Search

Your search keyword '"Jaka, Oihane"' showing total 25 results
Start Over Author "Jaka, Oihane"
25 results on '"Jaka, Oihane"'

3. Ret function in muscle stem cells points to tyrosine kinase inhibitor therapy for facioscapulohumeral muscular dystrophy.

Author

Moyle, Louise A, Blanc, Eric, Jaka, Oihane, Prueller, Johanna, Banerji, Christopher Rs, Tedesco, Francesco Saverio, Harridge, Stephen Dr, Knight, Robert D, and Zammit, Peter S

Subjects
Muscles, Cells, Cultured, Myoblasts, Satellite Cells, Skeletal Muscle, Animals, Humans, Mice, Muscular Dystrophy, Facioscapulohumeral, Pyrroles, Indoles, Homeodomain Proteins, Enzyme Inhibitors, Cell Differentiation, Cell Proliferation, Gene Expression, Proto-Oncogene Proteins c-ret, Sunitinib, DUX4, FSHD, RET, cell biology, facioscapulohumeral muscular dystrophy, human, human biology, medicine, mouse, therapy, Biochemistry and Cell Biology
Abstract

Facioscapulohumeral muscular dystrophy (FSHD) involves sporadic expression of DUX4, which inhibits myogenesis and is pro-apoptotic. To identify target genes, we over-expressed DUX4 in myoblasts and found that the receptor tyrosine kinase Ret was significantly up-regulated, suggesting a role in FSHD. RET is dynamically expressed during myogenic progression in mouse and human myoblasts. Constitutive expression of either RET9 or RET51 increased myoblast proliferation, whereas siRNA-mediated knockdown of Ret induced myogenic differentiation. Suppressing RET activity using Sunitinib, a clinically-approved tyrosine kinase inhibitor, rescued differentiation in both DUX4-expressing murine myoblasts and in FSHD patient-derived myoblasts. Importantly, Sunitinib also increased engraftment and differentiation of FSHD myoblasts in regenerating mouse muscle. Thus, DUX4-mediated activation of Ret prevents myogenic differentiation and could contribute to FSHD pathology by preventing satellite cell-mediated repair. Rescue of DUX4-induced pathology by Sunitinib highlights the therapeutic potential of tyrosine kinase inhibitors for treatment of FSHD.

Published
2016

13. VGLL3 operates via TEAD1, TEAD3 and TEAD4 to influence myogenesis in skeletal muscle

Author

Figeac, Nicolas, Mohamed, Abdalla D., Sun, Congshan, Schönfelder, Martin, Matallanas, David, Garcia-Munoz, Amaya, Missiaglia, Edoardo, Collie-Duguid, Elaina, De Mello, Vanessa, Pobbati, Ajaybabu V., Pruller, Johanna, Jaka, Oihane, Harridge, Stephen D. R., Hong, Wanjin, Shipley, Janet, Vargesson, Neil, Zammit, Peter S., Wackerhage, Henning, and Sportbiologie

Subjects
Skeletal muscle, Stem cells, TAZ, TEAD, VGLL3, WWTR1, YAP, Medizin und Gesundheit, Biowissenschaften, Biologie, ddc:790, ddc:570, ddc:610, Sport, Spiele, Unterhaltung
Abstract

VGLL proteins are transcriptional co-factors that bind TEAD family transcription factors to regulate events ranging from wing development in fly, to muscle fibre composition and immune function in mice. Here, we characterise Vgll3 in skeletal muscle. We found that mouse Vgll3 was expressed at low levels in healthy muscle but that its levels increased during hypertrophy or regeneration; in humans, VGLL3 was highly expressed in tissues from patients with various muscle diseases, such as in dystrophic muscle and alveolar rhabdomyosarcoma. Interaction proteomics revealed that VGLL3 bound TEAD1, TEAD3 and TEAD4 in myoblasts and/or myotubes. However, there was no interaction with proteins from major regulatory systems such as the Hippo kinase cascade, unlike what is found for the TEAD co-factors YAP (encoded by YAP1) and TAZ (encoded by WWTR1). Vgll3 overexpression reduced the activity of the Hippo negative-feedback loop, affecting expression of muscle-regulating genes including Myf5, Pitx2 and Pitx3, and genes encoding certain Wnts and IGFBPs. VGLL3 mainly repressed gene expression, regulating similar genes to those regulated by YAP and TAZ. siRNA-mediated Vgll3 knockdown suppressed myoblast proliferation, whereas Vgll3 overexpression strongly promoted myogenic differentiation. However, skeletal muscle was overtly normal in Vgll3-null mice, presumably due to feedback signalling and/or redundancy. This work identifies VGLL3 as a transcriptional co-factor operating with the Hippo signal transduction network to control myogenesis.

