PMID- 32353380
OWN - NLM
STAT- MEDLINE
DCOM- 20210517
LR  - 20220107
IS  - 1872-7972 (Electronic)
IS  - 0304-3940 (Print)
IS  - 0304-3940 (Linking)
VI  - 731
DP  - 2020 Jul 13
TI  - Multiple MuSK signaling pathways and the aging neuromuscular junction.
PG  - 135014
LID - S0304-3940(20)30284-6 [pii]
LID - 10.1016/j.neulet.2020.135014 [doi]
AB  - The neuromuscular junction (NMJ) is the vehicle for fast, reliable and robust 
      communication between motor neuron and muscle. The unparalleled accessibility of 
      this synapse to morphological, electrophysiological and genetic analysis has 
      yielded an in depth understanding of many molecular components mediating its 
      formation, maturation and stability. However, key questions surrounding the 
      signaling pathways mediating these events and how they play out across the 
      lifetime of the synapse remain unanswered. Such information is critical since the 
      NMJ is necessary for normal movement and is compromised in several settings 
      including myasthenia gravis, amyotrophic lateral sclerosis (ALS), spinal muscular 
      atrophy (SMA), muscular dystrophy, sarcopenia and aging. Muscle specific kinase 
      (MuSK) is a central player in most if not all contexts of NMJ formation and 
      stability. However, elucidating the function of this receptor in this range of 
      settings is challenging since MuSK participates in at least three signaling 
      pathways: as a tyrosine kinase-dependent receptor for agrin-LRP4 and Wnts; and, 
      as a kinase-independent BMP co-receptor. Here we focus on NMJ stability during 
      aging and discuss open questions regarding the molecular mechanisms that govern 
      active maintenance of the NMJ, with emphasis on MuSK and the potential role of 
      its multiple signaling contexts.
CI  - Copyright (c) 2020 Elsevier B.V. All rights reserved.
FAU - Fish, Lauren A
AU  - Fish LA
AD  - Department of Neuroscience, Brown University, Providence, RI 02912, United 
      States; Neuroscience Graduate Program, Brown University, Providence, RI 02912, 
      United States.
FAU - Fallon, Justin R
AU  - Fallon JR
AD  - Department of Neuroscience, Brown University, Providence, RI 02912, United 
      States. Electronic address: Justin_Fallon@brown.edu.
LA  - eng
GR  - T32 MH020068/MH/NIMH NIH HHS/United States
GR  - R01 HD023924/HD/NICHD NIH HHS/United States
GR  - U01 NS064295/NS/NINDS NIH HHS/United States
GR  - R21 NS112743/NS/NINDS NIH HHS/United States
GR  - R21 AR055878/AR/NIAMS NIH HHS/United States
PT  - Journal Article
PT  - Research Support, N.I.H., Extramural
PT  - Research Support, Non-U.S. Gov't
PT  - Review
DEP - 20200428
PL  - Ireland
TA  - Neurosci Lett
JT  - Neuroscience letters
JID - 7600130
RN  - 0 (Agrin)
RN  - 0 (Receptors, Cholinergic)
RN  - EC 2.7.10.1 (MUSK protein, human)
RN  - EC 2.7.10.1 (Receptor Protein-Tyrosine Kinases)
SB  - IM
MH  - Aging/physiology
MH  - Agrin/*metabolism
MH  - Animals
MH  - Humans
MH  - Motor Neurons/*metabolism
MH  - Neuromuscular Junction/*physiology
MH  - Receptor Protein-Tyrosine Kinases/*metabolism
MH  - Receptors, Cholinergic/*metabolism
PMC - PMC8730820
MID - NIHMS1599045
OTO - NOTNLM
OT  - Aging
OT  - BMP signaling
OT  - MuSK
OT  - Neuromuscular junction
OT  - Synaptic maintenance
EDAT- 2020/05/01 06:00
MHDA- 2021/05/18 06:00
PMCR- 2022/01/05
CRDT- 2020/05/01 06:00
PHST- 2020/03/02 00:00 [received]
PHST- 2020/04/23 00:00 [revised]
PHST- 2020/04/24 00:00 [accepted]
PHST- 2020/05/01 06:00 [pubmed]
PHST- 2021/05/18 06:00 [medline]
PHST- 2020/05/01 06:00 [entrez]
PHST- 2022/01/05 00:00 [pmc-release]
AID - S0304-3940(20)30284-6 [pii]
AID - 10.1016/j.neulet.2020.135014 [doi]
PST - ppublish
SO  - Neurosci Lett. 2020 Jul 13;731:135014. doi: 10.1016/j.neulet.2020.135014. Epub 
      2020 Apr 28.