دورية أكاديمية
أعرض في EDS

SHP2 regulates GluA2 tyrosine phosphorylation required for AMPA receptor endocytosis and mGluR-LTD.

التفاصيل البيبلوغرافية
العنوان: SHP2 regulates GluA2 tyrosine phosphorylation required for AMPA receptor endocytosis and mGluR-LTD.
المؤلفون: Lee S; Department of Biomedical Sciences, Seoul National University College of Medicine, Seoul 03080, South Korea.; Neuroscience Research Institute, Medical Research Center, Seoul National University College of Medicine, Seoul 03080, South Korea.; Transplantation Research Institute, Medical Research Center, Seoul National University College of Medicine, Seoul 03080, South Korea., Kim J; Department of Biomedical Sciences, Seoul National University College of Medicine, Seoul 03080, South Korea.; Neuroscience Research Institute, Medical Research Center, Seoul National University College of Medicine, Seoul 03080, South Korea.; Transplantation Research Institute, Medical Research Center, Seoul National University College of Medicine, Seoul 03080, South Korea., Ryu HH; Department of Biomedical Sciences, Seoul National University College of Medicine, Seoul 03080, South Korea.; Neuroscience Research Institute, Medical Research Center, Seoul National University College of Medicine, Seoul 03080, South Korea.; Department of Physiology, Seoul National University College of Medicine, Seoul 03080, South Korea., Jang H; Department of Biomedical Sciences, Seoul National University College of Medicine, Seoul 03080, South Korea.; Neuroscience Research Institute, Medical Research Center, Seoul National University College of Medicine, Seoul 03080, South Korea.; Department of Physiology, Seoul National University College of Medicine, Seoul 03080, South Korea., Lee D; Department of Biomedical Sciences, Seoul National University College of Medicine, Seoul 03080, South Korea.; Neuroscience Research Institute, Medical Research Center, Seoul National University College of Medicine, Seoul 03080, South Korea.; Transplantation Research Institute, Medical Research Center, Seoul National University College of Medicine, Seoul 03080, South Korea., Lee S; Department of Biomedical Sciences, Seoul National University College of Medicine, Seoul 03080, South Korea.; Neuroscience Research Institute, Medical Research Center, Seoul National University College of Medicine, Seoul 03080, South Korea.; Transplantation Research Institute, Medical Research Center, Seoul National University College of Medicine, Seoul 03080, South Korea., Song JM; Department of Biomedical Sciences, Seoul National University College of Medicine, Seoul 03080, South Korea.; Neuroscience Research Institute, Medical Research Center, Seoul National University College of Medicine, Seoul 03080, South Korea.; Transplantation Research Institute, Medical Research Center, Seoul National University College of Medicine, Seoul 03080, South Korea., Lee YS; Department of Biomedical Sciences, Seoul National University College of Medicine, Seoul 03080, South Korea.; Neuroscience Research Institute, Medical Research Center, Seoul National University College of Medicine, Seoul 03080, South Korea.; Department of Physiology, Seoul National University College of Medicine, Seoul 03080, South Korea., Suh YH; Department of Biomedical Sciences, Seoul National University College of Medicine, Seoul 03080, South Korea.; Neuroscience Research Institute, Medical Research Center, Seoul National University College of Medicine, Seoul 03080, South Korea.; Transplantation Research Institute, Medical Research Center, Seoul National University College of Medicine, Seoul 03080, South Korea.
المصدر: Proceedings of the National Academy of Sciences of the United States of America [Proc Natl Acad Sci U S A] 2024 Apr 30; Vol. 121 (18), pp. e2316819121. Date of Electronic Publication: 2024 Apr 24.
