LAMP2A-mediated autophagy involved in Huntington’s disease progression
Huntington’s disease (HD) is caused by a mutant huntingtin (mHtt) protein that contains abnormally extended polyglutamine (polyQ) repeats. The process of autophagy has been implicated in clearing mHtt aggregates, and microRNAs (miRNAs) have been reported as new players to regulate autophagy. However...
Ausführliche Beschreibung
Gespeichert in:
| Autor*in: |
Choi, Seung Ho [verfasserIn] |
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| Format: |
E-Artikel |
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| Sprache: |
Englisch |
| Erschienen: |
2021transfer abstract |
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| Schlagwörter: |
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| Umfang: |
7 |
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| Übergeordnetes Werk: |
Enthalten in: Preparation and characterization of glass-ceramics via co-sintering of coal fly ash and oil shale ash-derived amorphous slag - Zhang, Zhikun ELSEVIER, 2019, BBRC, Orlando, Fla |
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| Übergeordnetes Werk: |
volume:534 ; year:2021 ; day:1 ; month:01 ; pages:561-567 ; extent:7 |
| Links: |
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| DOI / URN: |
10.1016/j.bbrc.2020.11.042 |
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ELV052601390 |
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| 520 | |a Huntington’s disease (HD) is caused by a mutant huntingtin (mHtt) protein that contains abnormally extended polyglutamine (polyQ) repeats. The process of autophagy has been implicated in clearing mHtt aggregates, and microRNAs (miRNAs) have been reported as new players to regulate autophagy. However, the autophagy-associated target molecule of let7b miRNA remains unclear in HD. The present study showed that extended polyQ in mouse striatal neurons increased lysosomal membrane-associated protein 2A (LAMP2A) levels and influenced the inflammatory conditions, and these augmented levels correlated to the let7b miRNA expression level. The upregulated let7b increased LAMP2A and reduced the extended polyQ in mouse striatal cells. The let7b level was highly expressed in the striatum of pre-onset HD mice, whereas it was significantly reduced in the post-onset HD striatum. Considering the level changing pattern of let7b, LAMP2A protein levels were increased in the striatum of pre-onset HD mice, but decreased in the striatum of post-onset HD mice. These results suggest that LAMP2A related to chaperone-mediated autophagy (CMA) capacity might play an important role in HD symptom onset and progression. | ||
| 520 | |a Huntington’s disease (HD) is caused by a mutant huntingtin (mHtt) protein that contains abnormally extended polyglutamine (polyQ) repeats. The process of autophagy has been implicated in clearing mHtt aggregates, and microRNAs (miRNAs) have been reported as new players to regulate autophagy. However, the autophagy-associated target molecule of let7b miRNA remains unclear in HD. The present study showed that extended polyQ in mouse striatal neurons increased lysosomal membrane-associated protein 2A (LAMP2A) levels and influenced the inflammatory conditions, and these augmented levels correlated to the let7b miRNA expression level. The upregulated let7b increased LAMP2A and reduced the extended polyQ in mouse striatal cells. The let7b level was highly expressed in the striatum of pre-onset HD mice, whereas it was significantly reduced in the post-onset HD striatum. Considering the level changing pattern of let7b, LAMP2A protein levels were increased in the striatum of pre-onset HD mice, but decreased in the striatum of post-onset HD mice. These results suggest that LAMP2A related to chaperone-mediated autophagy (CMA) capacity might play an important role in HD symptom onset and progression. | ||
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| 773 | 0 | 8 | |i Enthalten in |n Academic Press |a Zhang, Zhikun ELSEVIER |t Preparation and characterization of glass-ceramics via co-sintering of coal fly ash and oil shale ash-derived amorphous slag |d 2019 |d BBRC |g Orlando, Fla |w (DE-627)ELV002811154 |
