Tonic ATP-mediated growth suppression in peripheral nerve glia requires arrestin-PP2 and is evaded in NF1

Abstract Normal Schwann cells (SCs) are quiescent in adult nerves, when ATP is released from the nerve in an activity dependent manner. We find that suppressing nerve activity in adult nerves causes SC to enter the cell cycle. In vitro, ATP activates the SC G-protein coupled receptor (GPCR) P2Y2. Do...
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Autor*in:	Coover, Robert A. [verfasserIn] Healy, Tabitha E. Guo, Li Chaney, Katherine E. Hennigan, Robert F. Thomson, Craig S. Aschbacher-Smith, Lindsey E. Jankowski, Michael P. Ratner, Nancy

Format:	E-Artikel
Sprache:	Englisch

Erschienen:	2018

Schlagwörter:	Glia Schwann PP2A AKT Purinergic Neurofibromatosis P2Y2 Arrestin ATP

Anmerkung:	© The Author(s). 2018

Übergeordnetes Werk:	Enthalten in: Acta Neuropathologica Communications - London : Biomed Central, 2013, 6(2018), 1 vom: 23. Nov.
Übergeordnetes Werk:	volume:6 ; year:2018 ; number:1 ; day:23 ; month:11

Links:	Volltext

DOI / URN:	10.1186/s40478-018-0635-9

Katalog-ID:	SPR036514276

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520			\|a Abstract Normal Schwann cells (SCs) are quiescent in adult nerves, when ATP is released from the nerve in an activity dependent manner. We find that suppressing nerve activity in adult nerves causes SC to enter the cell cycle. In vitro, ATP activates the SC G-protein coupled receptor (GPCR) P2Y2. Downstream of P2Y2, β-arrestin-mediated signaling results in PP2-mediated de-phosphorylation of AKT, and PP2 activity is required for SC growth suppression. NF1 deficient SC show reduced growth suppression by ATP, and are resistant to the effects of β-arrestin-mediated signaling, including PP2-mediated de-phosphorylation of AKT. In patients with the disorder Neurofibromatosis type 1, NF1 mutant SCs proliferate and form SC tumors called neurofibromas. Elevating ATP levels in vivo reduced neurofibroma cell proliferation. Thus, the low proliferation characteristic of differentiated adult peripheral nerve may require ongoing, nerve activity-dependent, ATP. Additionally, we identify a mechanism through which NF1 SCs may evade growth suppression in nerve tumors.
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allfields	10.1186/s40478-018-0635-9 doi (DE-627)SPR036514276 (SPR)s40478-018-0635-9-e DE-627 ger DE-627 rakwb eng Coover, Robert A. verfasserin aut Tonic ATP-mediated growth suppression in peripheral nerve glia requires arrestin-PP2 and is evaded in NF1 2018 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier © The Author(s). 2018 Abstract Normal Schwann cells (SCs) are quiescent in adult nerves, when ATP is released from the nerve in an activity dependent manner. We find that suppressing nerve activity in adult nerves causes SC to enter the cell cycle. In vitro, ATP activates the SC G-protein coupled receptor (GPCR) P2Y2. Downstream of P2Y2, β-arrestin-mediated signaling results in PP2-mediated de-phosphorylation of AKT, and PP2 activity is required for SC growth suppression. NF1 deficient SC show reduced growth suppression by ATP, and are resistant to the effects of β-arrestin-mediated signaling, including PP2-mediated de-phosphorylation of AKT. In patients with the disorder Neurofibromatosis type 1, NF1 mutant SCs proliferate and form SC tumors called neurofibromas. Elevating ATP levels in vivo reduced neurofibroma cell proliferation. Thus, the low proliferation characteristic of differentiated adult peripheral nerve may require ongoing, nerve activity-dependent, ATP. Additionally, we