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Re-evaluation of neuronal P2X7 expression using novel mouse models and a P2X7-specific nanobody

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Re-evaluation of neuronal P2X7 expression using novel mouse models and a P2X7-specific nanobody. / Kaczmarek-Hajek, Karina; Zhang, Jiong; Kopp, Robin; Grosche, Antje; Rissiek, Björn; Saul, Anika; Bruzzone, Santina; Engel, Tobias; Jooss, Tina; Krautloher, Anna; Schuster, Stefanie; Magnus, Tim; Stadelmann, Christine; Sirko, Swetlana; Koch-Nolte, Friedrich; Eulenburg, Volker; Nicke, Annette.

In: ELIFE, Vol. 7, 03.08.2018, p. e36217.

Research output: SCORING: Contribution to journal › SCORING: Journal article › Research › peer-review

Harvard

Kaczmarek-Hajek, K, Zhang, J, Kopp, R, Grosche, A, Rissiek, B, Saul, A, Bruzzone, S, Engel, T, Jooss, T, Krautloher, A, Schuster, S, Magnus, T, Stadelmann, C, Sirko, S, Koch-Nolte, F, Eulenburg, V & Nicke, A 2018, 'Re-evaluation of neuronal P2X7 expression using novel mouse models and a P2X7-specific nanobody', ELIFE, vol. 7, pp. e36217. https://doi.org/10.7554/eLife.36217

APA

Kaczmarek-Hajek, K., Zhang, J., Kopp, R., Grosche, A., Rissiek, B., Saul, A., Bruzzone, S., Engel, T., Jooss, T., Krautloher, A., Schuster, S., Magnus, T., Stadelmann, C., Sirko, S., Koch-Nolte, F., Eulenburg, V., & Nicke, A. (2018). Re-evaluation of neuronal P2X7 expression using novel mouse models and a P2X7-specific nanobody. ELIFE, 7, e36217. https://doi.org/10.7554/eLife.36217

Vancouver

Kaczmarek-Hajek K, Zhang J, Kopp R, Grosche A, Rissiek B, Saul A et al. Re-evaluation of neuronal P2X7 expression using novel mouse models and a P2X7-specific nanobody. ELIFE. 2018 Aug 3;7:e36217. https://doi.org/10.7554/eLife.36217

Bibtex

@article{34e2912d58cc4c7e9e080f0a2e12746a,
title = "Re-evaluation of neuronal P2X7 expression using novel mouse models and a P2X7-specific nanobody",
abstract = "The P2X7 channel is involved in the pathogenesis of various CNS diseases. An increasing number of studies suggest its presence in neurons where its putative functions remain controversial for more than a decade. To resolve this issue and to provide a model for analysis of P2X7 functions, we generated P2X7-BAC transgenic mice that allow visualization of functional EGFP-tagged P2X7 receptors in vivo. Extensive characterization of these mice revealed dominant P2X7-EGFP protein expression in microglia, Bergmann glia, and oligodendrocytes, but not in neurons. These findings were further validated by microglia- and oligodendrocyte-specific P2X7 deletion and a novel P2X7-specific nanobody. In addition to the first quantitative analysis of P2X7 protein expression in the CNS, we show potential consequences of its overexpression in ischemic retina and post-traumatic cerebral cortex grey matter. This novel mouse model overcomes previous limitations in P2X7 research and will help to determine its physiological roles and contribution to diseases.",
keywords = "Journal Article",
author = "Karina Kaczmarek-Hajek and Jiong Zhang and Robin Kopp and Antje Grosche and Bj{\"o}rn Rissiek and Anika Saul and Santina Bruzzone and Tobias Engel and Tina Jooss and Anna Krautloher and Stefanie Schuster and Tim Magnus and Christine Stadelmann and Swetlana Sirko and Friedrich Koch-Nolte and Volker Eulenburg and Annette Nicke",
note = "{\textcopyright} 2018, Kaczmarek-Hajek et al.",
year = "2018",
month = aug,
day = "3",
doi = "10.7554/eLife.36217",
language = "English",
volume = "7",
pages = "e36217",
journal = "ELIFE",
issn = "2050-084X",
publisher = "eLife Sciences Publications",

}

RIS

TY - JOUR

T1 - Re-evaluation of neuronal P2X7 expression using novel mouse models and a P2X7-specific nanobody

AU - Kaczmarek-Hajek, Karina

AU - Zhang, Jiong

AU - Kopp, Robin

AU - Grosche, Antje

AU - Rissiek, Björn

AU - Saul, Anika

AU - Bruzzone, Santina

AU - Engel, Tobias

AU - Jooss, Tina

AU - Krautloher, Anna

AU - Schuster, Stefanie

AU - Magnus, Tim

AU - Stadelmann, Christine

AU - Sirko, Swetlana

AU - Koch-Nolte, Friedrich

AU - Eulenburg, Volker

AU - Nicke, Annette

N1 - © 2018, Kaczmarek-Hajek et al.

PY - 2018/8/3

Y1 - 2018/8/3

N2 - The P2X7 channel is involved in the pathogenesis of various CNS diseases. An increasing number of studies suggest its presence in neurons where its putative functions remain controversial for more than a decade. To resolve this issue and to provide a model for analysis of P2X7 functions, we generated P2X7-BAC transgenic mice that allow visualization of functional EGFP-tagged P2X7 receptors in vivo. Extensive characterization of these mice revealed dominant P2X7-EGFP protein expression in microglia, Bergmann glia, and oligodendrocytes, but not in neurons. These findings were further validated by microglia- and oligodendrocyte-specific P2X7 deletion and a novel P2X7-specific nanobody. In addition to the first quantitative analysis of P2X7 protein expression in the CNS, we show potential consequences of its overexpression in ischemic retina and post-traumatic cerebral cortex grey matter. This novel mouse model overcomes previous limitations in P2X7 research and will help to determine its physiological roles and contribution to diseases.

AB - The P2X7 channel is involved in the pathogenesis of various CNS diseases. An increasing number of studies suggest its presence in neurons where its putative functions remain controversial for more than a decade. To resolve this issue and to provide a model for analysis of P2X7 functions, we generated P2X7-BAC transgenic mice that allow visualization of functional EGFP-tagged P2X7 receptors in vivo. Extensive characterization of these mice revealed dominant P2X7-EGFP protein expression in microglia, Bergmann glia, and oligodendrocytes, but not in neurons. These findings were further validated by microglia- and oligodendrocyte-specific P2X7 deletion and a novel P2X7-specific nanobody. In addition to the first quantitative analysis of P2X7 protein expression in the CNS, we show potential consequences of its overexpression in ischemic retina and post-traumatic cerebral cortex grey matter. This novel mouse model overcomes previous limitations in P2X7 research and will help to determine its physiological roles and contribution to diseases.

KW - Journal Article

U2 - 10.7554/eLife.36217

DO - 10.7554/eLife.36217

M3 - SCORING: Journal article

C2 - 30074479

VL - 7

SP - e36217

JO - ELIFE

JF - ELIFE

SN - 2050-084X

ER -