نوع المنشور: Journal Article; Research Support, Non-U.S. Gov't; Research Support, N.I.H., Extramural
اللغة: English
بيانات الدورية: Publisher: National Academy of Sciences Country of Publication: United States NLM ID: 7505876 Publication Model: Print-Electronic Cited Medium: Internet ISSN: 1091-6490 (Electronic) Linking ISSN: 00278424 NLM ISO Abbreviation: Proc Natl Acad Sci U S A Subsets: MEDLINE
أسماء مطبوعة: Original Publication: Washington, DC : National Academy of Sciences
مواضيع طبية MeSH: Receptors, AMPA*/metabolism , Endocytosis*/physiology , Long-Term Synaptic Depression*/physiology , Receptors, Metabotropic Glutamate*/metabolism , Protein Tyrosine Phosphatase, Non-Receptor Type 11*/metabolism , Protein Tyrosine Phosphatase, Non-Receptor Type 11*/genetics, Animals ; Phosphorylation ; Rats ; Tyrosine/metabolism ; Receptor, Metabotropic Glutamate 5/metabolism ; Synapses/metabolism ; Mice ; Humans ; Neurons/metabolism
مستخلص: Posttranslational modifications regulate the properties and abundance of synaptic α-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid (AMPA) receptors that mediate fast excitatory synaptic transmission and synaptic plasticity in the central nervous system. During long-term depression (LTD), protein tyrosine phosphatases (PTPs) dephosphorylate tyrosine residues in the C-terminal tail of AMPA receptor GluA2 subunit, which is essential for GluA2 endocytosis and group I metabotropic glutamate receptor (mGluR)-dependent LTD. However, as a selective downstream effector of mGluRs, the mGluR-dependent PTP responsible for GluA2 tyrosine dephosphorylation remains elusive at Schaffer collateral (SC)-CA1 synapses. In the present study, we find that mGluR5 stimulation activates Src homology 2 (SH2) domain-containing phosphatase 2 (SHP2) by increasing phospho-Y542 levels in SHP2. Under steady-state conditions, SHP2 plays a protective role in stabilizing phospho-Y869 of GluA2 by directly interacting with GluA2 phosphorylated at Y869, without affecting GluA2 phospho-Y876 levels. Upon mGluR5 stimulation, SHP2 dephosphorylates GluA2 at Y869 and Y876, resulting in GluA2 endocytosis and mGluR-LTD. Our results establish SHP2 as a downstream effector of mGluR5 and indicate a dual action of SHP2 in regulating GluA2 tyrosine phosphorylation and function. Given the implications of mGluR5 and SHP2 in synaptic pathophysiology, we propose SHP2 as a promising therapeutic target for neurodevelopmental and autism spectrum disorders.
Competing Interests: Competing interests statement:The authors declare no competing interest.
References: Neuron. 2004 Sep 30;44(1):5-21. (PMID: 15450156)
J Neurochem. 2006 Jan;96(1):179-94. (PMID: 16277605)
Nat Neurosci. 2001 Nov;4(11):1079-85. (PMID: 11687813)
J Biol Chem. 2016 Sep 2;291(36):18856-66. (PMID: 27417137)
Nature. 2016 Jul 7;535(7610):148-52. (PMID: 27362227)
Trends Neurosci. 2004 Jul;27(7):370-7. (PMID: 15219735)
Nature. 1999 Jan 7;397(6714):72-6. (PMID: 9892356)
Mol Cell. 2001 Oct;8(4):759-69. (PMID: 11684012)
Neuron. 2010 Feb 25;65(4):445-59. (PMID: 20188650)
Korean J Physiol Pharmacol. 2020 Mar;24(2):129-135. (PMID: 32140036)
Neuron. 2003 Jul 3;39(1):163-76. (PMID: 12848940)
Neuropharmacology. 1997 Mar;36(3):397-9. (PMID: 9175619)
Neuron. 1996 Nov;17(5):945-56. (PMID: 8938126)
Cell. 2020 Oct 15;183(2):490-502.e18. (PMID: 33002410)
J Biol Chem. 2020 Jul 17;295(29):10023-10031. (PMID: 32499374)
J Biol Chem. 2003 Feb 21;278(8):6516-20. (PMID: 12482860)
Neurosci Lett. 1991 Jun 10;127(1):61-6. (PMID: 1679224)
Neuron. 2010 Jun 10;66(5):768-80. (PMID: 20547133)
J Biol Chem. 2017 Sep 15;292(37):15481-15488. (PMID: 28768764)