identify a mechanism through which NF1 SCs may evade growth suppression in nerve tumors. Glia (dpeaa)DE-He213 Schwann (dpeaa)DE-He213 PP2A (dpeaa)DE-He213 AKT (dpeaa)DE-He213 Purinergic (dpeaa)DE-He213 Neurofibromatosis (dpeaa)DE-He213 P2Y2 (dpeaa)DE-He213 Arrestin (dpeaa)DE-He213 ATP (dpeaa)DE-He213 Healy, Tabitha E. aut Guo, Li aut Chaney, Katherine E. aut Hennigan, Robert F. aut Thomson, Craig S. aut Aschbacher-Smith, Lindsey E. aut Jankowski, Michael P. aut Ratner, Nancy aut Enthalten in Acta Neuropathologica Communications London : Biomed Central, 2013 6(2018), 1 vom: 23. Nov. (DE-627)746066465 (DE-600)2715589-4 2051-5960 nnns volume:6 year:2018 number:1 day:23 month:11 https://dx.doi.org/10.1186/s40478-018-0635-9 kostenfrei Volltext GBV_USEFLAG_A SYSFLAG_A GBV_SPRINGER SSG-OLC-PHA GBV_ILN_11 GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_73 GBV_ILN_74 GBV_ILN_95 GBV_ILN_105 GBV_ILN_110 GBV_ILN_151 GBV_ILN_161 GBV_ILN_170 GBV_ILN_206 GBV_ILN_213 GBV_ILN_230 GBV_ILN_285 GBV_ILN_293 GBV_ILN_602 GBV_ILN_2003 GBV_ILN_2005 GBV_ILN_2009 GBV_ILN_2014 GBV_ILN_2055 GBV_ILN_2111 GBV_ILN_4012 GBV_ILN_4037 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4249 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4338 GBV_ILN_4367 GBV_ILN_4700 AR 6 2018 1 23 11
spelling	10.1186/s40478-018-0635-9 doi (DE-627)SPR036514276 (SPR)s40478-018-0635-9-e DE-627 ger DE-627 rakwb eng Coover, Robert A. verfasserin aut Tonic ATP-mediated growth suppression in peripheral nerve glia requires arrestin-PP2 and is evaded in NF1 2018 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier © The Author(s). 2018 Abstract Normal Schwann cells (SCs) are quiescent in adult nerves, when ATP is released from the nerve in an activity dependent manner. We find that suppressing nerve activity in adult nerves causes SC to enter the cell cycle. In vitro, ATP activates the SC G-protein coupled receptor (GPCR) P2Y2. Downstream of P2Y2, β-arrestin-mediated signaling results in PP2-mediated de-phosphorylation of AKT, and PP2 activity is required for SC growth suppression. NF1 deficient SC show reduced growth suppression by ATP, and are resistant to the effects of β-arrestin-mediated signaling, including PP2-mediated de-phosphorylation of AKT. In patients with the disorder Neurofibromatosis type 1, NF1 mutant SCs proliferate and form SC tumors called neurofibromas. Elevating ATP levels in vivo reduced neurofibroma cell proliferation. Thus, the low proliferation characteristic of differentiated adult peripheral nerve may require ongoing, nerve activity-dependent, ATP. Additionally, we identify a mechanism through which NF1 SCs may evade growth suppression in nerve tumors. Glia (dpeaa)DE-He213 Schwann (dpeaa)DE-He213 PP2A (dpeaa)DE-He213 AKT (dpeaa)DE-He213 Purinergic (dpeaa)DE-He213 Neurofibromatosis (dpeaa)DE-He213 P2Y2 (dpeaa)DE-He213 Arrestin (dpeaa)DE-He213 ATP (dpeaa)DE-He213 Healy, Tabitha E. aut Guo, Li aut Chaney, Katherine E. aut Hennigan, Robert F. aut Thomson, Craig S. aut Aschbacher-Smith, Lindsey E. aut Jankowski, Michael P. aut Ratner, Nancy aut Enthalten in Acta Neuropathologica Communications London : Biomed Central, 2013 6(2018), 1 vom: 23. Nov. (DE-627)746066465 (DE-600)2715589-4 2051-5960 nnns volume:6 year:2018 number:1 day:23 month:11 https://dx.doi.org/10.1186/s40478-018-0635-9 kostenfrei Volltext GBV_USEFLAG_A SYSFLAG_A GBV_SPRINGER SSG-OLC-PHA GBV_ILN_11 GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_73 GBV_ILN_74 GBV_ILN_95 GBV_ILN_105 GBV_ILN_110 GBV_ILN_151 GBV_ILN_161 GBV_ILN_170 GBV_ILN_206 GBV_ILN_213 GBV_ILN_230 GBV_ILN_285 GBV_ILN_293 GBV_ILN_602 GBV_ILN_2003 GBV_ILN_2005 GBV_ILN_2009 GBV_ILN_2014 GBV_ILN_2055 GBV_ILN_2111 GBV_ILN_4012 GBV_ILN_4037 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4249 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4338 GBV_ILN_4367 GBV_ILN_4700 AR 6 2018 1 23 11
