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The control of alternative splicing by SRSF1 in myelinated afferents contributes to the development of neuropathic pain.

Neurobiology of disease (2016-10-19)
Richard P Hulse, Robert A R Drake, David O Bates, Lucy F Donaldson
RESUMEN

Neuropathic pain results from neuroplasticity in nociceptive neuronal networks. Here we demonstrate that control of alternative pre-mRNA splicing, through the splice factor serine-arginine splice factor 1 (SRSF1), is integral to the processing of nociceptive information in the spinal cord. Neuropathic pain develops following a partial saphenous nerve ligation injury, at which time SRSF1 is activated in damaged myelinated primary afferent neurons, with minimal found in small diameter (IB

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Sigma-Aldrich
Monoclonal Anti-Neurofilament 200 (Phos. and Non-Phos.) antibody produced in mouse, clone N52, ascites fluid
Sigma-Aldrich
SRPIN340, ≥98% (HPLC)