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Paclitaxel Reduces Axonal Bclw to Initiate IP

Neuron (2017-10-13)
Sarah E Pease-Raissi, Maria F Pazyra-Murphy, Yihang Li, Franziska Wachter, Yusuke Fukuda, Sara J Fenstermacher, Lauren A Barclay, Gregory H Bird, Loren D Walensky, Rosalind A Segal
ABSTRACT

Chemotherapy-induced peripheral neuropathy (CIPN) is a debilitating side effect of many cancer treatments. The hallmark of CIPN is degeneration of long axons required for transmission of sensory information; axonal degeneration causes impaired tactile sensation and persistent pain. Currently the molecular mechanisms of CIPN are not understood, and there are no available treatments. Here we show that the chemotherapeutic agent paclitaxel triggers CIPN by altering IP

MATERIALS
Product Number
Brand
Product Description

Sigma-Aldrich
MDL 28170, ≥90% (TLC)
Sigma-Aldrich
Paclitaxel, from Taxus brevifolia, ≥95% (HPLC), powder
Sigma-Aldrich
p-Xylene-bis(N-pyridinium bromide), ≥95% (TLC)
Sigma-Aldrich
Tetramethylrhodamine ethyl ester perchlorate, suitable for fluorescence, ≥90% (HPCE)
Sigma-Aldrich
8-Aminonaphthalene-1,3,6-trisulfonic acid disodium salt, BioReagent, suitable for fluorescence, ≥90% (CE)
Sigma-Aldrich
DL-Glyceraldehyde 3-phosphate solution, 45-55 mg/mL in H2O
Sigma-Aldrich
Puromycin dihydrochloride from Streptomyces alboniger, ≥98% (HPLC), powder