cAMP response element-binding protein activation in ligation preconditioning in neonatal brain

2004 ◽  
Vol 56 (5) ◽  
pp. 611-623 ◽  
Author(s):  
Hsueh-Te Lee ◽  
Ying-Chao Chang ◽  
Lin-Yu Wang ◽  
Shan-Tair Wang ◽  
Chao-Ching Huang ◽  
...  
Keyword(s):  
Binding Protein ◽  
Camp Response Element Binding ◽  
Neonatal Brain ◽  
Camp Response Element ◽  
Response Element ◽  
Protein Activation ◽  
Element Binding Protein

Febrile seizures impair memory and cAMP response-element binding protein activation

2003 ◽  
Vol 54 (6) ◽  
pp. 706-718 ◽  
Author(s):  
Ying-Chao Chang ◽  
A-Min Huang ◽  
Yu-Min Kuo ◽  
Shan-Tair Wang ◽  
Yung-Yee Chang ◽  
...  
Keyword(s):  
Binding Protein ◽  
Febrile Seizures ◽  
Camp Response Element Binding ◽  
Camp Response Element ◽  
Response Element ◽  
Protein Activation ◽  
Element Binding Protein

Involvement of cAMP Response Element-Binding Protein Activation in Salivary Secretion

Pathobiology ◽  
2006 ◽  
Vol 73 (1) ◽  
pp. 1-7 ◽  
Author(s):  
Koichi Yamada ◽  
Hiroko Inoue ◽  
Satoshi Kida ◽  
Shoichi Masushige ◽  
Tatsuaki Nishiyama ◽  
...  
Keyword(s):  
Binding Protein ◽  
Salivary Secretion ◽  
Camp Response Element Binding ◽  
Camp Response Element ◽  
Response Element ◽  
Protein Activation ◽  
Element Binding Protein

Scutellarin Mitigates Cancer-Induced Bone Pain by Suppressing CaMKII/CREB Pathway in Rat Models

2019 ◽  
Vol 17 (3) ◽  
pp. 249-253
Author(s):  
Liu Chenglong ◽  
Liu Haihua ◽  
Zhang Fei ◽  
Zheng Jie ◽  
Wei Fang
Keyword(s):  
Protein Kinase ◽  
Bone Pain ◽  
Binding Protein ◽  
Camp Response Element Binding ◽  
Camp Response Element ◽  
Dependent Protein Kinase ◽  
Response Element ◽  
Protein Kinase Ii ◽  
Element Binding Protein ◽  
Dependent Protein

Cancer-induced bone pain is a severe and complex pain caused by metastases to bone in cancer patients. The aim of this study was to investigate the analgesic effect of scutellarin on cancer-induced bone pain in rat models by intrathecal injection of Walker 256 carcinoma cells. Mechanical allodynia was determined by paw withdrawal threshold in response to mechanical stimulus, and thermal hyperalgesia was indicated by paw withdrawal latency in response to noxious thermal stimulus. The paw withdrawal threshold and paw withdrawal latencies were significantly decreased after inoculation of tumor cells, whereas administration of scutellarin significantly attenuated tumor cell inoculation-induced mechanical and heat hyperalgesia. Tumor cell inoculation-induced tumor growth was also significantly abrogated by scutellarin. Ca2+/calmodulin-dependent protein kinase II is a multifunctional kinase with up-regulated activity in bone pain models. The activation of Ca2+/calmodulin-dependent protein kinase II triggers phosphorylation of cAMP-response element binding protein. Scutellarin significantly reduced the expression of phosphorylated-Ca2+/calmodulin-dependent protein kinase II and phosphorylated-cAMP-response element binding protein in cancer-induced bone pain rats. Collectively, our study demonstrated that scutellarin attenuated tumor cell inoculation-induced bone pain by down-regulating the expression of phosphorylated-Ca2+/calmodulin-dependent protein kinase II and phosphorylated-cAMP-response element binding protein. The suppressive effect of scutellarin on phosphorylated-Ca2+/calmodulin-dependent protein kinase II/phosphorylated-cAMP-response element binding protein activation may serve as a novel therapeutic strategy for CIBP management.

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