2004.02364.x doi (DE-627)NLEJ243121938 DE-627 ger DE-627 rakwb Hallak, Hazem verfasserin aut Ethanol inhibits palmitoylation of G protein Gαs Oxford, UK Blackwell Science Ltd 2004 Online-Ressource nicht spezifiziert zzz rdacontent nicht spezifiziert z rdamedia nicht spezifiziert zu rdacarrier Neurobiological actions of ethanol have been linked to perturbations in cyclic AMP (cAMP)-dependent signaling processes. Chronic ethanol exposure leads to desensitization of cAMP production in response to physiological ligands (heterologous desensitization). Ethanol-induced alterations in neuronal expression of G proteins Gs and Gi have been invoked as a cause of heterologous desensitization. However, effects of ethanol on G protein expression vary considerably among different experimental protocols, various brain regions and diverse neuronal cell types. Dynamic palmitoylation of G protein α subunits is critical for membrane localization and protein–protein interactions, and represents a regulatory feature of G protein function. We studied the effect of ethanol on Gαs palmitoylation. In NG108-15 rat neuroblastoma × glioma hybrid cells, acute exposure to pharmacologically relevant concentrations of ethanol (25–100 mm) inhibited basal and prostaglandin E1-stimulated incorporation of palmitate into Gαs. Exposure of NG108-15 cells to ethanol for 72 h induced a shift in Gαs to its non-palmitoylated state, coincident with an inhibition of prostaglandin E1-induced cAMP production. Both parameters were restored following 24 h of ethanol withdrawal. Chronic ethanol exposure also induced the depalmitoylation of Gαs in human embryonic kidney (HEK)293 cells that overexpress wild-type Gαs and caused heterologous desensitization of adenylyl cyclase. By contrast, HEK293 cells that express a non-palmitoylated mutant of Gαs were insensitive to heterologous desensitization after chronic ethanol exposure. In summary, the findings identify a novel effect of ethanol on post-translational lipid modification of Gαs, and represent a mechanism by which ethanol might affect adenylyl cyclase activity. 2004 Blackwell Publishing Journal Backfiles 1879-2005 |2004|||||||||| cyclic AMP Rubin, Raphael verfasserin aut In Journal of neurochemistry Oxford : Wiley-Blackwell, 1956 89(2004), 4, Seite 0 Online-Ressource (DE-627)NLEJ243927584 (DE-600)2020528-4 1471-4159 nnns volume:89 year:2004 number:4 pages:0 http://dx.doi.org/10.1046/j.1471-4159.2004.02364.x text/html Verlag Deutschlandweit zugänglich Volltext GBV_USEFLAG_U ZDB-1-DJB GBV_NL_ARTICLE AR 89 2004 4 0 |
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10.1046/j.1471-4159.2004.02364.x doi (DE-627)NLEJ243121938 DE-627 ger DE-627 rakwb Hallak, Hazem verfasserin aut Ethanol inhibits palmitoylation of G protein Gαs Oxford, UK Blackwell Science Ltd 2004 Online-Ressource nicht spezifiziert zzz rdacontent nicht spezifiziert z rdamedia nicht spezifiziert zu rdacarrier Neurobiological actions of ethanol have been linked to perturbations in cyclic AMP (cAMP)-dependent signaling processes. Chronic ethanol exposure leads to desensitization of cAMP production in response to physiological ligands (heterologous desensitization). Ethanol-induced alterations in neuronal expression of G proteins Gs and Gi have been invoked as a cause of heterologous desensitization. However, effects of ethanol on G protein expression vary considerably among different experimental protocols, various brain regions and diverse neuronal cell types. Dynamic palmitoylation of G protein α subunits is critical for membrane localization and protein–protein interactions, and represents a regulatory feature of G protein function. We studied the effect of ethanol on Gαs palmitoylation. In NG108-15 rat neuroblastoma × glioma hybrid cells, acute exposure to pharmacologically relevant concentrations of ethanol (25–100 mm) inhibited basal and prostaglandin E1-stimulated incorporation of palmitate into Gαs. Exposure of NG108-15 cells to ethanol for 72 h induced a shift in Gαs to its non-palmitoylated state, coincident with an inhibition of prostaglandin E1-induced