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Deficiency of the miR-29a/b-1 cluster leads to ataxic features and cerebellar alterations in mice

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Deficiency of the miR-29a/b-1 cluster leads to ataxic features and cerebellar alterations in mice. / Papadopoulou, Aikaterini S; Serneels, Lutgarde; Achsel, Tilmann; Mandemakers, Wim; Callaerts-Vegh, Zsuzsanna; Dooley, James; Lau, Pierre; Ayoubi, Torik; Radaelli, Enrico; Spinazzi, Marco; Neumann, Melanie; Hébert, Sébastien S; Silahtaroglu, Asli; Liston, Adrian; D'Hooge, Rudi; Glatzel, Markus; De Strooper, Bart.

in: NEUROBIOL DIS, Jahrgang 73, 01.2015, S. 275-288.

Publikationen: SCORING: Beitrag in Fachzeitschrift/Zeitung › SCORING: Zeitschriftenaufsatz › Forschung › Begutachtung

Harvard

Papadopoulou, AS, Serneels, L, Achsel, T, Mandemakers, W, Callaerts-Vegh, Z, Dooley, J, Lau, P, Ayoubi, T, Radaelli, E, Spinazzi, M, Neumann, M, Hébert, SS, Silahtaroglu, A, Liston, A, D'Hooge, R, Glatzel, M & De Strooper, B 2015, 'Deficiency of the miR-29a/b-1 cluster leads to ataxic features and cerebellar alterations in mice', NEUROBIOL DIS, Jg. 73, S. 275-288. https://doi.org/10.1016/j.nbd.2014.10.006

APA

Papadopoulou, A. S., Serneels, L., Achsel, T., Mandemakers, W., Callaerts-Vegh, Z., Dooley, J., Lau, P., Ayoubi, T., Radaelli, E., Spinazzi, M., Neumann, M., Hébert, S. S., Silahtaroglu, A., Liston, A., D'Hooge, R., Glatzel, M., & De Strooper, B. (2015). Deficiency of the miR-29a/b-1 cluster leads to ataxic features and cerebellar alterations in mice. NEUROBIOL DIS, 73, 275-288. https://doi.org/10.1016/j.nbd.2014.10.006

Vancouver

Papadopoulou AS, Serneels L, Achsel T, Mandemakers W, Callaerts-Vegh Z, Dooley J et al. Deficiency of the miR-29a/b-1 cluster leads to ataxic features and cerebellar alterations in mice. NEUROBIOL DIS. 2015 Jan;73:275-288. https://doi.org/10.1016/j.nbd.2014.10.006

Bibtex

@article{7cff99baf51b46d6b1252ef252b29632,
title = "Deficiency of the miR-29a/b-1 cluster leads to ataxic features and cerebellar alterations in mice",
abstract = "miR-29 is expressed strongly in the brain and alterations in expression have been linked to several neurological disorders. To further explore the function of this miRNA in the brain, we generated miR-29a/b-1 knockout animals. Knockout mice develop a progressive disorder characterized by locomotor impairment and ataxia. The different members of the miR-29 family are strongly expressed in neurons of the olfactory bulb, the hippocampus and in the Purkinje cells of the cerebellum. Morphological analysis showed that Purkinje cells are smaller and display less dendritic arborisation compared to their wildtype littermates. In addition, a decreased number of parallel fibers form synapses on the Purkinje cells. We identified several mRNAs significantly up-regulated in the absence of the miR-29a/b-1 cluster. At the protein level, however, the voltage-gated potassium channel Kcnc3 (Kv3.3) was significantly up-regulated in the cerebella of the miR-29a/b knockout mice. Dysregulation of KCNC3 expression may contribute to the ataxic phenotype.",
author = "Papadopoulou, {Aikaterini S} and Lutgarde Serneels and Tilmann Achsel and Wim Mandemakers and Zsuzsanna Callaerts-Vegh and James Dooley and Pierre Lau and Torik Ayoubi and Enrico Radaelli and Marco Spinazzi and Melanie Neumann and H{\'e}bert, {S{\'e}bastien S} and Asli Silahtaroglu and Adrian Liston and Rudi D'Hooge and Markus Glatzel and {De Strooper}, Bart",
note = "Copyright {\textcopyright} 2014. Published by Elsevier Inc.",
year = "2015",
month = jan,
doi = "10.1016/j.nbd.2014.10.006",
language = "English",
volume = "73",
pages = "275--288",
journal = "NEUROBIOL DIS",
issn = "0969-9961",
publisher = "Academic Press Inc.",

}

RIS

TY - JOUR

T1 - Deficiency of the miR-29a/b-1 cluster leads to ataxic features and cerebellar alterations in mice

AU - Papadopoulou, Aikaterini S

AU - Serneels, Lutgarde

AU - Achsel, Tilmann

AU - Mandemakers, Wim

AU - Callaerts-Vegh, Zsuzsanna

AU - Dooley, James

AU - Lau, Pierre

AU - Ayoubi, Torik

AU - Radaelli, Enrico

AU - Spinazzi, Marco

AU - Neumann, Melanie

AU - Hébert, Sébastien S

AU - Silahtaroglu, Asli

AU - Liston, Adrian

AU - D'Hooge, Rudi

AU - Glatzel, Markus

AU - De Strooper, Bart

N1 - Copyright © 2014. Published by Elsevier Inc.

PY - 2015/1

Y1 - 2015/1

N2 - miR-29 is expressed strongly in the brain and alterations in expression have been linked to several neurological disorders. To further explore the function of this miRNA in the brain, we generated miR-29a/b-1 knockout animals. Knockout mice develop a progressive disorder characterized by locomotor impairment and ataxia. The different members of the miR-29 family are strongly expressed in neurons of the olfactory bulb, the hippocampus and in the Purkinje cells of the cerebellum. Morphological analysis showed that Purkinje cells are smaller and display less dendritic arborisation compared to their wildtype littermates. In addition, a decreased number of parallel fibers form synapses on the Purkinje cells. We identified several mRNAs significantly up-regulated in the absence of the miR-29a/b-1 cluster. At the protein level, however, the voltage-gated potassium channel Kcnc3 (Kv3.3) was significantly up-regulated in the cerebella of the miR-29a/b knockout mice. Dysregulation of KCNC3 expression may contribute to the ataxic phenotype.

AB - miR-29 is expressed strongly in the brain and alterations in expression have been linked to several neurological disorders. To further explore the function of this miRNA in the brain, we generated miR-29a/b-1 knockout animals. Knockout mice develop a progressive disorder characterized by locomotor impairment and ataxia. The different members of the miR-29 family are strongly expressed in neurons of the olfactory bulb, the hippocampus and in the Purkinje cells of the cerebellum. Morphological analysis showed that Purkinje cells are smaller and display less dendritic arborisation compared to their wildtype littermates. In addition, a decreased number of parallel fibers form synapses on the Purkinje cells. We identified several mRNAs significantly up-regulated in the absence of the miR-29a/b-1 cluster. At the protein level, however, the voltage-gated potassium channel Kcnc3 (Kv3.3) was significantly up-regulated in the cerebella of the miR-29a/b knockout mice. Dysregulation of KCNC3 expression may contribute to the ataxic phenotype.

U2 - 10.1016/j.nbd.2014.10.006

DO - 10.1016/j.nbd.2014.10.006

M3 - SCORING: Journal article

C2 - 25315682

VL - 73

SP - 275

EP - 288

JO - NEUROBIOL DIS

JF - NEUROBIOL DIS

SN - 0969-9961

ER -