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Condition: Huntington's Disease

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Total 63 results found since Jan 2013.

SIRT2 regulates insulin sensitivity in insulin-resistant neuronal cells.
In this study, we report the role of SIRT2 in regulating insulin-sensitivity in neuronal cells in vitro. Using approaches like pharmacological inhibition of SIRT2, siRNA mediated SIRT2 knockdown and over-expression of wild-type and catalytically-mutated SIRT2, we observed that downregulation of SIRT2 ameliorated the reduced activity of AKT and increased insulin-stimulated glucose uptake in insulin resistant neuro-2a cells. The data was supported by over expression of catalytically-inactive SIRT2 in insulin-resistant human SH-SY5Y neuronal cells. Data highlights a crucial role of SIRT2 in regulation of neuronal insulin sens...
Source: Biochemical and Biophysical Research communications - May 5, 2016 Category: Biochemistry Authors: Arora A, Dey CS Tags: Biochem Biophys Res Commun Source Type: research

Coupling of d2R short but not d2R Long receptor isoform to the Rho/Rock signaling pathway renders striatal neurons vulnerable to mutant huntingtin
This article is protected by copyright. All rights reserved.
Source: European Journal of Neuroscience - August 31, 2016 Category: Neuroscience Authors: Beatriz Galan ‐Rodriguez, Elodie Martin, Emmanuel Brouillet, Nicole Déglon, Sandrine Betuing, Jocelyne Caboche Tags: Special Issue Article Source Type: research

GSE98739 RNA-seq dataset for Identifying Novel Therapeutic Targets by Combining Transcriptional Data with Ordinal Clinical Measurements
We report an analytical approach to integrate ordinal clinical information with transcriptomics. We have applied this method to public data for a large cohort of Huntington ’s disease patients and controls, identifying and prioritizing phenotype-associated genes. To validate the approach, we have performed viability, siRNA knockdown, mRNA-seq, and ChIP-seq on striatal precursor cells expressing either full-length wild type (STHdh Q7) or mutant huntingtin (STHdh Q111) . We have verified the role of a high-ranked gene in dysregulation of sphingolipid metabolism in the disease and demonstrated that inhibiting the enzyme, SP...
Source: GEO: Gene Expression Omnibus - May 11, 2017 Category: Genetics & Stem Cells Tags: Expression profiling by high throughput sequencing Mus musculus Source Type: research

GSE98738 ChIP-seq dataset for H3K9ac in Identifying Novel Therapeutic Targets by Combining Transcriptional Data with Ordinal Clinical Measurements
We report an analytical approach to integrate ordinal clinical information with transcriptomics. We have applied this method to public data for a large cohort of Huntington ’s disease patients and controls, identifying and prioritizing phenotype-associated genes. To validate the approach, we have performed viability, siRNA knockdown, mRNA-seq, and ChIP-seq on striatal precursor cells expressing either full-length wild type (STHdh Q7) or mutant huntingtin (STHdh Q111) . We have verified the role of a high-ranked gene in dysregulation of sphingolipid metabolism in the disease and demonstrated that inhibiting the enzyme, SP...
Source: GEO: Gene Expression Omnibus - May 11, 2017 Category: Genetics & Stem Cells Tags: Genome binding/occupancy profiling by high throughput sequencing Mus musculus Source Type: research

Knockdown of HIP1 expression promotes ligand ‑induced endocytosis of EGFR in HeLa cells.
In this study, the effects of HIP1 on the degradation of EGFR, which have important roles in carcinogenesis after EGF stimulation, were examined. After screening 17 cell lines, the coexpression of HIP1 and EGFR was detected in HeLa cells. Accordingly, the expression of HIP1 was knocked down in HeLa cells using various HIP1 siRNA sequences. The endocytosis of EGFR and localization of clathrin in HeLa cells were examined after stimulation by EGF at various concentrations (i.e., 1.5 and 100 ng/ml). After HIP1 expression was blocked by siRNAs, EGFR endocytosis was accelerated and this effect was dependent on the EGF concentra...
Source: Oncology Reports - October 20, 2017 Category: Cancer & Oncology Tags: Oncol Rep Source Type: research

BGRF and SILS scientists analyze viability of shRNA therapy for Huntington's Disease
(Biogerontology Research Foundation) Researchers from the Biogerontology Research Foundation, Department of Molecular Neuroscience at the Swammerdam Institute for Life Sciences at the University of Amsterdam, and the Department of Neurobiology, Care Sciences and Society at the Karolinska Institute announce the publication of a paper in Translational Neurodegeneration, a BioMedCentral journal, titled RNAi mechanisms in Huntington's disease therapy: siRNA versus shRNA.
Source: EurekAlert! - Medicine and Health - December 1, 2017 Category: International Medicine & Public Health Source Type: news

Myeloid Derived Suppressor Cells Interactions With Natural Killer Cells and Pro-angiogenic Activities: Roles in Tumor Progression
Conclusions MDSC are major players in the immunosuppressive scenario in cancer, thanks to their phenotype heterogeneity and critical interaction with several innate immune cells, thus representing a crucial target in oncology. Here we reviewed the interactions of MDSCs with NK cells. The contribution of key cytokines, chemokines and mediators active in this process have been discussed. We also described the contribution of MDSC on angiogenesis directly or indirectly through interactions with NK and immunosuppressive activities. A parallel of the cancer associated to the decidual counterpart of these cells is discussed, a...
Source: Frontiers in Immunology - April 17, 2019 Category: Allergy & Immunology Source Type: research

