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  1. Article ; Online: Class IIa HDACs in myelination.

    Velasco-Aviles, Sergio / Gomez-Sanchez, Jose A / Cabedo, Hugo

    Aging

    2018  Volume 10, Issue 5, Page(s) 853–854

    MeSH term(s) Animals ; Histone Deacetylases/metabolism ; Humans ; Myelin Sheath/metabolism ; Neurogenesis/physiology
    Chemical Substances Histone Deacetylases (EC 3.5.1.98)
    Language English
    Publishing date 2018-05-03
    Publishing country United States
    Document type Editorial
    ISSN 1945-4589
    ISSN (online) 1945-4589
    DOI 10.18632/aging.101443
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  2. Article ; Online: A genetic compensatory mechanism regulated by

    Velasco-Aviles, Sergio / Patel, Nikiben / Casillas-Bajo, Angeles / Frutos-Rincón, Laura / Velasco, Enrique / Gallar, Juana / Arthur-Farraj, Peter / Gomez-Sanchez, Jose A / Cabedo, Hugo

    eLife

    2022  Volume 11

    Abstract: The class IIa histone deacetylases (HDACs) have pivotal roles in the development of different tissues. Of this family, Schwann cells ... ...

    Abstract The class IIa histone deacetylases (HDACs) have pivotal roles in the development of different tissues. Of this family, Schwann cells express
    MeSH term(s) Animals ; Female ; Gene Expression Regulation/physiology ; Genes, jun/genetics ; Histone Deacetylases/genetics ; Histone Deacetylases/metabolism ; MEF2 Transcription Factors/genetics ; MEF2 Transcription Factors/metabolism ; Male ; Mice ; Peripheral Nerves/physiology ; Remyelination ; Schwann Cells/metabolism
    Chemical Substances MEF2 Transcription Factors ; Mef2d protein, mouse ; Histone Deacetylases (EC 3.5.1.98)
    Language English
    Publishing date 2022-01-25
    Publishing country England
    Document type Journal Article ; Research Support, Non-U.S. Gov't
    ZDB-ID 2687154-3
    ISSN 2050-084X ; 2050-084X
    ISSN (online) 2050-084X
    ISSN 2050-084X
    DOI 10.7554/eLife.72917
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  3. Article ; Online: Class IIa histone deacetylases link cAMP signaling to the myelin transcriptional program of Schwann cells.

    Gomis-Coloma, Clara / Velasco-Aviles, Sergio / Gomez-Sanchez, Jose A / Casillas-Bajo, Angeles / Backs, Johannes / Cabedo, Hugo

    The Journal of cell biology

    2018  Volume 217, Issue 4, Page(s) 1249–1268

    Abstract: Schwann cells respond to cyclic adenosine monophosphate (cAMP) halting proliferation and expressing myelin proteins. Here we show that cAMP signaling induces the nuclear shuttling of the class IIa histone deacetylase (HDAC)-4 in these cells, where it ... ...

    Abstract Schwann cells respond to cyclic adenosine monophosphate (cAMP) halting proliferation and expressing myelin proteins. Here we show that cAMP signaling induces the nuclear shuttling of the class IIa histone deacetylase (HDAC)-4 in these cells, where it binds to the promoter and blocks the expression of
    MeSH term(s) Active Transport, Cell Nucleus ; Animals ; Binding Sites ; Cells, Cultured ; Cyclic AMP/metabolism ; Early Growth Response Protein 2/genetics ; Early Growth Response Protein 2/metabolism ; Histone Deacetylases/deficiency ; Histone Deacetylases/genetics ; Histone Deacetylases/metabolism ; MEF2 Transcription Factors/genetics ; MEF2 Transcription Factors/metabolism ; Mice, Knockout ; Myelin Sheath/genetics ; Myelin Sheath/metabolism ; Nerve Fibers, Myelinated/enzymology ; Nerve Fibers, Myelinated/ultrastructure ; Nuclear Receptor Co-Repressor 1/genetics ; Nuclear Receptor Co-Repressor 1/metabolism ; Promoter Regions, Genetic ; Proto-Oncogene Proteins c-jun/genetics ; Proto-Oncogene Proteins c-jun/metabolism ; Rats, Wistar ; Schwann Cells/enzymology ; Schwann Cells/ultrastructure ; Sciatic Nerve/enzymology ; Sciatic Nerve/ultrastructure ; Second Messenger Systems ; Tissue Culture Techniques ; Transcription, Genetic
    Chemical Substances Early Growth Response Protein 2 ; Egr2 protein, rat ; MEF2 Transcription Factors ; Ncor1 protein, rat ; Nuclear Receptor Co-Repressor 1 ; Proto-Oncogene Proteins c-jun ; Cyclic AMP (E0399OZS9N) ; HDAC4 protein, rat (EC 3.5.1.98) ; Hdac5 protein, mouse (EC 3.5.1.98) ; Hdac5 protein, rat (EC 3.5.1.98) ; Histone Deacetylases (EC 3.5.1.98)
    Language English
    Publishing date 2018-02-22
    Publishing country United States
    Document type Journal Article ; Research Support, Non-U.S. Gov't
    ZDB-ID 218154-x
    ISSN 1540-8140 ; 0021-9525
    ISSN (online) 1540-8140
    ISSN 0021-9525
    DOI 10.1083/jcb.201611150
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  4. Article: Novel EGR2 variant that associates with Charcot-Marie-Tooth disease when combined with lipopolysaccharide-induced TNF-α factor T49M polymorphism.