allfields_unstemmed	10.1186/s40478-018-0635-9 doi (DE-627)SPR036514276 (SPR)s40478-018-0635-9-e DE-627 ger DE-627 rakwb eng Coover, Robert A. verfasserin aut Tonic ATP-mediated growth suppression in peripheral nerve glia requires arrestin-PP2 and is evaded in NF1 2018 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier © The Author(s). 2018 Abstract Normal Schwann cells (SCs) are quiescent in adult nerves, when ATP is released from the nerve in an activity dependent manner. We find that suppressing nerve activity in adult nerves causes SC to enter the cell cycle. In vitro, ATP activates the SC G-protein coupled receptor (GPCR) P2Y2. Downstream of P2Y2, β-arrestin-mediated signaling results in PP2-mediated de-phosphorylation of AKT, and PP2 activity is required for SC growth suppression. NF1 deficient SC show reduced growth suppression by ATP, and are resistant to the effects of β-arrestin-mediated signaling, including PP2-mediated de-phosphorylation of AKT. In patients with the disorder Neurofibromatosis type 1, NF1 mutant SCs proliferate and form SC tumors called neurofibromas. Elevating ATP levels in vivo reduced neurofibroma cell proliferation. Thus, the low proliferation characteristic of differentiated adult peripheral nerve may require ongoing, nerve activity-dependent, ATP. Additionally, we identify a mechanism through which NF1 SCs may evade growth suppression in nerve tumors. Glia (dpeaa)DE-He213 Schwann (dpeaa)DE-He213 PP2A (dpeaa)DE-He213 AKT (dpeaa)DE-He213 Purinergic (dpeaa)DE-He213 Neurofibromatosis (dpeaa)DE-He213 P2Y2 (dpeaa)DE-He213 Arrestin (dpeaa)DE-He213 ATP (dpeaa)DE-He213 Healy, Tabitha E. aut Guo, Li aut Chaney, Katherine E. aut Hennigan, Robert F. aut Thomson, Craig S. aut Aschbacher-Smith, Lindsey E. aut Jankowski, Michael P. aut Ratner, Nancy aut Enthalten in Acta Neuropathologica Communications London : Biomed Central, 2013 6(2018), 1 vom: 23. Nov. (DE-627)746066465 (DE-600)2715589-4 2051-5960 nnns volume:6 year:2018 number:1 day:23 month:11 https://dx.doi.org/10.1186/s40478-018-0635-9 kostenfrei Volltext GBV_USEFLAG_A SYSFLAG_A GBV_SPRINGER SSG-OLC-PHA GBV_ILN_11 GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_73 GBV_ILN_74 GBV_ILN_95 GBV_ILN_105 GBV_ILN_110 GBV_ILN_151 GBV_ILN_161 GBV_ILN_170 GBV_ILN_206 GBV_ILN_213 GBV_ILN_230 GBV_ILN_285 GBV_ILN_293 GBV_ILN_602 GBV_ILN_2003 GBV_ILN_2005 GBV_ILN_2009 GBV_ILN_2014 GBV_ILN_2055 GBV_ILN_2111 GBV_ILN_4012 GBV_ILN_4037 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4249 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4338 GBV_ILN_4367 GBV_ILN_4700 AR 6 2018 1 23 11
allfieldsGer	10.1186/s40478-018-0635-9 doi (DE-627)SPR036514276 (SPR)s40478-018-0635-9-e DE-627 ger DE-627 rakwb eng Coover, Robert A. verfasserin aut Tonic ATP-mediated growth suppression in peripheral nerve glia requires arrestin-PP2 and is evaded in NF1 2018 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier © The Author(s). 