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10.1016/j.bbrc.2020.11.042 doi /cbs_pica/cbs_olc/import_discovery/elsevier/einzuspielen/GBV00000000001250.pica (DE-627)ELV052601390 (ELSEVIER)S0006-291X(20)32088-X DE-627 ger DE-627 rakwb eng 670 VZ 51.60 bkl 58.45 bkl Choi, Seung Ho verfasserin aut LAMP2A-mediated autophagy involved in Huntington’s disease progression 2021transfer abstract 7 nicht spezifiziert zzz rdacontent nicht spezifiziert z rdamedia nicht spezifiziert zu rdacarrier Huntington’s disease (HD) is caused by a mutant huntingtin (mHtt) protein that contains abnormally extended polyglutamine (polyQ) repeats. The process of autophagy has been implicated in clearing mHtt aggregates, and microRNAs (miRNAs) have been reported as new players to regulate autophagy. However, the autophagy-associated target molecule of let7b miRNA remains unclear in HD. The present study showed that extended polyQ in mouse striatal neurons increased lysosomal membrane-associated protein 2A (LAMP2A) levels and influenced the inflammatory conditions, and these augmented levels correlated to the let7b miRNA expression level. The upregulated let7b increased LAMP2A and reduced the extended polyQ in mouse striatal cells. The let7b level was highly expressed in the striatum of pre-onset HD mice, whereas it was significantly reduced in the post-onset HD striatum. Considering the level changing pattern of let7b, LAMP2A protein levels were increased in the striatum of pre-onset HD mice, but decreased in the striatum of post-onset HD mice. These results suggest that LAMP2A related to chaperone-mediated autophagy (CMA) capacity might play an important role in HD symptom onset and progression. Huntington’s disease (HD) is caused by a mutant huntingtin (mHtt) protein that contains abnormally extended polyglutamine (polyQ) repeats. The process of autophagy has been implicated in clearing mHtt aggregates, and microRNAs (miRNAs) have been reported as new players to regulate autophagy. However, the autophagy-associated target molecule of let7b miRNA remains unclear in HD. The present study showed that extended polyQ in mouse striatal neurons increased lysosomal membrane-associated protein 2A (LAMP2A) levels and influenced the inflammatory conditions, and these augmented levels correlated to the let7b miRNA expression level. The upregulated let7b increased LAMP2A and reduced the extended polyQ in mouse striatal cells. The let7b level was highly expressed in the striatum of pre-onset HD mice, whereas it was significantly reduced in the post-onset HD striatum. Considering the level changing pattern of let7b, LAMP2A protein levels were increased in the striatum of pre-onset HD mice, but decreased in the striatum of post-onset HD mice. These results suggest that LAMP2A related to chaperone-mediated autophagy (CMA) capacity might play an important role in HD symptom onset and progression. Huntingtin Elsevier let7b Elsevier miRNA Elsevier Autophagy Elsevier LAMP2A Elsevier Cho, KyoungJoo oth Enthalten in Academic Press Zhang, Zhikun ELSEVIER Preparation and characterization of glass-ceramics via co-sintering of coal fly ash and oil shale ash-derived amorphous slag 2019 BBRC Orlando, Fla (DE-627)ELV002811154 volume:534 year:2021 day:1 month:01 pages:561-567 extent:7 https://doi.org/10.1016/j.bbrc.2020.11.042 Volltext GBV_USEFLAG_U GBV_ELV SYSFLAG_U 51.60 Keramische Werkstoffe Hartstoffe Werkstoffkunde VZ 58.45 Gesteinshüttenkunde VZ AR 534 2021 1 0101 561-567 7 |
| spelling |
10.1016/j.bbrc.2020.11.042 doi /cbs_pica/cbs_olc/import_discovery/elsevier/einzuspielen/GBV00000000001250.pica (DE-627)ELV052601390 (ELSEVIER)S0006-291X(20)32088-X DE-627 ger DE-627 rakwb eng 670 VZ 51.60 bkl 58.45 bkl Choi, Seung Ho verfasserin aut LAMP2A-mediated autophagy involved in Huntington’s disease progression 2021transfer abstract 7 nicht spezifiziert zzz rdacontent nicht spezifiziert z rdamedia nicht spezifiziert zu rdacarrier Huntington’s disease (HD) is caused by a mutant huntingtin (mHtt) protein that contains abnormally extended polyglutamine (polyQ) repeats. The process of autophagy has been implicated in clearing mHtt aggregates, and microRNAs (miRNAs) have been reported as new players to regulate autophagy. However, the autophagy-associated target molecule of let7b miRNA remains unclear in HD. The present study showed that extended polyQ in mouse striatal neurons increased lysosomal membrane-associated protein 2A (LAMP2A) levels and influenced the inflammatory conditions, and these augmented levels correlated to the let7b