CaMK2-beta/gamma/delta (Phospho-Thr287) ELISA Kit

In our previous study using iTRAQ technique we found that the level of calmodulin-dependent protein kinase 2b (Camk2b) was lower in rats with hyperhomocysteinemia. We presumed that Camk2b might be involved in homocysteine-induced apoptosis and tried to explore its role in this study through the transfection with Camk2b gene. Results showed that neurons of HHcy group had lower activity measured by MTT, higher percentage of apoptotic neurons, lower expression levels of Camk2b mRNA and protein than those in normal group. Neurons with overexpression of Camk2b (Camk2b group) had lower percentage of apoptosis and higher activity than those in control group. After exposure to 2-Methoxyestradiol, the activity of neurons with overexpression of Camk2b was suppressed with more apoptotic cells observed. The expressions of BCL2, eNOS, EP300 and EPO were all elevated at both mRNA and protein levels in neurons of CamK2b group compared with other three groups. Thus, Camk2b protects neurons from Homocysteine-induced apoptosis with the involvement of HIF-1 alpha signal pathway.

Ginsenoside-Rb1 (Rb1) is known to be partially associated with the inhibition of heparin-binding epidermal growth factor-like growth factor (HB-EGF). Tetramethylpyrazine phosphate (TMPP) inhibits the activation of the calcium/calmodulin/calmodulin-dependent protein kinase (Ca2+/CaM/CaMKII) pathway. The alpha-myosin heavy chain cTnT(R141W) transgenic mouse was previously reported as a model for dilated cardiomyopathy (DCM), and it was used to test the effects of combinations of Rb1 and TMPP in reversing the progression of DCM and the potential mechanism. Survival, echocardiography, histologic features assessed the effectiveness of Rb1 and TMPP treatments. Western blot and reverse transcription polymerase chain reactions were used to determine expression levels of certain genes. This study clearly demonstrated that treatment with a combination of Rb1 and TMPP could inhibit the expression of HB-EGF, calmodulin1 (Calm1), and calcium/calmodulin-dependent protein kinase II beta (Camk2b). Rb1 alone mainly reduced the expression of HB-EGF, and TMPP alone mainly reduced the expression of Calm1 and Camk2b. Treatment with Rb1 and TMPP had synergistic effects on the amelioration of chamber dilation, contractile dysfunction, interstitial fibrosis, and ultrastructural degeneration in cTnT(R141W) mice when compared with the results of treatment with Rb1 or TMPP alone, and those were probably due to the inhibition of both HB-EGF and the Ca2+/CaM/CaMKII pathway.