The DOI matches its Crossref record; 6 of the 6 references it cites were found in a registry or an index.
Disruption of astrocyte-neuron cholesterol cross talk affects neuronal function in Huntington’s disease
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SREBP2 gene silencing in wild-type astrocytes has detrimental effects on HD neurons.
“SREBP2 gene silencing in wild-type (wt) astrocytes has detrimental effects on HD neurons 22 ,”
From SREBP2 gene therapy targeting striatal astrocytes ameliorates Huntington’s disease phenotypes (2021) · cites this paper as [22]
Forced expression of the N-terminal active fragment of SREBP2 in HD astrocytes reverses neurite outgrowth and synaptic defects in HD neurons.
“while the forced expression of the N-terminal active fragment of SREBP2 in HD astrocytes reverses neurite outgrowth and synaptic defects in HD neurons 22 .”
From SREBP2 gene therapy targeting striatal astrocytes ameliorates Huntington’s disease phenotypes (2021) · cites this paper as [22]
Reduced activity of SREBP2 in the presence of mutant HTT underlies the reduced cholesterol biosynthesis in HD, likely through sequestration of the SREBP2/importin b complex required for nuclear import.
“The underlying molecular mechanism implicates reduced activity of SREBP2 in the presence of mutant HTT 17,22 , likely through sequestration in the cytoplasm of the SREBP2/importin b complex required for nuclear import 23 .”
From SREBP2 gene therapy targeting striatal astrocytes ameliorates Huntington’s disease phenotypes (2021) · cites this paper as [22]
In these conditions, neuronal function and morphology are fully reestablished.
“In these conditions, we showed that neuronal function and morphology are fully reestablished 22 .”
From SREBP2 gene therapy targeting striatal astrocytes ameliorates Huntington’s disease phenotypes (2021) · cites this paper as [22]
This cross-talk is severely damaged in vitro in the presence of muHTT, due to reduced activity of SREBP2, but can be rescued when HD astrocytes overexpressing SREBP2 are co-cultured with HD neurons.
“This cross-talk is severely damaged in vitro in the presence of muHTT, due to reduced activity of SREBP2, but it can be rescued when HD astrocytes overexpressing SREBP2 are co-cultured with HD neurons.”
From SREBP2 gene therapy targeting striatal astrocytes ameliorates Huntington’s disease phenotypes (2021) · cites this paper as [22]
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Citations
Cites
Non–cell autonomous toxicity in neurodegenerative disorders: ALS and beyond
Ilieva, H., Polymenidou, M., & Cleveland, D. W. (2009) · Journal of Cell Biology · doi:10.1083/jcb.200908164 · Cited by 1,008
ApoE Promotes the Proteolytic Degradation of Aβ
Jiang, Q., Lee, C. Y. D., Mandrekar, S., Wilkinson, B., Cramer, P., Zelcer, N., Mann, K., Lamb, B., Willson, T. M., Collins, J. L., et al. (2008) · Neuron · doi:10.1016/j.neuron.2008.04.010 · Cited by 876
Regulation of synaptic connectivity by glia.
Eroglu, C., & Barres, B. A. (2010) · Nature · doi:10.1038/nature09612 · Cited by 813
Cholesterol metabolism in neurons and astrocytes
Pfrieger, F. W., & Ungerer, N. (2011) · Progress in Lipid Research · doi:10.1016/j.plipres.2011.06.002 · Cited by 500
Lipoprotein receptors in the nervous system
Herz, J., & Bock, H. H. (2002) · Annual Review of Biochemistry · doi:10.1146/annurev.biochem.71.110601.135342 · Cited by 457
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Wahrle, S. E., Jiang, H., Parsadanian, M., Kim, J., Li, A., Knoten, A., Jain, S., Hirsch-Reinshagen, V., Wellington, C. L., Bales, K. R., et al. (2008) · Journal of Clinical Investigation · doi:10.1172/jci33622 · Cited by 370 · cited 1×
“level in the GCM (GCMR6/2ABCA1) compared with GCMR6/2pcDNA (Figure 3f, left), in agreement with the evidence that greater than sixfold overexpression of ABCA1 in the mouse brain is required to alter apoE levels.(22)”
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Self-citationCotto, B., Natarajaseenivasan, K., Ferrero, K., Wesley, L., Sayre, M., & Langford, D. (2018) · Glia · doi:10.1002/glia.23291 · Cited by 30
“In agreement with human and animal studies, in vitro studies demonstrate that depletion of cholesterol has deleterious effects on neuronal function (Frank et al. 2008; Fukui, Ferris, & Kahn, 2016; Thiele, Hannah, Fahrenholz, & Huttner, 2000; Valenza et al. 2015).”
BackgroundResultCholesterol Metabolism in CNS Diseases: The Potential of SREBP2 and LXR as Therapeutic Targets
Wang, N.-Q., Sun, P.-X., Shen, Q.-Q., & Deng, M.-Y. (2025) · Molecular Neurobiology · doi:10.1007/s12035-024-04672-w · Cited by 19
Metadata
- Authors
- Valenza, M., Marullo, M., Di Paolo, E., Cesana, E., Zuccato, C., Biella, G., & Cattaneo, E.
- Venue
- Cell Death & Differentiation
- Published
- 2014-10-10
- Volume
- 22
- Issue
- 4
- Pages
- 690-702
- ISSN
- 1350-9047
- 1476-5403
- Cited by
- 133
- References
- 6
- Language
- en
- Licence
- www.springer.com/tdm (tdm)
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