Casein Kinase II

Publication Title: 
Biochemical and Biophysical Research Communications

Cellular senescence is a tumor suppression mechanism. We previously reported that CKII downregulation induces senescence in human lung fibroblast IMR-90 and colon cancer HCT116 cells. In this study, potential longevity drugs, including rapamycin, vitamin C, and vitamin E, blocked CKII downregulation-mediated senescence through reduction of reactive oxygen species (ROS) production in HCT116 cells.

Author(s): 
Park, Ji Hye
Kim, Jin Joo
Bae, Young-Seuk
Publication Title: 
Blood

JAK-STAT signaling is involved in the regulation of cell survival, proliferation, and differentiation. JAK tyrosine kinases can be transiently activated by cytokines or growth factors in normal cells, whereas they become constitutively activated as a result of mutations that affect their function in tumors. Specifically, the JAK2V617F mutation is present in the majority of patients with myeloproliferative disorders (MPDs) and is implicated in the pathogenesis of these diseases.

Author(s): 
Zheng, Ying
Qin, Hongwei
Frank, Stuart J.
Deng, Luqin
Litchfield, David W.
Tefferi, Ayalew
Pardanani, Animesh
Lin, Fang-Tsyr
Li, Jingzhi
Sha, Bingdong
Benveniste, Etty N.
Publication Title: 
The Journal of Pharmacology and Experimental Therapeutics

Clinically used calcineurin inhibitors, including tacrolimus (FK506) and cyclosporine A, can induce calcineurin inhibitor-induced pain syndrome (CIPS), which is characterized as severe pain and pain hypersensitivity. Increased synaptic N-methyl-D-aspartate receptor (NMDAR) activity in the spinal dorsal horn plays a critical role in the development of CIPS. Casein kinase II (CK2), a serine/threonine protein kinase, can regulate synaptic NMDAR activity in the brain.

Author(s): 
Hu, Yi-Min
Chen, Shao-Rui
Chen, Hong
Pan, Hui-lin
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