2018 Abstract Normal Schwann cells (SCs) are quiescent in adult nerves, when ATP is released from the nerve in an activity dependent manner. We find that suppressing nerve activity in adult nerves causes SC to enter the cell cycle. In vitro, ATP activates the SC G-protein coupled receptor (GPCR) P2Y2. Downstream of P2Y2, β-arrestin-mediated signaling results in PP2-mediated de-phosphorylation of AKT, and PP2 activity is required for SC growth suppression. NF1 deficient SC show reduced growth suppression by ATP, and are resistant to the effects of β-arrestin-mediated signaling, including PP2-mediated de-phosphorylation of AKT. In patients with the disorder Neurofibromatosis type 1, NF1 mutant SCs proliferate and form SC tumors called neurofibromas. Elevating ATP levels in vivo reduced neurofibroma cell proliferation. Thus, the low proliferation characteristic of differentiated adult peripheral nerve may require ongoing, nerve activity-dependent, ATP. Additionally, we identify a mechanism through which NF1 SCs may evade growth suppression in nerve tumors. Glia (dpeaa)DE-He213 Schwann (dpeaa)DE-He213 PP2A (dpeaa)DE-He213 AKT (dpeaa)DE-He213 Purinergic (dpeaa)DE-He213 Neurofibromatosis (dpeaa)DE-He213 P2Y2 (dpeaa)DE-He213 Arrestin (dpeaa)DE-He213 ATP (dpeaa)DE-He213 Healy, Tabitha E. aut Guo, Li aut Chaney, Katherine E. aut Hennigan, Robert F. aut Thomson, Craig S. aut Aschbacher-Smith, Lindsey E. aut Jankowski, Michael P. aut Ratner, Nancy aut Enthalten in Acta Neuropathologica Communications London : Biomed Central, 2013 6(2018), 1 vom: 23. Nov. (DE-627)746066465 (DE-600)2715589-4 2051-5960 nnns volume:6 year:2018 number:1 day:23 month:11 https://dx.doi.org/10.1186/s40478-018-0635-9 kostenfrei Volltext GBV_USEFLAG_A SYSFLAG_A GBV_SPRINGER SSG-OLC-PHA GBV_ILN_11 GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_73 GBV_ILN_74 GBV_ILN_95 GBV_ILN_105 GBV_ILN_110 GBV_ILN_151 GBV_ILN_161 GBV_ILN_170 GBV_ILN_206 GBV_ILN_213 GBV_ILN_230 GBV_ILN_285 GBV_ILN_293 GBV_ILN_602 GBV_ILN_2003 GBV_ILN_2005 GBV_ILN_2009 GBV_ILN_2014 GBV_ILN_2055 GBV_ILN_2111 GBV_ILN_4012 GBV_ILN_4037 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4249 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4338 GBV_ILN_4367 GBV_ILN_4700 AR 6 2018 1 23 11
allfieldsSound	10.1186/s40478-018-0635-9 doi (DE-627)SPR036514276 (SPR)s40478-018-0635-9-e DE-627 ger DE-627 rakwb eng Coover, Robert A. verfasserin aut Tonic ATP-mediated growth suppression in peripheral nerve glia requires arrestin-PP2 and is evaded in NF1 2018 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier © The Author(s). 2018 Abstract Normal Schwann cells (SCs) are quiescent in adult nerves, when ATP is released from the nerve in an activity dependent manner. We find that suppressing nerve activity in adult nerves causes SC to enter the cell cycle. In vitro, ATP activates the SC G-protein coupled receptor (GPCR) P2Y2. Downstream of P2Y2, β-arrestin-mediated signaling results in PP2-mediated de-phosphorylation of AKT, and PP2 activity is required for SC growth suppression. NF1 deficient SC show reduced growth suppression by ATP, and are resistant to the effects of β-arrestin-mediated signaling, including PP2-mediated de-phosphorylation of AKT. In patients with the disorder Neurofibromatosis type 1, NF1 mutant SCs proliferate and form SC tumors called neurofibromas. Elevating ATP levels in vivo reduced neurofibroma cell proliferation. Thus, the low proliferation characteristic of differentiated adult peripheral nerve may require ongoing, nerve activity-dependent, ATP. Additionally, we identify a mechanism through which NF1 SCs may evade growth suppression in nerve tumors. Glia (dpeaa)DE-He213 Schwann (dpeaa)DE-He213 PP2A (dpeaa)DE-He213 AKT (dpeaa)DE-He213 Purinergic (dpeaa)DE-He213 Neurofibromatosis (dpeaa)DE-He213 P2Y2 (dpeaa)DE-He213 Arrestin (dpeaa)DE-He213 ATP (dpeaa)DE-He213 Healy, Tabitha E. aut Guo, Li aut Chaney, Katherine E. aut Hennigan, Robert