Trends Biochem Sci. 2003 Jun;28(6):284-93. (PMID: 12826400)
Cell Rep. 2018 Aug 7;24(6):1523-1535. (PMID: 30089263)
Proc Natl Acad Sci U S A. 1994 Jul 19;91(15):7335-9. (PMID: 8041791)
Proc Natl Acad Sci U S A. 1992 May 15;89(10):4363-7. (PMID: 1350090)
Neuropharmacology. 2002 Aug;43(2):175-80. (PMID: 12213271)
EMBO J. 2004 Mar 10;23(5):1040-50. (PMID: 14976558)
Mol Cell Biol. 2015 May;35(9):1557-72. (PMID: 25713104)
Neuron. 1992 Nov;9(5):967-75. (PMID: 1419003)
Neuropharmacology. 1997 Nov-Dec;36(11-12):1517-32. (PMID: 9517422)
Neurosci Lett. 2022 May 14;779:136636. (PMID: 35439551)
Mol Pharmacol. 2006 Aug;70(2):562-70. (PMID: 16717135)
J Neurosci. 2006 Mar 1;26(9):2544-54. (PMID: 16510732)
Nat Rev Neurosci. 2010 Jul;11(7):459-73. (PMID: 20559335)
Neurosci Lett. 2017 May 10;649:41-47. (PMID: 28366775)
J Biol Chem. 2021 Jan-Jun;296:100538. (PMID: 33722610)
Neuron. 2013 Oct 30;80(3):704-17. (PMID: 24183021)
Proc Natl Acad Sci U S A. 2013 Mar 5;110(10):E948-57. (PMID: 23431139)
Trends Neurosci. 2011 Dec;34(12):629-37. (PMID: 22051158)
J Neurosci. 2020 May 27;40(22):4277-4296. (PMID: 32341099)
Nature. 2023 Sep;621(7977):146-153. (PMID: 37648853)
Elife. 2021 Mar 23;10:. (PMID: 33755016)
Cell Signal. 2008 Mar;20(3):453-9. (PMID: 17993263)
J Neurosci. 2004 Jul 7;24(27):6152-60. (PMID: 15240807)
Cell. 1998 Feb 20;92(4):441-50. (PMID: 9491886)
Eur J Pharmacol. 1993 Aug 3;239(1-3):265-6. (PMID: 8223907)
Mol Cell Neurosci. 2009 Feb;40(2):267-79. (PMID: 19063969)
J Proteome Res. 2008 Jan;7(1):311-8. (PMID: 18034455)
Pharmacol Rev. 2012 Jan;64(1):65-87. (PMID: 22090472)
Annu Rev Genomics Hum Genet. 2017 Aug 31;18:115-142. (PMID: 28859574)
J Neurosci. 2008 Oct 15;28(42):10561-6. (PMID: 18923032)
Front Synaptic Neurosci. 2018 Nov 13;10:41. (PMID: 30483111)
Proc Natl Acad Sci U S A. 2020 Mar 3;117(9):4948-4958. (PMID: 32071234)
Nat Neurosci. 2014 Dec;17(12):1736-43. (PMID: 25383899)
Eur J Med Genet. 2015 Oct;58(10):509-25. (PMID: 26341048)
Hippocampus. 2007;17(8):600-5. (PMID: 17534972)
Neuropharmacology. 1999 Apr;38(4):495-504. (PMID: 10221753)
Biochem Biophys Res Commun. 2021 Sep 10;569:72-78. (PMID: 34237430)
Annu Rev Genomics Hum Genet. 2013;14:355-69. (PMID: 23875798)
Mol Neurobiol. 2017 Nov;54(9):7235-7250. (PMID: 27796759)
Pain. 2012 May;153(5):1042-1053. (PMID: 22425446)
Neuron. 2018 Oct 24;100(2):314-329. (PMID: 30359599)
Brain Res Mol Brain Res. 1999 Jun 18;70(1):18-25. (PMID: 10381539)
Science. 2024 Mar;383(6686):eadk1291. (PMID: 38422154)
J Physiol. 2008 May 15;586(10):2499-510. (PMID: 18356198)
Neuropharmacology. 1999 Oct;38(10):1577-83. (PMID: 10530819)
معلومات مُعتمدة: NRF-2018R1A2B6004759 National Research Foundation of Korea (NRF); NRF-2020R1A5A1019023 National Research Foundation of Korea (NRF); NRF-2022R1A2C1004913 National Research Foundation of Korea (NRF); NRF-2023R1A2C2003229 National Research Foundation of Korea (NRF); NRF-2018R1A5A2025964 National Research Foundation of Korea (NRF); HU21C0071 Korea Dementia Research Center (KDRC)
فهرسة مساهمة: Keywords: GluA2; SHP2; mGluR-LTD; mGluR5; trafficking
المشرفين على المادة: 0 (Receptors, AMPA)
P6W5IXV8V9 (glutamate receptor ionotropic, AMPA 2)
0 (Receptors, Metabotropic Glutamate)
EC 3.1.3.48 (Protein Tyrosine Phosphatase, Non-Receptor Type 11)
42HK56048U (Tyrosine)
0 (Receptor, Metabotropic Glutamate 5)
تواريخ الأحداث: Date Created: 20240424 Date Completed: 20240424 Latest Revision: 20240508
رمز التحديث: 20240509
مُعرف محوري في PubMed: PMC11066993
DOI: 10.1073/pnas.2316819121
PMID: 38657042
قاعدة البيانات: MEDLINE
الوصف
تدمد:1091-6490
DOI:10.1073/pnas.2316819121