    Blanco-Cantó, Maria Empar / Patel, Nikiben / Velasco-Aviles, Sergio / Casillas-Bajo, Angeles / Salas-Felipe, Juan / García-Escrivá, Alexandre / Díaz-Marín, Carmen / Cabedo, Hugo

    Neurology. Genetics

    2020  Volume 6, Issue 2, Page(s) e407

    Abstract: Objective: To identify novel genetic mechanisms causing Charcot-Marie-Tooth (CMT) disease.: Methods: We performed a next-generation sequencing study of 34 genes associated with CMT in a patient with peripheral neuropathy.: Results: We found a non- ... ...

    Abstract Objective: To identify novel genetic mechanisms causing Charcot-Marie-Tooth (CMT) disease.
    Methods: We performed a next-generation sequencing study of 34 genes associated with CMT in a patient with peripheral neuropathy.
    Results: We found a non-previously described mutation in EGR2 (p.P397H). P397H mutation is located within the loop that connects zinc fingers 2 and 3, a pivotal domain for the activity of this transcription factor. Using promoter activity luciferase assays, we found that this mutation promotes decreased transcriptional activity of EGR2. In this patient, we also found a previously described nonpathogenic polymorphism in lipopolysaccharide-induced TNF-α factor (LITAF) (p.T49M). We show that the p.T49M mutation decreases the steady-state levels of the LITAF protein in Schwann cells. Loss of function of LITAF has been shown to produce deregulation in the NRG1-erbB signaling, a pivotal pathway for EGR2 expression by Schwann cells. Surprisingly, our segregation study demonstrates that p.P397H mutation in EGR2 is not sufficient to produce CMT disease. Most notably, only those patients expressing simultaneously the LITAF T49M polymorphism develop peripheral neuropathy.
    Conclusions: Our data support that the LITAF loss-of-function interferes with the expression of the transcriptional-deficient EGR2 P397H mutant hampering Schwann cell differentiation and suggest that in vivo both genes act in tandem to allow the proper development of myelin.
    Language English
    Publishing date 2020-03-03
    Publishing country United States
    Document type Journal Article
    ZDB-ID 2818607-2
    ISSN 2376-7839
    ISSN 2376-7839
    DOI 10.1212/NXG.0000000000000407
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  5. Article ; Online: Failures of nerve regeneration caused by aging or chronic denervation are rescued by restoring Schwann cell c-Jun.

    Wagstaff, Laura J / Gomez-Sanchez, Jose A / Fazal, Shaline V / Otto, Georg W / Kilpatrick, Alastair M / Michael, Kirolos / Wong, Liam YN / Ma, Ki H / Turmaine, Mark / Svaren, John / Gordon, Tessa / Arthur-Farraj, Peter / Velasco-Aviles, Sergio / Cabedo, Hugo / Benito, Cristina / Mirsky, Rhona / Jessen, Kristjan R

    eLife

    2021  Volume 10

    Abstract: After nerve injury, myelin and Remak Schwann cells reprogram to repair cells specialized for regeneration. Normally providing strong regenerative support, these cells fail in aging animals, and during chronic denervation that results from slow axon ... ...