F. aut Thomson, Craig S. aut Aschbacher-Smith, Lindsey E. aut Jankowski, Michael P. aut Ratner, Nancy aut Enthalten in Acta Neuropathologica Communications London : Biomed Central, 2013 6(2018), 1 vom: 23. Nov. (DE-627)746066465 (DE-600)2715589-4 2051-5960 nnns volume:6 year:2018 number:1 day:23 month:11 https://dx.doi.org/10.1186/s40478-018-0635-9 kostenfrei Volltext GBV_USEFLAG_A SYSFLAG_A GBV_SPRINGER SSG-OLC-PHA GBV_ILN_11 GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_73 GBV_ILN_74 GBV_ILN_95 GBV_ILN_105 GBV_ILN_110 GBV_ILN_151 GBV_ILN_161 GBV_ILN_170 GBV_ILN_206 GBV_ILN_213 GBV_ILN_230 GBV_ILN_285 GBV_ILN_293 GBV_ILN_602 GBV_ILN_2003 GBV_ILN_2005 GBV_ILN_2009 GBV_ILN_2014 GBV_ILN_2055 GBV_ILN_2111 GBV_ILN_4012 GBV_ILN_4037 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4249 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4338 GBV_ILN_4367 GBV_ILN_4700 AR 6 2018 1 23 11
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authorswithroles_txt_mv	Coover, Robert A. @@aut@@ Healy, Tabitha E. @@aut@@ Guo, Li @@aut@@ Chaney, Katherine E. @@aut@@ Hennigan, Robert F. @@aut@@ Thomson, Craig S. @@aut@@ Aschbacher-Smith, Lindsey E. @@aut@@ Jankowski, Michael P. @@aut@@ Ratner, Nancy @@aut@@
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author	Coover, Robert A.
spellingShingle	Coover, Robert A. misc Glia misc Schwann misc PP2A misc AKT misc Purinergic misc Neurofibromatosis misc P2Y2 misc Arrestin misc ATP Tonic ATP-mediated growth suppression in peripheral nerve glia requires arrestin-PP2 and is evaded in NF1
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topic_title	Tonic ATP-mediated growth suppression in peripheral nerve glia requires arrestin-PP2 and is evaded in NF1 Glia (dpeaa)DE-He213 Schwann (dpeaa)DE-He213 PP2A (dpeaa)DE-He213 AKT (dpeaa)DE-He213 Purinergic (dpeaa)DE-He213 Neurofibromatosis (dpeaa)DE-He213 P2Y2 (dpeaa)DE-He213 Arrestin (dpeaa)DE-He213 ATP (dpeaa)DE-He213
topic	misc Glia misc Schwann misc PP2A misc AKT misc Purinergic misc Neurofibromatosis misc P2Y2 misc Arrestin misc ATP
topic_unstemmed	misc Glia misc Schwann misc PP2A misc AKT misc Purinergic misc Neurofibromatosis misc P2Y2 misc Arrestin misc ATP
topic_browse	misc Glia misc Schwann misc PP2A misc AKT misc Purinergic misc Neurofibromatosis misc P2Y2 misc Arrestin misc ATP
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title	Tonic ATP-mediated growth suppression in peripheral nerve glia requires arrestin-PP2 and is evaded in NF1
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title_full	Tonic ATP-mediated growth suppression in peripheral nerve glia requires arrestin-PP2 and is evaded in NF1
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author_browse	Coover, Robert A. Healy, Tabitha E. Guo, Li Chaney, Katherine E. Hennigan, Robert F. Thomson, Craig S. Aschbacher-Smith, Lindsey E. Jankowski, Michael P. Ratner, Nancy
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title_sort	tonic atp-mediated growth suppression in peripheral nerve glia requires arrestin-pp2 and is evaded in nf1
title_auth	Tonic ATP-mediated growth suppression in peripheral nerve glia requires arrestin-PP2 and is evaded in NF1