miRNA expression level. The upregulated let7b increased LAMP2A and reduced the extended polyQ in mouse striatal cells. The let7b level was highly expressed in the striatum of pre-onset HD mice, whereas it was significantly reduced in the post-onset HD striatum. Considering the level changing pattern of let7b, LAMP2A protein levels were increased in the striatum of pre-onset HD mice, but decreased in the striatum of post-onset HD mice. These results suggest that LAMP2A related to chaperone-mediated autophagy (CMA) capacity might play an important role in HD symptom onset and progression. Huntington’s disease (HD) is caused by a mutant huntingtin (mHtt) protein that contains abnormally extended polyglutamine (polyQ) repeats. The process of autophagy has been implicated in clearing mHtt aggregates, and microRNAs (miRNAs) have been reported as new players to regulate autophagy. However, the autophagy-associated target molecule of let7b miRNA remains unclear in HD. The present study showed that extended polyQ in mouse striatal neurons increased lysosomal membrane-associated protein 2A (LAMP2A) levels and influenced the inflammatory conditions, and these augmented levels correlated to the let7b miRNA expression level. The upregulated let7b increased LAMP2A and reduced the extended polyQ in mouse striatal cells. The let7b level was highly expressed in the striatum of pre-onset HD mice, whereas it was significantly reduced in the post-onset HD striatum. Considering the level changing pattern of let7b, LAMP2A protein levels were increased in the striatum of pre-onset HD mice, but decreased in the striatum of post-onset HD mice. These results suggest that LAMP2A related to chaperone-mediated autophagy (CMA) capacity might play an important role in HD symptom onset and progression. Huntingtin Elsevier let7b Elsevier miRNA Elsevier Autophagy Elsevier LAMP2A Elsevier Cho, KyoungJoo oth Enthalten in Academic Press Zhang, Zhikun ELSEVIER Preparation and characterization of glass-ceramics via co-sintering of coal fly ash and oil shale ash-derived amorphous slag 2019 BBRC Orlando, Fla (DE-627)ELV002811154 volume:534 year:2021 day:1 month:01 pages:561-567 extent:7 https://doi.org/10.1016/j.bbrc.2020.11.042 Volltext GBV_USEFLAG_U GBV_ELV SYSFLAG_U 51.60 Keramische Werkstoffe Hartstoffe Werkstoffkunde VZ 58.45 Gesteinshüttenkunde VZ AR 534 2021 1 0101 561-567 7 |
| allfields_unstemmed |
10.1016/j.bbrc.2020.11.042 doi /cbs_pica/cbs_olc/import_discovery/elsevier/einzuspielen/GBV00000000001250.pica (DE-627)ELV052601390 (ELSEVIER)S0006-291X(20)32088-X DE-627 ger DE-627 rakwb eng 670 VZ 51.60 bkl 58.45 bkl Choi, Seung Ho verfasserin aut LAMP2A-mediated autophagy involved in Huntington’s disease progression 2021transfer abstract 7 nicht spezifiziert zzz rdacontent nicht spezifiziert z rdamedia nicht spezifiziert zu rdacarrier Huntington’s disease (HD) is caused by a mutant huntingtin (mHtt) protein that contains abnormally extended polyglutamine (polyQ) repeats. The process of autophagy has been implicated in clearing mHtt aggregates, and microRNAs (miRNAs) have been reported as new players to regulate autophagy. However, the autophagy-associated target molecule of let7b miRNA remains unclear in HD. The present study showed that extended polyQ in mouse striatal neurons increased lysosomal membrane-associated protein 2A (LAMP2A) levels and influenced the inflammatory conditions, and these augmented levels correlated to the let7b miRNA expression level. The upregulated let7b increased LAMP2A and reduced the extended polyQ in mouse striatal cells. The let7b level was highly expressed in the striatum of pre-onset HD mice, whereas it was significantly reduced in the post-onset HD striatum. Considering the level changing pattern of let7b, LAMP2A protein levels were increased in the striatum of pre-onset HD mice, but decreased in the striatum of post-onset HD mice. These results suggest that LAMP2A related to chaperone-mediated autophagy (CMA) capacity might play an important role in HD symptom onset and progression. Huntington’s disease (HD) is caused by a mutant huntingtin (mHtt) protein that contains abnormally extended polyglutamine (polyQ) repeats. The process of autophagy has been implicated in clearing mHtt aggregates, and microRNAs (miRNAs) have been reported as new players to regulate autophagy. However, the autophagy-associated