Wei Tang
Baylor College of Medicine
9 Papers
87 Citations
Wei Tang is an academic researcher from Baylor College of Medicine. The author has contributed to research in topics: Ryanodine receptor & Chemistry. The author has an hindex of 7, co-authored 7 publications.
Chat about Author
Papers
Removal of FKBP12 enhances mTOR-Raptor interactions, LTP, memory, and perseverative/repetitive behavior.
Charles A. Hoeffer,Wei Tang,Helen Wong,Arturo Santillan,Richard J. Patterson,Luis A. Martinez,Maria V. Tejada-Simon,Richard Paylor,Susan L. Hamilton,Eric Klann,Eric Klann +10 more
TL;DR: The results indicate that FKBP12 plays a critical role in the regulation of mTOR-Raptor interactions, LTP, memory, and perseverative behaviors.
221
Apocalmodulin and Ca2+Calmodulin-Binding Sites on the CaV1.2 Channel
Wei Tang,D. Brent Halling,D.J. Black,Patricia Pate,Jia-Zheng Zhang,Steen E. Pedersen,Ruth A. Altschuld,Susan L. Hamilton +7 more
TL;DR: The data are consistent with a model in which apoCaM binding to the region around the IQ motif is necessary for the rapid binding of Ca(2+) to the C-lobe of CaM, which is likely to engage the A-C region.
89
Altered excitation-contraction coupling with skeletal muscle specific FKBP12 deficiency.
Wei Tang,Christopher P. Ingalls,William J. Durham,Jessica Snider,Michael B. Reid,Gang Yi Wu,Martin M. Matzuk,Susan L. Hamilton +7 more
TL;DR: FKBP12 deficiency alters both orthograde and retrograde coupling between the L‐type Ca2+ channel and RyR1 and the consequences of these changes depend on muscle type and activity.
49
Calmodulin modulation of proteins involved in excitation-contraction coupling.
TL;DR: Calmodulin binds to a region on RyR1 corresponding to amino acids 3614-3643 and to a regions in the carboxy-terminal tail of the L-type Ca2+ channel, suggesting that they represent more general protein-protein interaction motifs.
43
Upregulation of P2X3 receptors in primary afferent pathways involves in colon-to-bladder cross-sensitization in rats
TL;DR: The upregulation of the P2X3 receptor in an afferent pathway involved in bladder overactivity evoked by TNBS-induced colonic inflammation is found, suggesting that the P1x3 receptor antagonist may be an available and novel strategy for the control of bladder over activity.