Sirtuins: double players in Huntington's disease
Sirtuins are a conserved family of NAD+-dependent class III lysine deacetylases, known to regulate longevity. In mammals, the sirtuin family has seven members (SIRT1–7), which vary in enzymatic activity, subcellular distribution and targets. Pharmacological and genetic modulation of SIRTs has been w...
Ausführliche Beschreibung
Gespeichert in:
| Autor*in: |
Naia, Luana [verfasserIn] |
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E-Artikel |
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| Sprache: |
Englisch |
| Erschienen: |
2015transfer abstract |
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| Umfang: |
12 |
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| Übergeordnetes Werk: |
Enthalten in: Mixed polymer brushes with integrated antibacterial and antifouling properties - Fu, Yanhong ELSEVIER, 2019, BBA, Amsterdam |
|---|---|
| Übergeordnetes Werk: |
volume:1852 ; year:2015 ; number:10 ; pages:2183-2194 ; extent:12 |
| Links: |
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| DOI / URN: |
10.1016/j.bbadis.2015.07.003 |
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| 520 | |a Sirtuins are a conserved family of NAD+-dependent class III lysine deacetylases, known to regulate longevity. In mammals, the sirtuin family has seven members (SIRT1–7), which vary in enzymatic activity, subcellular distribution and targets. Pharmacological and genetic modulation of SIRTs has been widely spread as a promising approach to slow aging and neurodegenerative processes. Huntington's disease (HD) is a neurodegenerative disorder linked to expression of polyglutamine-expanded huntingtin (HTT) protein for which there is still no disease-reversing treatment. Studies in different animal models provide convincing evidence that SIRT1 protects both cellular and animal models from mutant HTT toxicity, however controversial results were recently reported. Indeed, as a consequence of a variety of SIRT-activation pathways, either activation or inhibition of a specific SIRT appears to be neuroprotective. Therefore, this review summarizes the recent progress and knowledge in sirtuins (particularly SIRT1–3) and their implications for HD treatment. | ||
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10.1016/j.bbadis.2015.07.003 doi GBVA2015014000027.pica (DE-627)ELV029079926 (ELSEVIER)S0925-4439(15)00195-7 DE-627 ger DE-627 rakwb eng 570 610 570 DE-600 610 DE-600 540 VZ 52.78 bkl Naia, Luana verfasserin aut Sirtuins: double players in Huntington's disease 2015transfer abstract 12 nicht spezifiziert zzz rdacontent nicht spezifiziert z rdamedia nicht spezifiziert zu rdacarrier Sirtuins are a conserved family of NAD+-dependent class III lysine deacetylases, known to regulate longevity. In mammals, the sirtuin family has seven members (SIRT1–7), which vary in enzymatic activity, subcellular distribution and targets. Pharmacological and genetic modulation of SIRTs has been widely spread as a promising approach to slow aging and neurodegenerative processes. Huntington's disease (HD) is a neurodegenerative disorder linked to expression of polyglutamine-expanded huntingtin (HTT) protein for which there is still no disease-reversing treatment. Studies in different animal models provide convincing evidence that SIRT1 protects both cellular and animal models from mutant HTT toxicity, however controversial results were recently reported. Indeed, as a consequence of a variety of SIRT-activation pathways, either activation or inhibition of a specific SIRT appears to be neuroprotective. Therefore, this review summarizes the recent progress and knowledge in sirtuins (particularly SIRT1–3) and their implications for HD treatment. Sirtuins are a conserved family of NAD+-dependent class III lysine deacetylases, known to regulate longevity. In mammals, the sirtuin family has seven members (SIRT1–7), which vary in enzymatic activity, subcellular distribution and targets. Pharmacological and genetic modulation of SIRTs has been widely spread as a promising approach to slow aging and neurodegenerative processes. Huntington's disease (HD) is a neurodegenerative disorder linked to expression of polyglutamine-expanded huntingtin (HTT) protein for which there is still no