target molecule of let7b miRNA remains unclear in HD. The present study showed that extended polyQ in mouse striatal neurons increased lysosomal membrane-associated protein 2A (LAMP2A) levels and influenced the inflammatory conditions, and these augmented levels correlated to the let7b miRNA expression level. The upregulated let7b increased LAMP2A and reduced the extended polyQ in mouse striatal cells. The let7b level was highly expressed in the striatum of pre-onset HD mice, whereas it was significantly reduced in the post-onset HD striatum. Considering the level changing pattern of let7b, LAMP2A protein levels were increased in the striatum of pre-onset HD mice, but decreased in the striatum of post-onset HD mice. These results suggest that LAMP2A related to chaperone-mediated autophagy (CMA) capacity might play an important role in HD symptom onset and progression. Huntingtin Elsevier let7b Elsevier miRNA Elsevier Autophagy Elsevier LAMP2A Elsevier Cho, KyoungJoo oth Enthalten in Academic Press Zhang, Zhikun ELSEVIER Preparation and characterization of glass-ceramics via co-sintering of coal fly ash and oil shale ash-derived amorphous slag 2019 BBRC Orlando, Fla (DE-627)ELV002811154 volume:534 year:2021 day:1 month:01 pages:561-567 extent:7 https://doi.org/10.1016/j.bbrc.2020.11.042 Volltext GBV_USEFLAG_U GBV_ELV SYSFLAG_U 51.60 Keramische Werkstoffe Hartstoffe Werkstoffkunde VZ 58.45 Gesteinshüttenkunde VZ AR 534 2021 1 0101 561-567 7 |
| allfieldsGer |
10.1016/j.bbrc.2020.11.042 doi /cbs_pica/cbs_olc/import_discovery/elsevier/einzuspielen/GBV00000000001250.pica (DE-627)ELV052601390 (ELSEVIER)S0006-291X(20)32088-X DE-627 ger DE-627 rakwb eng 670 VZ 51.60 bkl 58.45 bkl Choi, Seung Ho verfasserin aut LAMP2A-mediated autophagy involved in Huntington’s disease progression 2021transfer abstract 7 nicht spezifiziert zzz rdacontent nicht spezifiziert z rdamedia nicht spezifiziert zu rdacarrier Huntington’s disease (HD) is caused by a mutant huntingtin (mHtt) protein that contains abnormally extended polyglutamine (polyQ) repeats. The process of autophagy has been implicated in clearing mHtt aggregates, and microRNAs (miRNAs) have been reported as new players to regulate autophagy. However, the autophagy-associated target molecule of let7b miRNA remains unclear in HD. The present study showed that extended polyQ in mouse striatal neurons increased lysosomal membrane-associated protein 2A (LAMP2A) levels and influenced the inflammatory conditions, and these augmented levels correlated to the let7b miRNA expression level. The upregulated let7b increased LAMP2A and reduced the extended polyQ in mouse striatal cells. The let7b level was highly expressed in the striatum of pre-onset HD mice, whereas it was significantly reduced in the post-onset HD striatum. Considering the level changing pattern of let7b, LAMP2A protein levels were increased in the striatum of pre-onset HD mice, but decreased in the striatum of post-onset HD mice. These results suggest that LAMP2A related to chaperone-mediated autophagy (CMA) capacity might play an important role in HD symptom onset and progression. Huntington’s disease (HD) is caused by a mutant huntingtin (mHtt) protein that contains abnormally extended polyglutamine (polyQ) repeats. The process of autophagy has been implicated in clearing mHtt aggregates, and microRNAs (miRNAs) have been reported as new players to regulate autophagy. However, the autophagy-associated target molecule of let7b miRNA remains unclear in HD. The present study showed that extended polyQ in mouse striatal neurons increased lysosomal membrane-associated protein 2A (LAMP2A) levels and influenced the inflammatory conditions, and these augmented levels correlated to the let7b miRNA expression level. The upregulated let7b increased LAMP2A and reduced the extended polyQ in mouse striatal cells. The let7b level was highly expressed in the striatum of pre-onset HD mice, whereas it was significantly reduced in the post-onset HD striatum. Considering the level changing pattern of let7b, LAMP2A protein levels were increased in the striatum of pre-onset HD mice, but decreased in the striatum of post-onset HD mice. These results suggest that LAMP2A related to chaperone-mediated autophagy (CMA) capacity might play an important role in HD symptom onset and progression. Huntingtin Elsevier let7b Elsevier miRNA Elsevier Autophagy Elsevier LAMP2A Elsevier Cho, KyoungJoo oth Enthalten in Academic Press Zhang, Zhikun ELSEVIER Preparation and characterization of glass-ceramics via co-sintering of coal fly ash and oil shale ash-derived amorphous slag 2019 BBRC Orlando, Fla (DE-627)ELV002811154 volume:534 year:2021 day:1 month:01 pages:561-567 extent:7 https://doi.org/10.1016/j.bbrc.2020.11.042 Volltext GBV_USEFLAG_U GBV_ELV SYSFLAG_U 51.60 Keramische Werkstoffe Hartstoffe Werkstoffkunde VZ 58.45 Gesteinshüttenkunde VZ AR 534 2021 1 0101 561-567 7 |