    Abstract After nerve injury, myelin and Remak Schwann cells reprogram to repair cells specialized for regeneration. Normally providing strong regenerative support, these cells fail in aging animals, and during chronic denervation that results from slow axon growth. This impairs axonal regeneration and causes significant clinical problems. In mice, we find that repair cells express reduced c-Jun protein as regenerative support provided by these cells declines during aging and chronic denervation. In both cases, genetically restoring Schwann cell c-Jun levels restores regeneration to control levels. We identify potential gene candidates mediating this effect and implicate Shh in the control of Schwann cell c-Jun levels. This establishes that a common mechanism, reduced c-Jun in Schwann cells, regulates success and failure of nerve repair both during aging and chronic denervation. This provides a molecular framework for addressing important clinical problems, suggesting molecular pathways that can be targeted to promote repair in the PNS.
    MeSH term(s) Aging ; Animals ; Female ; Male ; Mice ; Nerve Regeneration ; Proto-Oncogene Proteins c-jun/genetics ; Proto-Oncogene Proteins c-jun/metabolism ; Schwann Cells/metabolism
    Chemical Substances Proto-Oncogene Proteins c-jun
    Language English
    Publishing date 2021-01-21
    Publishing country England
    Document type Journal Article ; Research Support, Non-U.S. Gov't
    ZDB-ID 2687154-3
    ISSN 2050-084X ; 2050-084X
    ISSN (online) 2050-084X
    ISSN 2050-084X
    DOI 10.7554/eLife.62232
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  6. Article ; Online: Neddylation orchestrates the complex transcriptional and posttranscriptional program that drives Schwann cell myelination.

    Ayuso-García, Paula / Sánchez-Rueda, Alejandro / Velasco-Avilés, Sergio / Tamayo-Caro, Miguel / Ferrer-Pinós, Aroa / Huarte-Sebastian, Cecilia / Alvarez, Vanesa / Riobello, Cristina / Jiménez-Vega, Selene / Buendia, Izaskun / Cañas-Martin, Jorge / Fernández-Susavila, Héctor / Aparicio-Rey, Adrián / Esquinas-Román, Eva M / Ponte, Carlos Rodríguez / Guhl, Romane / Laville, Nicolas / Pérez-Andrés, Encarni / Lavín, José L /
    González-Lopez, Monika / Cámara, Nuria Macías / Aransay, Ana M / Lozano, Juan José / Sutherland, James D / Barrio, Rosa / Martinez-Chantar, María Luz / Azkargorta, Mikel / Elortza, Félix / Soriano-Navarro, Mario / Matute, Carlos / Sánchez-Gómez, María Victoria / Bayón-Cordero, Laura / Pérez-Samartín, Alberto / Bravo, Susana B / Kurz, Thimo / Lama-Díaz, Tomas / Blanco, Miguel G / Haddad, Saif / Record, Christopher J / van Hasselt, Peter M / Reilly, Mary M / Varela-Rey, Marta / Woodhoo, Ashwin

    Science advances

    2024  Volume 10, Issue 15, Page(s) eadm7600

    Abstract: Myelination is essential for neuronal function and health. In peripheral nerves, >100 causative mutations have been identified that cause Charcot-Marie-Tooth disease, a disorder that can affect myelin sheaths. Among these, a number of mutations are ... ...

    Abstract Myelination is essential for neuronal function and health. In peripheral nerves, >100 causative mutations have been identified that cause Charcot-Marie-Tooth disease, a disorder that can affect myelin sheaths. Among these, a number of mutations are related to essential targets of the posttranslational modification neddylation, although how these lead to myelin defects is unclear. Here, we demonstrate that inhibiting neddylation leads to a notable absence of peripheral myelin and axonal loss both in developing and regenerating mouse nerves. Our data indicate that neddylation exerts a global influence on the complex transcriptional and posttranscriptional program by simultaneously regulating the expression and function of multiple essential myelination signals, including the master transcription factor EGR2 and the negative regulators c-Jun and Sox2, and inducing global secondary changes in downstream pathways, including the mTOR and YAP/TAZ signaling pathways. This places neddylation as a critical regulator of myelination and delineates the potential pathogenic mechanisms involved in CMT mutations related to neddylation.
    MeSH term(s) Animals ; Mice ; Schwann Cells ; Myelin Sheath/genetics ; Charcot-Marie-Tooth Disease/genetics ; Mutation ; Protein Processing, Post-Translational
    Language English
    Publishing date 2024-04-12
    Publishing country United States
    Document type Journal Article
    ZDB-ID 2810933-8
    ISSN 2375-2548 ; 2375-2548
    ISSN (online) 2375-2548
    ISSN 2375-2548
    DOI 10.1126/sciadv.adm7600
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  7. Article ; Online: Hepatic levels of S-adenosylmethionine regulate the adaptive response to fasting.