disease-reversing treatment. Studies in different animal models provide convincing evidence that SIRT1 protects both cellular and animal models from mutant HTT toxicity, however controversial results were recently reported. Indeed, as a consequence of a variety of SIRT-activation pathways, either activation or inhibition of a specific SIRT appears to be neuroprotective. Therefore, this review summarizes the recent progress and knowledge in sirtuins (particularly SIRT1–3) and their implications for HD treatment. Rego, A. Cristina oth Enthalten in Elsevier Fu, Yanhong ELSEVIER Mixed polymer brushes with integrated antibacterial and antifouling properties 2019 BBA Amsterdam (DE-627)ELV001872222 volume:1852 year:2015 number:10 pages:2183-2194 extent:12 https://doi.org/10.1016/j.bbadis.2015.07.003 Volltext GBV_USEFLAG_U GBV_ELV SYSFLAG_U SSG-OLC-PHA 52.78 Oberflächentechnik Wärmebehandlung VZ AR 1852 2015 10 2183-2194 12 045F 570 |
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10.1016/j.bbadis.2015.07.003 doi GBVA2015014000027.pica (DE-627)ELV029079926 (ELSEVIER)S0925-4439(15)00195-7 DE-627 ger DE-627 rakwb eng 570 610 570 DE-600 610 DE-600 540 VZ 52.78 bkl Naia, Luana verfasserin aut Sirtuins: double players in Huntington's disease 2015transfer abstract 12 nicht spezifiziert zzz rdacontent nicht spezifiziert z rdamedia nicht spezifiziert zu rdacarrier Sirtuins are a conserved family of NAD+-dependent class III lysine deacetylases, known to regulate longevity. In mammals, the sirtuin family has seven members (SIRT1–7), which vary in enzymatic activity, subcellular distribution and targets. Pharmacological and genetic modulation of SIRTs has been widely spread as a promising approach to slow aging and neurodegenerative processes. Huntington's disease (HD) is a neurodegenerative disorder linked to expression of polyglutamine-expanded huntingtin (HTT) protein for which there is still no disease-reversing treatment. Studies in different animal models provide convincing evidence that SIRT1 protects both cellular and animal models from mutant HTT toxicity, however controversial results were recently reported. Indeed, as a consequence of a variety of SIRT-activation pathways, either activation or inhibition of a specific SIRT appears to be neuroprotective. Therefore, this review summarizes the recent progress and knowledge in sirtuins (particularly SIRT1–3) and their implications for HD treatment. Sirtuins are a conserved family of NAD+-dependent class III lysine deacetylases, known to regulate longevity. In mammals, the sirtuin family has seven members (SIRT1–7), which vary in enzymatic activity, subcellular distribution and targets. Pharmacological and genetic modulation of SIRTs has been widely spread as a promising approach to slow aging and neurodegenerative processes. Huntington's disease (HD) is a neurodegenerative disorder linked to expression of polyglutamine-expanded huntingtin (HTT) protein for which there is still no disease-reversing treatment. Studies in different animal models provide convincing evidence that SIRT1 protects both cellular and animal models from mutant HTT toxicity, however controversial results were recently reported. Indeed, as a consequence of a variety of SIRT-activation pathways, either activation or inhibition of a specific SIRT appears to be neuroprotective. Therefore, this review summarizes the recent progress and knowledge in sirtuins (particularly SIRT1–3) and their implications for HD treatment. Rego, A. Cristina oth Enthalten in Elsevier Fu, Yanhong ELSEVIER Mixed polymer brushes with integrated antibacterial and antifouling properties 2019 BBA Amsterdam (DE-627)ELV001872222 volume:1852 year:2015 number:10 pages:2183-2194 extent:12 https://doi.org/10.1016/j.bbadis.2015.07.003 Volltext GBV_USEFLAG_U GBV_ELV SYSFLAG_U SSG-OLC-PHA 52.78 Oberflächentechnik Wärmebehandlung VZ AR 1852 2015 10 2183-2194 12 045F 570 |
