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Gene Information

Gene symbol: CAMK2G

Gene name: calcium/calmodulin-dependent protein kinase II gamma

HGNC ID: 1463

Related Genes

# Gene Symbol Number of hits
1 AKT1 1 hits
2 CREB1 1 hits
3 IGF1R 1 hits
4 INS 1 hits
5 NOS2A 1 hits

Related Sentences

# PMID Sentence
1 19545622 Because the effect of CaM is mediated through CaM-dependent protein kinase II (CaMKII), we have investigated here the potential role of CaMKII in H(2)O(2)-induced ERK1/2 and PKB phosphorylation by using pharmacological inhibitors of CaM and CaMKII, a CaMKII inhibitor peptide, and siRNA knockdown strategies for CaMKII alpha.
2 19545622 These results demonstrate that CaMKII plays a critical upstream role in mediating the effects of H(2)O(2) on ERK1/2, PKB, and IGF-1R phosphorylation.
3 20215576 These results demonstrate that CaMKII does not regulate insulin-stimulated glucose uptake in skeletal muscle.
4 21301804 Cyclic AMP response element-binding protein (CREB) stimulates beta cell Irs2 expression and is a major calcium/calmodulin-dependent kinase (CaMK)(IV) target in neurons.
5 21301804 We therefore hypothesised that CaMK(IV) mediates glucose-induced Irs2 expression in beta cells via CREB activation.
6 21301804 Similarly, overproduction of a constitutively active form of CaMK(IV) promoted sustained CREB phosphorylation and a significant increase in Irs2 but not Irs1 expression.
7 21301804 Finally, overproduction of a dominant negative form of CREB completely suppressed glucose and CaMK(IV) stimulation of Irs2 expression.
8 21331776 The aim of this study was to investigate whether CaMKII affects iNOS-mediated pericyte death in the retina of diabetic mice with early stage disease.
9 21331776 Total- and phospho-CaMKII, iNOS, and active caspase-3 protein levels were assessed by Western blotting, and CaMKII activity was measured by kinase assay. iNOS-related pericyte death was assessed by double immunofluorescent staining for iNOS and ?-smooth muscle actin, followed by the TUNEL assay.
10 21331776 Our results demonstrate that CaMKII contributes to iNOS-related death of pericytes in the diabetic retina and that inactivation of this enzyme may be a potential treatment for retinal vascular lesion.