Raquel Machado

Dr. Raquel Machado

University of Luxembourg
orcid

Research Focus & Metrics

Academic Career Length

15Years (2012-Present)

(Calculated once Scilit publication data is synced: current year − year of first publication + 1)

Representative Publications

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2 December 2012 in Nature
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Journal Article
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MKMarlen Knobloch
Marlen Knobloch
SBSimon Braun
Simon Braun
LZLuis Zurkirchen
Luis Zurkirchen
CSCarolin von Schoultz
Carolin von Schoultz
NZNicola Zamboni
Nicola Zamboni
SJSebastian Jessberger
Sebastian Jessberger

15 November 2021 in Nature Chemical Biology
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Journal Article
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DDDavid Dilworth
David Dilworth
RHRonan P. Hanley
Ronan P. Hanley
RFRenato Ferreira de Freitas
Renato Ferreira de Freitas
AAAbdellah Allali-Hassani
Abdellah Allali-Hassani
MZMengqi Zhou
Mengqi Zhou
MSMatthieu Schapira
Matthieu Schapira

1 May 2021 in Cell Stem Cell
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Journal Article
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MIMuhammad Khadeesh bin Imtiaz
Muhammad Khadeesh bin Imtiaz
BJBaptiste N. Jaeger
Baptiste N. Jaeger
SBSara Bottes
Sara Bottes
Raquel MachadoRaquel Machado
Raquel Machado
MVMojca Vidmar
Mojca Vidmar
SJSebastian Jessberger
Sebastian Jessberger

1 June 2015 in Cell Reports
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Journal Article
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SBSimon Braun
Simon Braun
GPGregor-Alexander Pilz
Gregor-Alexander Pilz
Raquel MachadoRaquel Machado
Raquel Machado
JMJonathan Moss
Jonathan Moss
BBBurkhard Becher
Burkhard Becher
SJSebastian Jessberger
Sebastian Jessberger
Demyelinating diseases are characterized by a loss of oligodendrocytes leading to axonal degeneration and impaired brain function. Current strategies used for the treatment of demyelinating disease such as multiple sclerosis largely rely on modulation of the immune system. Only limited treatment options are available for treating the later stages of the disease, and these treatments require regenerative therapies to ameliorate the consequences of oligodendrocyte loss and axonal impairment. Directed differentiation of adult hippocampal neural stem/progenitor cells (NSPCs) into oligodendrocytes may represent an endogenous source of glial cells for cell-replacement strategies aiming to treat demyelinating disease. Here, we show that Ascl1-mediated conversion of hippocampal NSPCs into mature oligodendrocytes enhances remyelination in a diphtheria-toxin (DT)-inducible, genetic model for demyelination. These findings highlight the potential of targeting hippocampal NSPCs for the treatment of demyelinated lesions in the adult brain.

21 May 2024 in Nature Chemical Biology
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DODominic D. G. Owens
Dominic D. G. Owens
MMMatthew E. R. Maitland
Matthew E. R. Maitland
AYAliakbar Khalili Yazdi
Aliakbar Khalili Yazdi
XSXiaosheng Song
Xiaosheng Song
VRViviane Reber
Viviane Reber
CACheryl H. Arrowsmith
Cheryl H. Arrowsmith

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CDCarlos DeOcesano-Pereira
Carlos DeOcesano-Pereira
Raquel MachadoRaquel Machado
Raquel Machado
ACAna Chudzinski-Tavassi
Ana Chudzinski-Tavassi
MSMari Sogayar
Mari Sogayar
Non-coding RNAs (ncRNAs) comprise a diversity of RNA species, which do not have the potential to encode proteins. Non-coding RNAs include two classes of RNAs, namely: short regulatory ncRNAs and long non-coding RNAs (lncRNAs). The short regulatory RNAs, containing up to 200 nucleotides, include small RNAs, such as microRNAs (miRNA), short interfering RNAs (siRNAs), piwi-interacting RNAs (piRNAs), and small nucleolar RNAs (snoRNAs). The lncRNAs include long antisense RNAs and long intergenic RNAs (lincRNAs). Non-coding RNAs have been implicated as master regulators of several biological processes, their expression being strictly regulated under physiological conditions. In recent years, particularly in the last decade, substantial effort has been made to investigate the function of ncRNAs in several human diseases, including cancer. Glioblastoma is the most common and aggressive type of brain cancer in adults, with deregulated expression of small and long ncRNAs having been implicated in onset, progression, invasiveness, and recurrence of this tumor. The aim of this review is to guide the reader through important aspects of miRNA and lncRNA biology, focusing on the molecular mechanism associated with the progression of this highly malignant cancer type.