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10.1016/j.bbadis.2015.07.003 doi GBVA2015014000027.pica (DE-627)ELV029079926 (ELSEVIER)S0925-4439(15)00195-7 DE-627 ger DE-627 rakwb eng 570 610 570 DE-600 610 DE-600 540 VZ 52.78 bkl Naia, Luana verfasserin aut Sirtuins: double players in Huntington's disease 2015transfer abstract 12 nicht spezifiziert zzz rdacontent nicht spezifiziert z rdamedia nicht spezifiziert zu rdacarrier Sirtuins are a conserved family of NAD+-dependent class III lysine deacetylases, known to regulate longevity. In mammals, the sirtuin family has seven members (SIRT1–7), which vary in enzymatic activity, subcellular distribution and targets. Pharmacological and genetic modulation of SIRTs has been widely spread as a promising approach to slow aging and neurodegenerative processes. Huntington's disease (HD) is a neurodegenerative disorder linked to expression of polyglutamine-expanded huntingtin (HTT) protein for which there is still no disease-reversing treatment. Studies in different animal models provide convincing evidence that SIRT1 protects both cellular and animal models from mutant HTT toxicity, however controversial results were recently reported. Indeed, as a consequence of a variety of SIRT-activation pathways, either activation or inhibition of a specific SIRT appears to be neuroprotective. Therefore, this review summarizes the recent progress and knowledge in sirtuins (particularly SIRT1–3) and their implications for HD treatment. Sirtuins are a conserved family of NAD+-dependent class III lysine deacetylases, known to regulate longevity. In mammals, the sirtuin family has seven members (SIRT1–7), which vary in enzymatic activity, subcellular distribution and targets. Pharmacological and genetic modulation of SIRTs has been widely spread as a promising approach to slow aging and neurodegenerative processes. Huntington's disease (HD) is a neurodegenerative disorder linked to expression of polyglutamine-expanded huntingtin (HTT) protein for which there is still no disease-reversing treatment. Studies in different animal models provide convincing evidence that SIRT1 protects both cellular and animal models from mutant HTT toxicity, however controversial results were recently reported. Indeed, as a consequence of a variety of SIRT-activation pathways, either activation or inhibition of a specific SIRT appears to be neuroprotective. Therefore, this review summarizes the recent progress and knowledge in sirtuins (particularly SIRT1–3) and their implications for HD treatment. Rego, A. Cristina oth Enthalten in Elsevier Fu, Yanhong ELSEVIER Mixed polymer brushes with integrated antibacterial and antifouling properties 2019 BBA Amsterdam (DE-627)ELV001872222 volume:1852 year:2015 number:10 pages:2183-2194 extent:12 https://doi.org/10.1016/j.bbadis.2015.07.003 Volltext GBV_USEFLAG_U GBV_ELV SYSFLAG_U SSG-OLC-PHA 52.78 Oberflächentechnik Wärmebehandlung VZ AR 1852 2015 10 2183-2194 12 045F 570 |
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10.1016/j.bbadis.2015.07.003 doi GBVA2015014000027.pica (DE-627)ELV029079926 (ELSEVIER)S0925-4439(15)00195-7 DE-627 ger DE-627 rakwb eng 570 610 570 DE-600 610 DE-600 540 VZ 52.78 bkl Naia, Luana verfasserin aut Sirtuins: double players in Huntington's disease 2015transfer abstract 12 nicht spezifiziert zzz rdacontent nicht spezifiziert z rdamedia nicht spezifiziert zu rdacarrier Sirtuins are a conserved family of NAD+-dependent class III lysine deacetylases, known to regulate longevity. In mammals, the sirtuin family has seven members (SIRT1–7), which vary in enzymatic activity, subcellular distribution and targets. Pharmacological and genetic modulation of SIRTs has been widely spread as a promising approach to slow aging and neurodegenerative processes. Huntington's disease (HD) is a neurodegenerative disorder linked to expression of polyglutamine-expanded huntingtin (HTT) protein for which there is still no disease-reversing treatment. Studies in different animal models provide convincing evidence that SIRT1 protects both cellular and animal models from mutant HTT toxicity, however controversial results were recently reported. Indeed, as a consequence of a variety of SIRT-activation pathways, either activation or inhibition of a specific SIRT appears to be neuroprotective. Therefore, this review summarizes the recent progress and knowledge in sirtuins (particularly SIRT1–3) and their implications for HD treatment. Sirtuins are a conserved family of NAD+-dependent class III lysine deacetylases, known to regulate longevity. In mammals, the sirtuin family has seven members (SIRT1–7), which vary in