abstract	Abstract Normal Schwann cells (SCs) are quiescent in adult nerves, when ATP is released from the nerve in an activity dependent manner. We find that suppressing nerve activity in adult nerves causes SC to enter the cell cycle. In vitro, ATP activates the SC G-protein coupled receptor (GPCR) P2Y2. Downstream of P2Y2, β-arrestin-mediated signaling results in PP2-mediated de-phosphorylation of AKT, and PP2 activity is required for SC growth suppression. NF1 deficient SC show reduced growth suppression by ATP, and are resistant to the effects of β-arrestin-mediated signaling, including PP2-mediated de-phosphorylation of AKT. In patients with the disorder Neurofibromatosis type 1, NF1 mutant SCs proliferate and form SC tumors called neurofibromas. Elevating ATP levels in vivo reduced neurofibroma cell proliferation. Thus, the low proliferation characteristic of differentiated adult peripheral nerve may require ongoing, nerve activity-dependent, ATP. Additionally, we identify a mechanism through which NF1 SCs may evade growth suppression in nerve tumors. © The Author(s). 2018
abstractGer	Abstract Normal Schwann cells (SCs) are quiescent in adult nerves, when ATP is released from the nerve in an activity dependent manner. We find that suppressing nerve activity in adult nerves causes SC to enter the cell cycle. In vitro, ATP activates the SC G-protein coupled receptor (GPCR) P2Y2. Downstream of P2Y2, β-arrestin-mediated signaling results in PP2-mediated de-phosphorylation of AKT, and PP2 activity is required for SC growth suppression. NF1 deficient SC show reduced growth suppression by ATP, and are resistant to the effects of β-arrestin-mediated signaling, including PP2-mediated de-phosphorylation of AKT. In patients with the disorder Neurofibromatosis type 1, NF1 mutant SCs proliferate and form SC tumors called neurofibromas. Elevating ATP levels in vivo reduced neurofibroma cell proliferation. Thus, the low proliferation characteristic of differentiated adult peripheral nerve may require ongoing, nerve activity-dependent, ATP. Additionally, we identify a mechanism through which NF1 SCs may evade growth suppression in nerve tumors. © The Author(s). 2018
abstract_unstemmed	Abstract Normal Schwann cells (SCs) are quiescent in adult nerves, when ATP is released from the nerve in an activity dependent manner. We find that suppressing nerve activity in adult nerves causes SC to enter the cell cycle. In vitro, ATP activates the SC G-protein coupled receptor (GPCR) P2Y2. Downstream of P2Y2, β-arrestin-mediated signaling results in PP2-mediated de-phosphorylation of AKT, and PP2 activity is required for SC growth suppression. NF1 deficient SC show reduced growth suppression by ATP, and are resistant to the effects of β-arrestin-mediated signaling, including PP2-mediated de-phosphorylation of AKT. In patients with the disorder Neurofibromatosis type 1, NF1 mutant SCs proliferate and form SC tumors called neurofibromas. Elevating ATP levels in vivo reduced neurofibroma cell proliferation. Thus, the low proliferation characteristic of differentiated adult peripheral nerve may require ongoing, nerve activity-dependent, ATP. Additionally, we identify a mechanism through which NF1 SCs may evade growth suppression in nerve tumors. © The Author(s). 2018
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title_short	Tonic ATP-mediated growth suppression in peripheral nerve glia requires arrestin-PP2 and is evaded in NF1
url	https://dx.doi.org/10.1186/s40478-018-0635-9
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author2	Healy, Tabitha E. Guo, Li Chaney, Katherine E. Hennigan, Robert F. Thomson, Craig S. Aschbacher-Smith, Lindsey E. Jankowski, Michael P. Ratner, Nancy
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up_date	2024-07-03T18:05:30.667Z
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Tonic ATP-mediated growth suppression in peripheral nerve glia requires arrestin-PP2 and is evaded in NF1

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