| allfieldsSound |
10.1016/j.bbrc.2020.11.042 doi /cbs_pica/cbs_olc/import_discovery/elsevier/einzuspielen/GBV00000000001250.pica (DE-627)ELV052601390 (ELSEVIER)S0006-291X(20)32088-X DE-627 ger DE-627 rakwb eng 670 VZ 51.60 bkl 58.45 bkl Choi, Seung Ho verfasserin aut LAMP2A-mediated autophagy involved in Huntington’s disease progression 2021transfer abstract 7 nicht spezifiziert zzz rdacontent nicht spezifiziert z rdamedia nicht spezifiziert zu rdacarrier Huntington’s disease (HD) is caused by a mutant huntingtin (mHtt) protein that contains abnormally extended polyglutamine (polyQ) repeats. The process of autophagy has been implicated in clearing mHtt aggregates, and microRNAs (miRNAs) have been reported as new players to regulate autophagy. However, the autophagy-associated target molecule of let7b miRNA remains unclear in HD. The present study showed that extended polyQ in mouse striatal neurons increased lysosomal membrane-associated protein 2A (LAMP2A) levels and influenced the inflammatory conditions, and these augmented levels correlated to the let7b miRNA expression level. The upregulated let7b increased LAMP2A and reduced the extended polyQ in mouse striatal cells. The let7b level was highly expressed in the striatum of pre-onset HD mice, whereas it was significantly reduced in the post-onset HD striatum. Considering the level changing pattern of let7b, LAMP2A protein levels were increased in the striatum of pre-onset HD mice, but decreased in the striatum of post-onset HD mice. These results suggest that LAMP2A related to chaperone-mediated autophagy (CMA) capacity might play an important role in HD symptom onset and progression. Huntington’s disease (HD) is caused by a mutant huntingtin (mHtt) protein that contains abnormally extended polyglutamine (polyQ) repeats. The process of autophagy has been implicated in clearing mHtt aggregates, and microRNAs (miRNAs) have been reported as new players to regulate autophagy. However, the autophagy-associated target molecule of let7b miRNA remains unclear in HD. The present study showed that extended polyQ in mouse striatal neurons increased lysosomal membrane-associated protein 2A (LAMP2A) levels and influenced the inflammatory conditions, and these augmented levels correlated to the let7b miRNA expression level. The upregulated let7b increased LAMP2A and reduced the extended polyQ in mouse striatal cells. The let7b level was highly expressed in the striatum of pre-onset HD mice, whereas it was significantly reduced in the post-onset HD striatum. Considering the level changing pattern of let7b, LAMP2A protein levels were increased in the striatum of pre-onset HD mice, but decreased in the striatum of post-onset HD mice. These results suggest that LAMP2A related to chaperone-mediated autophagy (CMA) capacity might play an important role in HD symptom onset and progression. Huntingtin Elsevier let7b Elsevier miRNA Elsevier Autophagy Elsevier LAMP2A Elsevier Cho, KyoungJoo oth Enthalten in Academic Press Zhang, Zhikun ELSEVIER Preparation and characterization of glass-ceramics via co-sintering of coal fly ash and oil shale ash-derived amorphous slag 2019 BBRC Orlando, Fla (DE-627)ELV002811154 volume:534 year:2021 day:1 month:01 pages:561-567 extent:7 https://doi.org/10.1016/j.bbrc.2020.11.042 Volltext GBV_USEFLAG_U GBV_ELV SYSFLAG_U 51.60 Keramische Werkstoffe Hartstoffe Werkstoffkunde VZ 58.45 Gesteinshüttenkunde VZ AR 534 2021 1 0101 561-567 7 |
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Enthalten in Preparation and characterization of glass-ceramics via co-sintering of coal fly ash and oil shale ash-derived amorphous slag Orlando, Fla volume:534 year:2021 day:1 month:01 pages:561-567 extent:7 |