Assessing Triplet Repeat Expansions in Human SVG-A Cell Culture.
Abstract Determining the molecular mechanisms that contribute to trinucleotide repeat (TNR) expansions is essential to understanding the origin of genetically inherited diseases, such as Huntington's disease, and to inform efforts in developing therapeutic treatments. As one resource to probe the mechanisms of TNR expansions, we describe an expansion assay in human tissue culture cells. The cell line SVG-A, derived from human astrocytes, has the important property of supporting expansions in culture, unlike many cell lines derived from patients. SVG-A cells are also amenable to standard genetic and biochemical tec...
Source: Mol Biol Cell - October 7, 2019 Category: Molecular Biology Authors: Williams GM, Lahue RS Tags: Methods Mol Biol Source Type: research

Loss of huntingtin function slows synaptic vesicle endocytosis in striatal neurons from the httQ140/Q140 mouse model of Huntington's disease.
Abstract Huntington's disease (HD) is caused by CAG repeat expansion within the HTT gene, with the dysfunction and eventual loss of striatal medium spiny neurons a notable feature. Since medium spiny neurons receive high amounts of synaptic input, we hypothesised that this vulnerability originates from an inability to sustain presynaptic performance during intense neuronal activity. To test this hypothesis, primary cultures of either hippocampal or striatal neurons were prepared from either wild-type mice or a knock-in HD mouse model which contains 140 poly-glutamine repeats in the huntingtin protein (httQ140/Q140...
Source: Neurobiology of Disease - October 11, 2019 Category: Neurology Authors: McAdam RL, Morton A, Gordon SL, Alterman JF, Khvorova A, Cousin MA, Smillie KJ Tags: Neurobiol Dis Source Type: research

GSE162349 mRNA Sequencing of control and huntington's disease iPSC-derived medium spiny neuron-like cells and Q175 HET or WT mice. Plus and minus knockdown of PIAS1.
Contributors : Ryan G Lim ; Jie Wu ; Leslie M ThompsonSeries Type : Expression profiling by high throughput sequencingOrganism : Homo sapiens ; Mus musculusHD and control patient-derived induced pluripotent stem cells were used to generate medium spiny neuron-like cells. four control in duplicate and three HD samples in duplicate with CAG repeat length in juvenile onset range were differentiated as biological growth replicates (separate differentiations) into medium spiny neuron-like cells. Cells were treated with LNPs with siRNA for knockdown of PIAS1 or a luciferase control. Total RNA was isolated using the Qiagen RNeasy...
Source: GEO: Gene Expression Omnibus - January 1, 2021 Category: Genetics & Stem Cells Tags: Expression profiling by high throughput sequencing Homo sapiens Mus musculus Source Type: research

Modulating FKBP5/FKBP51 and autophagy lowers HTT (huntingtin) levels
Autophagy. 2021 May 24:1-22. doi: 10.1080/15548627.2021.1904489. Online ahead of print.ABSTRACTCurrent disease-modifying therapies for Huntington disease (HD) focus on lowering mutant HTT (huntingtin; mHTT) levels, and the immunosuppressant drug rapamycin is an intriguing therapeutic for aging and neurological disorders. Rapamycin interacts with FKBP1A/FKBP12 and FKBP5/FKBP51, inhibiting the MTORC1 complex and increasing cellular clearance mechanisms. Whether the levels of FKBP (FK506 binding protein) family members are altered in HD models and if these proteins are potential therapeutic targets for HD have not been invest...
Source: Autophagy - May 24, 2021 Category: Cytology Authors: Barbara J Bailus Stephen M Scheeler Jesse Simons Maria A Sanchez Kizito-Tshitoko Tshilenge Jordi Creus-Muncunill Swati Naphade Alejandro Lopez-Ramirez Ningzhe Zhang Kuruwitage Lakshika Madushani Stanislav Moroz Ashley Loureiro Katherine H Schreiber Felix Source Type: research

CRISPR-Cas9 mediated genome editing of Huntington's disease neurospheres
CONCLUSION: Our study confirmed that CAG repeat of R6/2 mouse-derived neurospheres can be edited through CRISPR-Cas9. Editing of CAG repeat sequence decreases polyglutamine aggregation and cellular apoptosis of HD neurospheres, which may be related to the increased expressions of PGC-1α and BDNF. Our data provide the evidence that CRISPR-Cas9 mediated genome editing has therapeutic potential on HD neuronal cells.PMID:36550260 | DOI:10.1007/s11033-022-08175-6
Source: Molecular Biology Reports - December 22, 2022 Category: Molecular Biology Authors: Ji Yun Han Jaewoo Seo Yoori Choi Wooseok Im Jae-Jun Ban Jung-Joon Sung Source Type: research

A Feedback Loop between TGF- β1 and < em > ATG5 < /em > Mediated by miR-122-5p Regulates Fibrosis and EMT in Human Trabecular Meshwork Cells
Curr Issues Mol Biol. 2023 Mar 13;45(3):2381-2392. doi: 10.3390/cimb45030154.ABSTRACTAutophagy is a cell's evolutionary conserved process for degrading and recycling cellular proteins and removing damaged organelles. There has been an increasing interest in identifying the basic cellular mechanism of autophagy and its implications in health and illness during the last decade. Many proteinopathies such as Alzheimer's and Huntington's disease are reported to be associated with impaired autophagy. The functional significance of autophagy in exfoliation syndrome/exfoliation glaucoma (XFS/XFG), remains unknown though it is pres...
Source: Current Issues in Molecular Biology - March 28, 2023 Category: Molecular Biology Authors: Munmun Chakraborthy Aparna Rao Source Type: research