    Capelo-Diz, Alba / Lachiondo-Ortega, Sofía / Fernández-Ramos, David / Cañas-Martín, Jorge / Goikoetxea-Usandizaga, Naroa / Serrano-Maciá, Marina / González-Rellan, Maria J / Mosca, Laura / Blazquez-Vicens, Joan / Tinahones-Ruano, Alberto / Fondevila, Marcos F / Buyan, Mason / Delgado, Teresa C / Gutierrez de Juan, Virginia / Ayuso-García, Paula / Sánchez-Rueda, Alejandro / Velasco-Avilés, Sergio / Fernández-Susavila, Héctor / Riobello-Suárez, Cristina /
    Dziechciarz, Bartlomiej / Montiel-Duarte, Cristina / Lopitz-Otsoa, Fernando / Bizkarguenaga, Maider / Bilbao-García, Jon / Bernardo-Seisdedos, Ganeko / Senra, Ana / Soriano-Navarro, Mario / Millet, Oscar / Díaz-Lagares, Ángel / Crujeiras, Ana B / Bao-Caamano, Aida / Cabrera, Diana / van Liempd, Sebastiaan / Tamayo-Carro, Miguel / Borzacchiello, Luigi / Gomez-Santos, Beatriz / Buqué, Xabier / Sáenz de Urturi, Diego / González-Romero, Francisco / Simon, Jorge / Rodríguez-Agudo, Rubén / Ruiz, Asier / Matute, Carlos / Beiroa, Daniel / Falcon-Perez, Juan M / Aspichueta, Patricia / Rodríguez-Cuesta, Juan / Porcelli, Marina / Pajares, María A / Ameneiro, Cristina / Fidalgo, Miguel / Aransay, Ana M / Lama-Díaz, Tomas / Blanco, Miguel G / López, Miguel / Villa-Bellosta, Ricardo / Müller, Timo D / Nogueiras, Rubén / Woodhoo, Ashwin / Martínez-Chantar, María Luz / Varela-Rey, Marta

    Cell metabolism

    2023  Volume 35, Issue 8, Page(s) 1373–1389.e8

    Abstract: There has been an intense focus to uncover the molecular mechanisms by which fasting triggers the adaptive cellular responses in the major organs of the body. Here, we show that in mice, hepatic S-adenosylmethionine (SAMe)-the principal methyl donor-acts ...

    Abstract There has been an intense focus to uncover the molecular mechanisms by which fasting triggers the adaptive cellular responses in the major organs of the body. Here, we show that in mice, hepatic S-adenosylmethionine (SAMe)-the principal methyl donor-acts as a metabolic sensor of nutrition to fine-tune the catabolic-fasting response by modulating phosphatidylethanolamine N-methyltransferase (PEMT) activity, endoplasmic reticulum-mitochondria contacts, β-oxidation, and ATP production in the liver, together with FGF21-mediated lipolysis and thermogenesis in adipose tissues. Notably, we show that glucagon induces the expression of the hepatic SAMe-synthesizing enzyme methionine adenosyltransferase α1 (MAT1A), which translocates to mitochondria-associated membranes. This leads to the production of this metabolite at these sites, which acts as a brake to prevent excessive β-oxidation and mitochondrial ATP synthesis and thereby endoplasmic reticulum stress and liver injury. This work provides important insights into the previously undescribed function of SAMe as a new arm of the metabolic adaptation to fasting.
    MeSH term(s) Mice ; Animals ; S-Adenosylmethionine/metabolism ; Liver/metabolism ; Liver Neoplasms/metabolism ; Fasting ; Adenosine Triphosphate/metabolism ; Methionine Adenosyltransferase/metabolism ; Phosphatidylethanolamine N-Methyltransferase/metabolism
    Chemical Substances S-Adenosylmethionine (7LP2MPO46S) ; Adenosine Triphosphate (8L70Q75FXE) ; Methionine Adenosyltransferase (EC 2.5.1.6) ; PEMT protein, mouse (EC 2.1.1.17) ; Phosphatidylethanolamine N-Methyltransferase (EC 2.1.1.17)
    Language English
    Publishing date 2023-07-31
    Publishing country United States
    Document type Journal Article ; Research Support, Non-U.S. Gov't
    ZDB-ID 2176834-1
    ISSN 1932-7420 ; 1550-4131
    ISSN (online) 1932-7420
    ISSN 1550-4131
    DOI 10.1016/j.cmet.2023.07.002
    Database MEDical Literature Analysis and Retrieval System OnLINE

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    Zs.A 6169: Show issues Location:
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