cAMP production. Both parameters were restored following 24 h of ethanol withdrawal. Chronic ethanol exposure also induced the depalmitoylation of Gαs in human embryonic kidney (HEK)293 cells that overexpress wild-type Gαs and caused heterologous desensitization of adenylyl cyclase. By contrast, HEK293 cells that express a non-palmitoylated mutant of Gαs were insensitive to heterologous desensitization after chronic ethanol exposure. In summary, the findings identify a novel effect of ethanol on post-translational lipid modification of Gαs, and represent a mechanism by which ethanol might affect adenylyl cyclase activity. 2004 Blackwell Publishing Journal Backfiles 1879-2005 |2004|||||||||| cyclic AMP Rubin, Raphael verfasserin aut In Journal of neurochemistry Oxford : Wiley-Blackwell, 1956 89(2004), 4, Seite 0 Online-Ressource (DE-627)NLEJ243927584 (DE-600)2020528-4 1471-4159 nnns volume:89 year:2004 number:4 pages:0 http://dx.doi.org/10.1046/j.1471-4159.2004.02364.x text/html Verlag Deutschlandweit zugänglich Volltext GBV_USEFLAG_U ZDB-1-DJB GBV_NL_ARTICLE AR 89 2004 4 0 |
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10.1046/j.1471-4159.2004.02364.x doi (DE-627)NLEJ243121938 DE-627 ger DE-627 rakwb Hallak, Hazem verfasserin aut Ethanol inhibits palmitoylation of G protein Gαs Oxford, UK Blackwell Science Ltd 2004 Online-Ressource nicht spezifiziert zzz rdacontent nicht spezifiziert z rdamedia nicht spezifiziert zu rdacarrier Neurobiological actions of ethanol have been linked to perturbations in cyclic AMP (cAMP)-dependent signaling processes. Chronic ethanol exposure leads to desensitization of cAMP production in response to physiological ligands (heterologous desensitization). Ethanol-induced alterations in neuronal expression of G proteins Gs and Gi have been invoked as a cause of heterologous desensitization. However, effects of ethanol on G protein expression vary considerably among different experimental protocols, various brain regions and diverse neuronal cell types. Dynamic palmitoylation of G protein α subunits is critical for membrane localization and protein–protein interactions, and represents a regulatory feature of G protein function. We studied the effect of ethanol on Gαs palmitoylation. In NG108-15 rat neuroblastoma × glioma hybrid cells, acute exposure to pharmacologically relevant concentrations of ethanol (25–100 mm) inhibited basal and prostaglandin E1-stimulated incorporation of palmitate into Gαs. Exposure of NG108-15 cells to ethanol for 72 h induced a shift in Gαs to its non-palmitoylated state, coincident with an inhibition of prostaglandin E1-induced cAMP production. Both parameters were restored following 24 h of ethanol withdrawal. Chronic ethanol exposure also induced the depalmitoylation of Gαs in human embryonic kidney (HEK)293 cells that overexpress wild-type Gαs and caused heterologous desensitization of adenylyl cyclase. By contrast, HEK293 cells that express a non-palmitoylated mutant of Gαs were insensitive to heterologous desensitization after chronic ethanol exposure. In summary, the findings identify a novel effect of ethanol on post-translational lipid modification of Gαs, and represent a mechanism by which ethanol might affect adenylyl cyclase activity. 2004 Blackwell Publishing Journal Backfiles 1879-2005 |2004|||||||||| cyclic AMP Rubin, Raphael verfasserin aut In Journal of neurochemistry Oxford : Wiley-Blackwell, 1956 89(2004), 4, Seite 0 Online-Ressource (DE-627)NLEJ243927584 (DE-600)2020528-4 1471-4159 nnns volume:89 year:2004 number:4 pages:0 http://dx.doi.org/10.1046/j.1471-4159.2004.02364.x text/html Verlag Deutschlandweit zugänglich Volltext GBV_USEFLAG_U ZDB-1-DJB GBV_NL_ARTICLE AR 89 2004 4 0 |
