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Pain hypersensitivity is the consequence of early posttranslational changes, both in the peripheral terminals of the nociceptor and in dorsal horn neurons, as well as later transcription-dependent changes in effector genes, again in primary sensory and dorsal horn neurons (4)

5-CCTGAGGATTGTTGGAATAAA-3) were cloned into pLKO.1 vector

Afterwards, DAPI was utilized to counterstain the nuclei for a period of 10 min

It was also suggested that cystinosin(7) traffics to the lysosome and then is degraded at the organelle through an unknown mechanism (20)