Published
2018

15. Vgll3 operates via Tead1, Tead3 and Tead4 to influence myogenesis in skeletal muscle

Author

Figeac, Nicolas, primary, Mohamed, Abdalla D., additional, Sun, Congshan, additional, Schönfelder, Martin, additional, Matallanas, David, additional, Garcia-Munoz, Amaya, additional, Missiaglia, Edoardo, additional, Collie-Duguid, Elaina, additional, De Mello, Vanessa, additional, Pobbati, Ajaybabu V., additional, Pruller, Johanna, additional, Jaka, Oihane, additional, Harridge, Stephen D. R., additional, Hong, Wanjin, additional, Shipley, Janet, additional, Vargesson, Neil, additional, Zammit, Peter S., additional, and Wackerhage, Henning, additional

Published
2019
Full Text
View/download PDF

16. VGLL3 operates via TEAD1, TEAD3 and TEAD4 to influence myogenesis in skeletal muscle

Author

Sportbiologie, Figeac, Nicolas;Mohamed, Abdalla D.;Sun, Congshan;Schönfelder, Martin;Matallanas, David;Garcia-Munoz, Amaya;Missiaglia, Edoardo;Collie-Duguid, Elaina;De Mello, Vanessa;Pobbati, Ajaybabu V.;Pruller, Johanna;Jaka, Oihane;Harridge, Stephen D. R.;Hong, Wanjin;Shipley, Janet;Vargesson, Neil;Zammit, Peter S.;Wackerhage, Henning, Sportbiologie, and Figeac, Nicolas;Mohamed, Abdalla D.;Sun, Congshan;Schönfelder, Martin;Matallanas, David;Garcia-Munoz, Amaya;Missiaglia, Edoardo;Collie-Duguid, Elaina;De Mello, Vanessa;Pobbati, Ajaybabu V.;Pruller, Johanna;Jaka, Oihane;Harridge, Stephen D. R.;Hong, Wanjin;Shipley, Janet;Vargesson, Neil;Zammit, Peter S.;Wackerhage, Henning

Abstract

VGLL proteins are transcriptional co-factors that bind TEAD family transcription factors to regulate events ranging from wing development in fly, to muscle fibre composition and immune function in mice. Here, we characterise Vgll3 in skeletal muscle. We found that mouse Vgll3 was expressed at low levels in healthy muscle but that its levels increased during hypertrophy or regeneration; in humans, VGLL3 was highly expressed in tissues from patients with various muscle diseases, such as in dystrophic muscle and alveolar rhabdomyosarcoma. Interaction proteomics revealed that VGLL3 bound TEAD1, TEAD3 and TEAD4 in myoblasts and/or myotubes. However, there was no interaction with proteins from major regulatory systems such as the Hippo kinase cascade, unlike what is found for the TEAD co-factors YAP (encoded by YAP1) and TAZ (encoded by WWTR1). Vgll3 overexpression reduced the activity of the Hippo negative-feedback loop, affecting expression of muscle-regulating genes including Myf5, Pitx2 and Pitx3, and genes encoding certain Wnts and IGFBPs. VGLL3 mainly repressed gene expression, regulating similar genes to those regulated by YAP and TAZ. siRNA-mediated Vgll3 knockdown suppressed myoblast proliferation, whereas Vgll3 overexpression strongly promoted myogenic differentiation. However, skeletal muscle was overtly normal in Vgll3-null mice, presumably due to feedback signalling and/or redundancy. This work identifies VGLL3 as a transcriptional co-factor operating with the Hippo signal transduction network to control myogenesis.

Published
2018

17. Altitude exposure and increased heart rate: the role of the parasympathetic nervous system

Author

Attias, Julia, Bieles, Julie, Carvil, Philip, Laing, Charles, Lewis, Fiona, Jaka, Oihane, O'Brien, Katie, and Ruchaya, Prashant

Abstract

Elevated heart rate (HR) has been demonstrated in response to acute hypoxia exposure, which is reportedly due to sympathetic nervous system activation (SNS) and concurrent withdrawal of parasympathetic nervous system activity (PSNS). This article is protected by copyright. All rights reserved.

Published
2017
Full Text
View/download PDF

20. LGMD2A gaixotasunaren diagnostiko molekularra

Author

Jaka, Oihane and Jaka, Oihane

Abstract

Limb-girdle muscular dystrophy type 2A (LGMD2A) is an autosomal recessive disorder caused by mutations in the CAPN3 gene. This gene encodes a protein expressed in skeletal muscle called calpain 3. In the present work we performed the molecular diagnosis of LGMD2A patients and we applied MLPA analysis for the detection of genomic rearrangements. This technique was efficient in identifying four different deletions. Based on our results we propose an algorithm for the molecular diagnosis of LGMD2A.; 2A motako gerrietako muskulu-distrofia (LGMD2A) CAPN3 geneko mutazioen ondorio den gaixotasun autosomiko azpirakorra da. CAPN3 geneak muskulu eskeletikoan adierazten den kalpaina 3 proteina kodetzen du. Ikerlan honetan, LGMD2A gaixoen diagnostiko molekularra egin da eta MLPA erabili da berrordenatze posibleak identifikatzeko. Teknika horri esker lau delezio mota identifikatu dira. Gure emaitzetan oinarrituz, LGMD2A gaixotasunaren diagnostiko molekularra egiteko algoritmo bat proposatzen dugu.

Published
2016

24. Expanded CTG repeats trigger miRNA alterations in Drosophila that are conserved in myotonic dystrophy type 1 patients

Author

Fernandez-Costa, Juan M., primary, Garcia-Lopez, Amparo, additional, Zuñiga, Sheila, additional, Fernandez-Pedrosa, Victoria, additional, Felipo-Benavent, Amelia, additional, Mata, Manuel, additional, Jaka, Oihane, additional, Aiastui, Ana, additional, Hernandez-Torres, Francisco, additional, Aguado, Begoña, additional, Perez-Alonso, Manuel, additional, Vilchez, Jesus J., additional, Lopez de Munain, Adolfo, additional, and Artero, Ruben D., additional

Published
2012
Full Text
View/download PDF

Catalog

Books, media, physical & digital resources
See catalog results