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Specialty: Cytology
Condition: Ataxia
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Total 7 results found since Jan 2013.
Chronic suppression of STIM1-mediated calcium signaling in Purkinje cells rescues the cerebellar pathology in spinocerebellar ataxia type 2
Biochim Biophys Acta Mol Cell Res. 2023 Mar 18:119466. doi: 10.1016/j.bbamcr.2023.119466. Online ahead of print.ABSTRACTDistorted neuronal calcium signaling has been reported in many neurodegenerative disorders, including different types of spinocerebellar ataxias (SCAs). Cerebellar Purkinje cells (PCs) are primarily affected in SCAs and the disturbances in the calcium homeostasis were observed in SCA PCs. Our previous results have revealed that 3,5-dihydroxyphenylglycine (DHPG) induced greater calcium responses in SCA2-58Q PC cultures than in wild type (WT) PC cultures. Here we observed that glutamate-induced calcium rele...
Source: Cell Research - March 20, 2023 Category: Cytology Authors: Polina A Egorova Ksenia S Marinina Ilya B Bezprozvanny Source Type: research
APTX acts in DNA double-strand break repair in a manner distinct from XRCC4
J Radiat Res. 2023 Mar 20:rrad007. doi: 10.1093/jrr/rrad007. Online ahead of print.ABSTRACTAprataxin (APTX), the product of the causative gene for hereditary neurogenerative syndromes Ataxia-oculomotor apraxia 1 and early onset ataxia with oculomotor apraxia and hypoalbuminemia, has an enzymatic activity of removing adenosine monophosphate from DNA 5'-end, which arises from abortive ligation by DNA ligases. It is also reported that APTX physically binds to XRCC1 and XRCC4, suggesting its involvement in DNA single-strand break repair (SSBR) and DNA double-strand break repair (DSBR) via non-homologous end joining pathway. Al...
Source: Cell Research - March 20, 2023 Category: Cytology Authors: Rikiya Imamura Mizuki Saito Mikio Shimada Junya Kobayashi Masamichi Ishiai Yoshihisa Matsumoto Source Type: research
ATR inhibition sensitizes liposarcoma to doxorubicin by increasing DNA damage
In this study, we investigated the expression, function, and potential of ATR as a therapeutic target in liposarcoma. Activation and expression of ATR in liposarcoma was analyzed by immunohistochemistry, which was further explored for correlation with patient clinical characteristics. ATR-specific siRNA and the ATR inhibitor VE-822 were applied to determine the effect of ATR inhibition on liposarcoma cell proliferation and anti-apoptotic activity. Migration activity and clonogenicity were examined using wound healing and clonogenic assays. ATR (p-ATR) was overexpressed in 88.1% of the liposarcoma specimens and correlated w...
Source: Cell Research - May 9, 2022 Category: Cytology Authors: Juncheng Cui Dylan Dean Francis J Hornicek Raphael E Pollock Robert M Hoffman Zhenfeng Duan Source Type: research
Olaparib-induced Apoptosis Through EBNA1-ATR-p38 MAPK Signaling Pathway in Epstein-Barr Virus-positive Gastric Cancer Cells
CONCLUSION: Olaparib treatment led to different cellular responses depending on EBV infection in gastric cancer cell lines. These results provide new insights into the mechanism of olaparib-induced apoptosis in gastric cancer cells and suggest that EBV infection should be considered when developing new potential therapeutic agents for gastric cancer.PMID:34969765 | DOI:10.21873/anticanres.15513
Source: Cell Research - December 31, 2021 Category: Cytology Authors: Sung Ho Moon Nam-Sook Park Min Hye Noh Yeong Seok Kim Soon Ho Cheong Dae Young Hur Source Type: research
RNA-Dependent Epigenetic Silencing Directs Transcriptional Downregulation Caused by Intronic Repeat Expansions
Publication date: Available online 26 July 2018Source: CellAuthor(s): Hannes Eimer, Sridevi Sureshkumar, Avilash Singh Yadav, Calvin Kraupner-Taylor, Champa Bandaranayake, Andrei Seleznev, Tamblyn Thomason, Stephen J. Fletcher, Stephanie Frances Gordon, Bernard J. Carroll, Sureshkumar BalasubramanianSummaryTranscriptional downregulation caused by intronic triplet repeat expansions underlies diseases such as Friedreich’s ataxia. This downregulation of gene expression is coupled with epigenetic changes, but the underlying mechanisms are unknown. Here, we show that an intronic GAA/TTC triplet expansion within the IIL1 gene...
Source: Cell - July 26, 2018 Category: Cytology Source Type: research
E3 Ligase RNF126 Directly Ubiquitinates Frataxin, Promoting Its Degradation: Identification of a Potential Therapeutic Target for Friedreich Ataxia
Publication date: 21 February 2017 Source:Cell Reports, Volume 18, Issue 8 Author(s): Monica Benini, Silvia Fortuni, Ivano Condò, Giulia Alfedi, Florence Malisan, Nicola Toschi, Dario Serio, Damiano Sergio Massaro, Gaetano Arcuri, Roberto Testi, Alessandra Rufini Friedreich ataxia (FRDA) is a severe genetic neurodegenerative disease caused by reduced expression of the mitochondrial protein frataxin. To date, there is no therapy to treat this condition. The amount of residual frataxin critically affects the severity of the disease; thus, attempts to restore physiological frataxin levels are considered therapeutically rele...
Source: Cell Reports - February 21, 2017 Category: Cytology Source Type: research