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Enthalten in Preparation and characterization of glass-ceramics via co-sintering of coal fly ash and oil shale ash-derived amorphous slag Orlando, Fla volume:534 year:2021 day:1 month:01 pages:561-567 extent:7 |
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Preparation and characterization of glass-ceramics via co-sintering of coal fly ash and oil shale ash-derived amorphous slag |
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LAMP2A-mediated autophagy involved in Huntington’s disease progression |
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Huntington’s disease (HD) is caused by a mutant huntingtin (mHtt) protein that contains abnormally extended polyglutamine (polyQ) repeats. The process of autophagy has been implicated in clearing mHtt aggregates, and microRNAs (miRNAs) have been reported as new players to regulate autophagy. However, the autophagy-associated target molecule of let7b miRNA remains unclear in HD. The present study showed that extended polyQ in mouse striatal neurons increased lysosomal membrane-associated protein 2A (LAMP2A) levels and influenced the inflammatory conditions, and these augmented levels correlated to the let7b miRNA expression level. The upregulated let7b increased LAMP2A and reduced the extended polyQ in mouse striatal cells. The let7b level was highly expressed in the striatum of pre-onset HD mice, whereas it was significantly reduced in the post-onset HD striatum. Considering the level changing pattern of let7b, LAMP2A protein levels were increased in the striatum of pre-onset HD mice, but decreased in the striatum of post-onset HD mice. These results suggest that LAMP2A related to chaperone-mediated autophagy (CMA) capacity might play an important role in HD symptom onset and progression. |
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Huntington’s disease (HD) is caused by a mutant huntingtin (mHtt) protein that contains abnormally extended polyglutamine (polyQ) repeats. The process of autophagy has been implicated in clearing mHtt aggregates, and microRNAs (miRNAs) have been reported as new players to regulate autophagy. However, the autophagy-associated target molecule of let7b miRNA remains unclear in HD. The present study showed that extended polyQ in mouse striatal neurons increased lysosomal membrane-associated protein 2A (LAMP2A) levels and influenced the inflammatory conditions, and these augmented levels correlated to the let7b miRNA expression level. The upregulated let7b increased LAMP2A and reduced the extended polyQ in mouse striatal cells. The let7b level was highly expressed in the striatum of pre-onset HD mice, whereas it was significantly reduced in the post-onset HD striatum. Considering the level changing pattern of let7b, LAMP2A protein levels were increased in the striatum of pre-onset HD mice, but decreased in the striatum of post-onset HD mice. These results suggest that LAMP2A related to chaperone-mediated autophagy (CMA) capacity might play an important role in HD symptom onset and progression. |
| abstract_unstemmed |
Huntington’s disease (HD) is caused by a mutant huntingtin (mHtt) protein that contains abnormally extended polyglutamine (polyQ) repeats. The process of autophagy has been implicated in clearing mHtt aggregates, and microRNAs (miRNAs) have been reported as new players to regulate autophagy. However, the autophagy-associated target molecule of let7b miRNA remains unclear in HD. The present study showed that extended polyQ in mouse striatal neurons increased lysosomal membrane-associated protein 2A (LAMP2A) levels and influenced the inflammatory conditions, and these augmented levels correlated to the let7b miRNA expression level. The upregulated let7b increased LAMP2A and reduced the extended polyQ in mouse striatal cells. The let7b level was highly expressed in the striatum of pre-onset HD mice, whereas it was significantly reduced in the post-onset HD striatum. Considering the level changing pattern of let7b, LAMP2A protein levels were increased in the striatum of pre-onset HD mice, but decreased in the striatum of post-onset HD mice. These results suggest that LAMP2A related to chaperone-mediated autophagy (CMA) capacity might play an important role in HD symptom onset and progression. |
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LAMP2A-mediated autophagy involved in Huntington’s disease progression |
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