Dipti Tillu

Pharmacology University of Arizona, Tucson, AZ 
Pain Neuroscience
"Dipti Tillu"
Mean distance: 17.86 (cluster 32)
Cross-listing: Chemistry Tree

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Moy JK, Szabo-Pardi T, Tillu DV, et al. (2019) Temporal and sex differences in the role of BDNF/TrkB signaling in hyperalgesic priming in mice and rats. Neurobiology of Pain (Cambridge, Mass.). 5: 100024
Burton MD, Tillu DV, Mazhar K, et al. (2017) Pharmacological activation of AMPK inhibits incision-evoked mechanical hypersensitivity and the development of hyperalgesic priming in mice. Neuroscience
Hanamura K, Washburn HR, Sheffler-Collins SI, et al. (2017) Extracellular phosphorylation of a receptor tyrosine kinase controls synaptic localization of NMDA receptors and regulates pathological pain. Plos Biology. 15: e2002457
Boitano S, Hoffman J, Flynn AN, et al. (2015) The novel PAR2 ligand C391 blocks multiple PAR2 signaling pathways in vitro and in vivo. British Journal of Pharmacology
Kim JY, Tillu DV, Quinn TL, et al. (2015) Spinal dopaminergic projections control the transition to pathological pain plasticity via a D1/D5-mediated mechanism. The Journal of Neuroscience : the Official Journal of the Society For Neuroscience. 35: 6307-17
Tillu DV, Hassler SN, Burgos-Vega CC, et al. (2015) Protease-activated receptor 2 activation is sufficient to induce the transition to a chronic pain state. Pain. 156: 859-67
Wei X, Yan J, Tillu D, et al. (2015) Meningeal norepinephrine produces headache behaviors in rats via actions both on dural afferents and fibroblasts. Cephalalgia : An International Journal of Headache
Melemedjian OK, Tillu DV, Moy JK, et al. (2014) Local translation and retrograde axonal transport of CREB regulates IL-6-induced nociceptive plasticity. Molecular Pain. 10: 45
Boitano S, Hoffman J, Tillu DV, et al. (2014) Development and evaluation of small peptidomimetic ligands to protease-activated receptor-2 (PAR2) through the use of lipid tethering. Plos One. 9: e99140
Melemedjian OK, Tillu DV, Asiedu MN, et al. (2013) BDNF regulates atypical PKC at spinal synapses to initiate and maintain a centralized chronic pain state. Molecular Pain. 9: 12
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