enzymatic activity, subcellular distribution and targets. Pharmacological and genetic modulation of SIRTs has been widely spread as a promising approach to slow aging and neurodegenerative processes. Huntington's disease (HD) is a neurodegenerative disorder linked to expression of polyglutamine-expanded huntingtin (HTT) protein for which there is still no disease-reversing treatment. Studies in different animal models provide convincing evidence that SIRT1 protects both cellular and animal models from mutant HTT toxicity, however controversial results were recently reported. Indeed, as a consequence of a variety of SIRT-activation pathways, either activation or inhibition of a specific SIRT appears to be neuroprotective. Therefore, this review summarizes the recent progress and knowledge in sirtuins (particularly SIRT1–3) and their implications for HD treatment. Rego, A. Cristina oth Enthalten in Elsevier Fu, Yanhong ELSEVIER Mixed polymer brushes with integrated antibacterial and antifouling properties 2019 BBA Amsterdam (DE-627)ELV001872222 volume:1852 year:2015 number:10 pages:2183-2194 extent:12 https://doi.org/10.1016/j.bbadis.2015.07.003 Volltext GBV_USEFLAG_U GBV_ELV SYSFLAG_U SSG-OLC-PHA 52.78 Oberflächentechnik Wärmebehandlung VZ AR 1852 2015 10 2183-2194 12 045F 570 |
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10.1016/j.bbadis.2015.07.003 doi GBVA2015014000027.pica (DE-627)ELV029079926 (ELSEVIER)S0925-4439(15)00195-7 DE-627 ger DE-627 rakwb eng 570 610 570 DE-600 610 DE-600 540 VZ 52.78 bkl Naia, Luana verfasserin aut Sirtuins: double players in Huntington's disease 2015transfer abstract 12 nicht spezifiziert zzz rdacontent nicht spezifiziert z rdamedia nicht spezifiziert zu rdacarrier Sirtuins are a conserved family of NAD+-dependent class III lysine deacetylases, known to regulate longevity. In mammals, the sirtuin family has seven members (SIRT1–7), which vary in enzymatic activity, subcellular distribution and targets. Pharmacological and genetic modulation of SIRTs has been widely spread as a promising approach to slow aging and neurodegenerative processes. Huntington's disease (HD) is a neurodegenerative disorder linked to expression of polyglutamine-expanded huntingtin (HTT) protein for which there is still no disease-reversing treatment. Studies in different animal models provide convincing evidence that SIRT1 protects both cellular and animal models from mutant HTT toxicity, however controversial results were recently reported. Indeed, as a consequence of a variety of SIRT-activation pathways, either activation or inhibition of a specific SIRT appears to be neuroprotective. Therefore, this review summarizes the recent progress and knowledge in sirtuins (particularly SIRT1–3) and their implications for HD treatment. Sirtuins are a conserved family of NAD+-dependent class III lysine deacetylases, known to regulate longevity. In mammals, the sirtuin family has seven members (SIRT1–7), which vary in enzymatic activity, subcellular distribution and targets. Pharmacological and genetic modulation of SIRTs has been widely spread as a promising approach to slow aging and neurodegenerative processes. Huntington's disease (HD) is a neurodegenerative disorder linked to expression of polyglutamine-expanded huntingtin (HTT) protein for which there is still no disease-reversing treatment. Studies in different animal models provide convincing evidence that SIRT1 protects both cellular and animal models from mutant HTT toxicity, however controversial results were recently reported. Indeed, as a consequence of a variety of SIRT-activation pathways, either activation or inhibition of a specific SIRT appears to be neuroprotective. Therefore, this review summarizes the recent progress and knowledge in sirtuins (particularly SIRT1–3) and their implications for HD treatment. Rego, A. Cristina oth Enthalten in Elsevier Fu, Yanhong ELSEVIER Mixed polymer brushes with integrated antibacterial and antifouling properties 2019 BBA Amsterdam (DE-627)ELV001872222 volume:1852 year:2015 number:10 pages:2183-2194 extent:12 https://doi.org/10.1016/j.bbadis.2015.07.003 Volltext GBV_USEFLAG_U GBV_ELV SYSFLAG_U SSG-OLC-PHA 52.78 Oberflächentechnik Wärmebehandlung VZ AR 1852 2015 10 2183-2194 12 045F 570 |
