The Composition, Development, and Regeneration of Neuromuscular Junctions.

The Composition, Development, and Regeneration of Neuromuscular Junctions. Curr Top Dev Biol. 2018;126:99-124 Authors: Liu W, Chakkalakal JV Abstract The neuromuscular junction (NMJ) is the specialized site that connects the terminal of a motor neuron axon to skeletal muscle. As a synapse NMJ integrity is essential for transducing motor neuron signals that initiate skeletal muscle contraction. Many diseases and skeletal muscle aging are linked to impaired NMJ function and the associated muscle wasting. In this chapter we review the components of an NMJ and, the processes of NMJ development, maturation, and regeneration. Also, we briefly discuss the cellular and molecular mechanisms of NMJ decline in the context of disease and aging. PMID: 29305005 [PubMed - in process]
Source: Current Topics in Developmental Biology - Category: Biology Authors: Tags: Curr Top Dev Biol Source Type: research

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This article has been withdrawn by the authors. The Journal questioned Figs. 2A and 7A. The original data and originally submitted figures were not available for evaluation. The authors stand by the reproducibility of the experimental data and the conclusions of the paper. The paper, with confirmatory data supporting the results, can be obtained by contacting the authors.
Source: Journal of Biological Chemistry - Category: Chemistry Authors: Tags: Withdrawals/Retractions Source Type: research
Conclusion: RA-induced differentiation in neurons could exert a suppressive effect on the activity of IKCa channels.Cell Physiol Biochem 2018;48:2374 –2388
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CONCLUSIONS: Plastin 3 overexpression in NSC-34 cells did not elicit an antioxidative effect following serum deprivation. PMID: 30106460 [PubMed - as supplied by publisher]
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PMID: 30105827 [PubMed - as supplied by publisher]
Source: CNS Neuroscience and Therapeutics - Category: Neuroscience Authors: Tags: CNS Neurosci Ther Source Type: research
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Source: Journal of Molecular Neuroscience - Category: Neuroscience Source Type: research
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Spasticity can be a complicating symptom of a variety of neurological conditions such as multiple sclerosis, motor neuron disease, Creutzfeldt-Jakob disease, or post-stroke. Several pharmacological treatment options are available, including baclofen, tizanidine, gabapentin, botulinum toxin A and tetrahydrocannabinol/canabidiol (1, 2). However, treatment feasibility decreases as the end of life approaches, e.g. when patients are no longer able to tolerate oral medications, the onset of action would be too long, or the initiation of parenteral drug therapy (intravenous, intrathecal) is no longer indicated or appropriate.
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ina Dolei The human endogenous retrovirus (HERV)-K, human mouse mammary tumor virus like-2 (HML-2) subgroup of HERVs is activated in several tumors and has been related to prostate cancer progression and motor neuron diseases. The cellular splicing factor 2/alternative splicing factor (SF2/ASF) is a positive regulator of gene expression, coded by a potent proto-oncogene, amplified, and abnormally expressed in tumors. TAR DNA-binding protein-43 (TDP-43) is a DNA/RNA-binding protein, negative regulator of alternative splicing, known for causing neurodegeneration, and with complex roles in oncogenesis. We used the cluster...
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Abstract Mutations in the Fused in Sarcoma (FUS) gene have been identified in familial ALS in human. Drosophila contains a single ortholog of human FUS called Cabeza (Caz). We previously established Drosophila models of ALS targeted to Caz, which developed the locomotive dysfunction and caused anatomical defects in presynaptic terminals of motoneurons. Accumulating evidence suggests that ALS and cancer share defects in many cellular processes. The Hippo pathway was originally discovered in Drosophila and plays a role as a tumor suppressor in mammals. We aimed to determine whether Hippo pathway genes modify the ALS...
Source: Experimental Cell Research - Category: Cytology Authors: Tags: Exp Cell Res Source Type: research
Spinal muscular atrophy (SMA) is an autosomal recessive neuromuscular disorder caused by an insufficient level of survival motor neuron (SMN) protein. It is characterized by progressive degeneration of lower motor neurons in the spinal cord, resulting in skeletal muscle atrophy and muscle weakness [1].
Source: Neuromuscular Disorders - Category: Neurology Authors: Source Type: research
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