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10.1046/j.1471-4159.2004.02364.x doi (DE-627)NLEJ243121938 DE-627 ger DE-627 rakwb Hallak, Hazem verfasserin aut Ethanol inhibits palmitoylation of G protein Gαs Oxford, UK Blackwell Science Ltd 2004 Online-Ressource nicht spezifiziert zzz rdacontent nicht spezifiziert z rdamedia nicht spezifiziert zu rdacarrier Neurobiological actions of ethanol have been linked to perturbations in cyclic AMP (cAMP)-dependent signaling processes. Chronic ethanol exposure leads to desensitization of cAMP production in response to physiological ligands (heterologous desensitization). Ethanol-induced alterations in neuronal expression of G proteins Gs and Gi have been invoked as a cause of heterologous desensitization. However, effects of ethanol on G protein expression vary considerably among different experimental protocols, various brain regions and diverse neuronal cell types. Dynamic palmitoylation of G protein α subunits is critical for membrane localization and protein–protein interactions, and represents a regulatory feature of G protein function. We studied the effect of ethanol on Gαs palmitoylation. In NG108-15 rat neuroblastoma × glioma hybrid cells, acute exposure to pharmacologically relevant concentrations of ethanol (25–100 mm) inhibited basal and prostaglandin E1-stimulated incorporation of palmitate into Gαs. Exposure of NG108-15 cells to ethanol for 72 h induced a shift in Gαs to its non-palmitoylated state, coincident with an inhibition of prostaglandin E1-induced cAMP production. Both parameters were restored following 24 h of ethanol withdrawal. Chronic ethanol exposure also induced the depalmitoylation of Gαs in human embryonic kidney (HEK)293 cells that overexpress wild-type Gαs and caused heterologous desensitization of adenylyl cyclase. By contrast, HEK293 cells that express a non-palmitoylated mutant of Gαs were insensitive to heterologous desensitization after chronic ethanol exposure. In summary, the findings identify a novel effect of ethanol on post-translational lipid modification of Gαs, and represent a mechanism by which ethanol might affect adenylyl cyclase activity. 2004 Blackwell Publishing Journal Backfiles 1879-2005 |2004|||||||||| cyclic AMP Rubin, Raphael verfasserin aut In Journal of neurochemistry Oxford : Wiley-Blackwell, 1956 89(2004), 4, Seite 0 Online-Ressource (DE-627)NLEJ243927584 (DE-600)2020528-4 1471-4159 nnns volume:89 year:2004 number:4 pages:0 http://dx.doi.org/10.1046/j.1471-4159.2004.02364.x text/html Verlag Deutschlandweit zugänglich Volltext GBV_USEFLAG_U ZDB-1-DJB GBV_NL_ARTICLE AR 89 2004 4 0 |
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Neurobiological actions of ethanol have been linked to perturbations in cyclic AMP (cAMP)-dependent signaling processes. Chronic ethanol exposure leads to desensitization of cAMP production in response to physiological ligands (heterologous desensitization). Ethanol-induced alterations in neuronal expression of G proteins Gs and Gi have been invoked as a cause of heterologous desensitization. However, effects of ethanol on G protein expression vary considerably among different experimental protocols, various brain regions and diverse neuronal cell types. Dynamic palmitoylation of G protein α subunits is critical for membrane localization and protein–protein interactions, and represents a regulatory feature of G protein function. We studied the effect of ethanol on Gαs palmitoylation. In NG108-15 rat neuroblastoma × glioma hybrid cells, acute exposure to pharmacologically relevant concentrations of ethanol (25–100 mm) inhibited basal and prostaglandin E1-stimulated incorporation of palmitate into Gαs. Exposure of NG108-15 cells to ethanol for 72 h induced a shift in Gαs to its non-palmitoylated state, coincident with an inhibition of prostaglandin E1-induced cAMP production. Both parameters were restored following 24 h of ethanol withdrawal. Chronic ethanol exposure also induced the depalmitoylation of Gαs in human embryonic kidney (HEK)293 cells that overexpress wild-type Gαs and caused heterologous desensitization of adenylyl cyclase. By contrast, HEK293 cells that express a non-palmitoylated mutant of Gαs were insensitive to heterologous desensitization after chronic ethanol exposure. In summary, the findings identify a novel effect of ethanol on post-translational lipid modification of Gαs, and represent a mechanism by which ethanol might affect adenylyl cyclase activity. |
