# overview
Research in  our lab centers on the molecular and cellular mechanisms underlying the formation, maintenance and pathology of synapses, the connections between nerve cells and their targets.  Because of its simplicity and experimental accessibility we have used the vertebrate neuromuscular junction (NMJ) as our model system. The NMJ is the synapse between a motor neuron and a skeletal muscle fiber. We address these problems using state-of-the-art mouse molecular genetic techniques in combination with standard molecular, cellular, and immunological approaches.

# keywords[]
S100 Calcium Binding Protein Beta Subunit

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Reverse Transcriptase Polymerase Chain Reaction

# educationAndTraining[].organization.label
University of Maryland, Baltimore - (Baltimore, Maryland, United States)

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Stanford University - (Stanford, California, United States)

# educationAndTraining[].organization.label
New Mexico State University - (Las Cruces, New Mexico, United States)

# educationAndTraining[].organization.label
New York University - (New York, New York, United States)

# educationAndTraining[].organization.label
University of the Andes - (Mérida, Venezuela)

# publications[].label
Neuregulins at the neuromuscular synapse: past, present, and future.

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Emerging roles for MAP kinases in agrin signaling.

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Improvement of neuromuscular synaptic phenotypes without enhanced survival and motor function in severe spinal muscular atrophy mice selectively rescued in motor neurons.

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Neuregulin-2 is synthesized by motor neurons and terminal Schwann cells and activates acetylcholine receptor transcription in muscle cells expressing ErbB4.

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Regulation of the size and distribution of agrin-induced postsynaptic-like apparatus in adult skeletal muscle by electrical muscle activity.

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Extracellular signal-regulated kinases 1 and 2 regulate neuromuscular junction and myofiber phenotypes in mammalian skeletal muscle.

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gamma-AChR/epsilon-AChR switch at agrin-induced postsynaptic-like apparatus in skeletal muscle.

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Agrin-induced postsynaptic-like apparatus in skeletal muscle fibers in vivo.

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Regulation of the intermediate filament protein nestin at rodent neuromuscular junctions by innervation and activity.

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CUGBP1 overexpression in mouse skeletal muscle reproduces features of myotonic dystrophy type 1.

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Modulation of agrin-induced acetylcholine receptor clustering by extracellular signal-regulated kinases 1 and 2 in cultured myotubes.

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Defective Acetylcholine Receptor Subunit Switch Precedes Atrophy of Slow-Twitch Skeletal Muscle Fibers Lacking ERK1/2 Kinases in Soleus Muscle.

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Neuregulins and erbB receptors at neuromuscular junctions and at agrin-induced postsynaptic-like apparatus in skeletal muscle.

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Cloning and analysis of chicken acetylcholinesterase transcripts from muscle and brain.

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Neuregulin-1 immunoglobulin-like domain mutant mice: clozapine sensitivity and impaired latent inhibition.

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Validation of terminal Schwann cell gene marker expression by fluorescent in situ hybridization using RNAscope.

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Induction of zinc-finger proliferation 1 expression in non-myelinating Schwann cells after denervation.

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Defective neuromuscular synaptogenesis in mice expressing constitutively active ErbB2 in skeletal muscle fibers.

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Denervation of chicken skeletal muscle causes an increase in acetylcholinesterase mRNA synthesis.

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Corrigendum: Defective Acetylcholine Receptor Subunit Switch Precedes Atrophy of Slow-Twitch Skeletal Muscle Fibers Lacking ERK1/2 Kinases in Soleus Muscle.

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Neuregulins: primary or secondary signals for the control of synapse-specific gene expression.

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BioABACUS: a database of abbreviations and acronyms in biotechnology and computer science.

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Agrin-induced aggregation of acetylcholine receptors in muscles of rats with experimental autoimmune myasthenia gravis.

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Stimulation of acetylcholine receptor transcription by neuregulin-2 requires an N-box response element and is regulated by alternative splicing.

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Schwann cell-derived neuregulin-2alpha can function as a cell-attached activator of muscle acetylcholine receptor expression.

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Muscle-derived extracellular signal-regulated kinases 1 and 2 are required for the maintenance of adult myofibers and their neuromuscular junctions.

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Muscles in a mouse model of spinal muscular atrophy show profound defects in neuromuscular development even in the absence of failure in neuromuscular transmission or loss of motor neurons.

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Evidence for muscle-dependent neuromuscular synaptic site determination in mammals.

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Nerve sprouting capacity in a pharmacologically induced mouse model of spinal muscular atrophy.

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Induction of neuregulin signaling in mouse schwann cells in vivo mimics responses to denervation.

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Transcripts for the acetylcholine receptor and acetylcholine esterase show distribution differences in cultured chick muscle cells.

# publications[].label
Erratum Volume9, Number 4 (1997), in Article No. CN970623: Ilana Cohen, Mendell Rimer, Terjo Lmo, and U. J. McMahan, Agrin-Induced Postsynaptic-like Apparatus in Skeletal Muscle Fibersin Vivo, pp. 237253

# researcherOn[].label
Isolation of Terminal Schwann Cells by Fluorescence-Activated Cell Sorting

# researcherOn[].awardedBy.label
National Institutes of Health - (Bethesda, Maryland, United States)

# researcherOn[].awardedBy.preferredLabel
DHHS-NIH-National Institute of Neurological Disorders and Stroke

# researcherOn[].label
Role of Erk1/2 In Neuromuscular Synapses and Myofiber Development In Vivo

# researcherOn[].awardedBy.label
National Institutes of Health - (Bethesda, Maryland, United States)

# researcherOn[].awardedBy.preferredLabel
DHHS-NIH-National Institute of Neurological Disorders and Stroke

# streetAddress
Texas A&M Health Science Center; Neuroscience & Experimental Therapeutics; 1359 TAMUS

# etdChairOf[].label
Paez, Ximena (2014-06). Motor Neuron-Specific Restoration of SMN in Two SMA Mouse Models: Insights into the Role of Motor Neurons in Spinal Muscular Atrophy. Doctoral Dissertation.

# etdChairOf[].label
Wang, Shuo (2018-05). The Potential Role of Erk1/2 Map Kinases in the Regulation of Neuromuscular Junction Integrity and Bone Morphogenetic Protein Signaling. Doctoral Dissertation.