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Sirtuins: double players in Huntington's disease |
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Sirtuins: double players in Huntington's disease |
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Naia, Luana |
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Mixed polymer brushes with integrated antibacterial and antifouling properties |
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Mixed polymer brushes with integrated antibacterial and antifouling properties |
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sirtuins: double players in huntington's disease |
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Sirtuins: double players in Huntington's disease |
| abstract |
Sirtuins are a conserved family of NAD+-dependent class III lysine deacetylases, known to regulate longevity. In mammals, the sirtuin family has seven members (SIRT1–7), which vary in enzymatic activity, subcellular distribution and targets. Pharmacological and genetic modulation of SIRTs has been widely spread as a promising approach to slow aging and neurodegenerative processes. Huntington's disease (HD) is a neurodegenerative disorder linked to expression of polyglutamine-expanded huntingtin (HTT) protein for which there is still no disease-reversing treatment. Studies in different animal models provide convincing evidence that SIRT1 protects both cellular and animal models from mutant HTT toxicity, however controversial results were recently reported. Indeed, as a consequence of a variety of SIRT-activation pathways, either activation or inhibition of a specific SIRT appears to be neuroprotective. Therefore, this review summarizes the recent progress and knowledge in sirtuins (particularly SIRT1–3) and their implications for HD treatment. |
| abstractGer |
Sirtuins are a conserved family of NAD+-dependent class III lysine deacetylases, known to regulate longevity. In mammals, the sirtuin family has seven members (SIRT1–7), which vary in enzymatic activity, subcellular distribution and targets. Pharmacological and genetic modulation of SIRTs has been widely spread as a promising approach to slow aging and neurodegenerative processes. Huntington's disease (HD) is a neurodegenerative disorder linked to expression of polyglutamine-expanded huntingtin (HTT) protein for which there is still no disease-reversing treatment. Studies in different animal models provide convincing evidence that SIRT1 protects both cellular and animal models from mutant HTT toxicity, however controversial results were recently reported. Indeed, as a consequence of a variety of SIRT-activation pathways, either activation or inhibition of a specific SIRT appears to be neuroprotective. Therefore, this review summarizes the recent progress and knowledge in sirtuins (particularly SIRT1–3) and their implications for HD treatment. |
| abstract_unstemmed |
Sirtuins are a conserved family of NAD+-dependent class III lysine deacetylases, known to regulate longevity. In mammals, the sirtuin family has seven members (SIRT1–7), which vary in enzymatic activity, subcellular distribution and targets. Pharmacological and genetic modulation of SIRTs has been widely spread as a promising approach to slow aging and neurodegenerative processes. Huntington's disease (HD) is a neurodegenerative disorder linked to expression of polyglutamine-expanded huntingtin (HTT) protein for which there is still no disease-reversing treatment. Studies in different animal models provide convincing evidence that SIRT1 protects both cellular and animal models from mutant HTT toxicity, however controversial results were recently reported. Indeed, as a consequence of a variety of SIRT-activation pathways, either activation or inhibition of a specific SIRT appears to be neuroprotective. Therefore, this review summarizes the recent progress and knowledge in sirtuins (particularly SIRT1–3) and their implications for HD treatment. |
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Sirtuins: double players in Huntington's disease |
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Rego, A. Cristina |
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2024-07-06T20:29:28.406Z |
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