| abstractGer |
Neurobiological actions of ethanol have been linked to perturbations in cyclic AMP (cAMP)-dependent signaling processes. Chronic ethanol exposure leads to desensitization of cAMP production in response to physiological ligands (heterologous desensitization). Ethanol-induced alterations in neuronal expression of G proteins Gs and Gi have been invoked as a cause of heterologous desensitization. However, effects of ethanol on G protein expression vary considerably among different experimental protocols, various brain regions and diverse neuronal cell types. Dynamic palmitoylation of G protein α subunits is critical for membrane localization and protein–protein interactions, and represents a regulatory feature of G protein function. We studied the effect of ethanol on Gαs palmitoylation. In NG108-15 rat neuroblastoma × glioma hybrid cells, acute exposure to pharmacologically relevant concentrations of ethanol (25–100 mm) inhibited basal and prostaglandin E1-stimulated incorporation of palmitate into Gαs. Exposure of NG108-15 cells to ethanol for 72 h induced a shift in Gαs to its non-palmitoylated state, coincident with an inhibition of prostaglandin E1-induced cAMP production. Both parameters were restored following 24 h of ethanol withdrawal. Chronic ethanol exposure also induced the depalmitoylation of Gαs in human embryonic kidney (HEK)293 cells that overexpress wild-type Gαs and caused heterologous desensitization of adenylyl cyclase. By contrast, HEK293 cells that express a non-palmitoylated mutant of Gαs were insensitive to heterologous desensitization after chronic ethanol exposure. In summary, the findings identify a novel effect of ethanol on post-translational lipid modification of Gαs, and represent a mechanism by which ethanol might affect adenylyl cyclase activity. |
| abstract_unstemmed |
Neurobiological actions of ethanol have been linked to perturbations in cyclic AMP (cAMP)-dependent signaling processes. Chronic ethanol exposure leads to desensitization of cAMP production in response to physiological ligands (heterologous desensitization). Ethanol-induced alterations in neuronal expression of G proteins Gs and Gi have been invoked as a cause of heterologous desensitization. However, effects of ethanol on G protein expression vary considerably among different experimental protocols, various brain regions and diverse neuronal cell types. Dynamic palmitoylation of G protein α subunits is critical for membrane localization and protein–protein interactions, and represents a regulatory feature of G protein function. We studied the effect of ethanol on Gαs palmitoylation. In NG108-15 rat neuroblastoma × glioma hybrid cells, acute exposure to pharmacologically relevant concentrations of ethanol (25–100 mm) inhibited basal and prostaglandin E1-stimulated incorporation of palmitate into Gαs. Exposure of NG108-15 cells to ethanol for 72 h induced a shift in Gαs to its non-palmitoylated state, coincident with an inhibition of prostaglandin E1-induced cAMP production. Both parameters were restored following 24 h of ethanol withdrawal. Chronic ethanol exposure also induced the depalmitoylation of Gαs in human embryonic kidney (HEK)293 cells that overexpress wild-type Gαs and caused heterologous desensitization of adenylyl cyclase. By contrast, HEK293 cells that express a non-palmitoylated mutant of Gαs were insensitive to heterologous desensitization after chronic ethanol exposure. In summary, the findings identify a novel effect of ethanol on post-translational lipid modification of Gαs, and represent a mechanism by which ethanol might affect adenylyl cyclase activity. |
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| title_short |
Ethanol inhibits palmitoylation of G protein Gαs |
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http://dx.doi.org/10.1046/j.1471-4159.2004.02364.x |
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Rubin, Raphael |
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10.1046/j.1471-4159.2004.02364.x |
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