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CKIalpha (show CSNK1A1 ELISA Kits)-mediated NS5A S235 phosphorylation is critical for HCV replication. CaMKII (show CAMK2G ELISA Kits) gamma and delta may have negative roles in the HCV life cycle.
TGFbeta (show TGFB1 ELISA Kits) elevated the expression of CamK (show CAMK4 ELISA Kits) IIbeta and CamK (show CAMK4 ELISA Kits) IIdelta, while siRNA silencing of those two subtypes significantly reduced TGFbeta (show TGFB1 ELISA Kits)-mediated expression of collagen A1 and fibronectin 1 (show FN1 ELISA Kits).
CEACAM1 (show CEACAM1 ELISA Kits) is able to maintain the active transcription of ID4 (show ID4 ELISA Kits) by an epigenetic mechanism involving HDAC4 (show HDAC4 ELISA Kits) and CaMK2D, and the same kinase enables lumen formation by CEACAM1 (show CEACAM1 ELISA Kits)
CaMKIId (show CAMK2 ELISA Kits) activity is up-regulated in the myocardium of diabetic patients and mouse models of diabetes, where it promotes pathological signaling that includes hypertrophy, fibrosis and apoptosis.
Study found a significant association with disordered gambling and rs167771 (DRD3 (show DRD3 ELISA Kits)) and with rs381572 (CAMK2D) in humans
This study showed that AKAP12 (show AKAP12 ELISA Kits),CAMK2D and a molecular pathway(cyclic amp (show APRT ELISA Kits))association to outcome of depressive during citalopram treatment.
CaMKIID (show CAMK2 ELISA Kits) specifically phosphorylates Thr (show TRH ELISA Kits)-457 on CEACAM1 (show CEACAM1 ELISA Kits)-SF, which in turn regulates the process of lumen formation via apoptosis of the central acinar cells.
Our studies suggest that CaMKII (show CAMK2G ELISA Kits) is a molecular signal that couples increased reactive oxygen species with atrial fibrillation and that therapeutic strategies to decrease oxidized CaMKII (show CAMK2G ELISA Kits) may prevent or reduce it.
End-stage failing human hearts had mor (show TTN ELISA Kits)e phosphorylation at CaMKII-dependent titin sites, (show CAMK2G ELISA Kits) contributing to their mechanical dysfunction & establishing a new role for CaMKIIdelta in regulating diastolic passive properties of healthy & diseased hearts.
suggest that CaMKII and calcineurin provide a switch-like mechanism that controls Ca-dependent LIMK1, SSH1L and cofilin activation, and subsequently actin cytoskeletal reorganization
CaMKIIdelta isoforms have similar effects on hypertrophic gene expression but disparate effects on Ca(2 (show CA2 ELISA Kits)+) handling
we demonstrate that the deltaC isoform of CaMKII (show CAMK2G ELISA Kits) contributes significantly to myocardial damage following ex vivo I/R. Signaling occurs through NF-kappaB (show NFKB1 ELISA Kits) and TNF-alpha (show TNF ELISA Kits) and acute inhibition of the generation or function of thesemolecules has a very robust protective effect inWT animals and in those expressing CaMKIIdeltaC.
Phosphorylating Titin's Cardiac N2B Element by ERK2 (show MAPK1 ELISA Kits) or CaMKIIdelta Lowers the Single Molecule and Cardiac Muscle Force
CaMK2d (show CAMK2B ELISA Kits)-dependent phosphorylation of RyR2 (show RYR2 ELISA Kits)-S2814 is significant in cardiomyopathy, independent of hypertrophy, induced by prolonged beta-adrenergic receptor stimulation.
Data indicate that combined cardiomyocyte-specific deletion of CaM Kinase II CaMKIIdelta/gamma does not affect ischemia/reperfusion (I/R) injury.
CaMKIIdelta activation and phosphorylation of downstream targets was enhanced in aromatase (show CYP19A1 ELISA Kits) knockout hearts subjected to ischemia-reperfusion
Cardiac CaM Kinase II genes delta and gamma contribute to adverse remodeling but redundantly inhibit calcineurin-induced myocardial hypertrophy.
CaMKIIdeltagamma couples noncanonical Wnt signaling to histone deacetylase 4 and myosin enhancer factor 2.
we show selective upregulation of CaMKIIdelta in adult cardiac fibroblasts following cardiac hypertrophy and assign a previously unrecognised role to CaMKII (show CAMK2G ELISA Kits) in regulating adult cardiac fibroblast function in normal and diseased mouse hearts.
Camk2d (show CAMK2B ELISA Kits) expression and activity increase during arteriogenesis
A specific inhibitor of CaMKII (show CAMK2G ELISA Kits) can effectively inhibit the occurrence of EADs.
The product of this gene belongs to the serine/threonine protein kinase family and to the Ca(2+)/calmodulin-dependent protein kinase subfamily. Calcium signaling is crucial for several aspects of plasticity at glutamatergic synapses. In mammalian cells, the enzyme is composed of four different chains: alpha, beta, gamma, and delta. The product of this gene is a delta chain. Alternative splicing results in multiple transcript variants encoding distinct isoforms. Distinct isoforms of this chain have different expression patterns.
calcium/calmodulin-dependent protein kinase (CaM kinase) II delta
, calcium/calmodulin-dependent protein kinase II, delta
, calcium/calmodulin-dependent protein kinase II delta
, caM kinase II subunit delta
, caM-kinase II delta chain
, caMK-II subunit delta
, calcium/calmodulin-dependent protein kinase II delta12 subunit
, calcium/calmodulin-dependent protein kinase type II delta chain
, CaM kinase II delta subunit
, CaM-kinase II delta chain
, CaMK-II delta subunit
, calcium/calmodulin-dependent protein kinase type II subunit delta
, Ca++/calmodulin-dependent protein kinase 2 delta subunit
, Ca++/calmodulin-dependent protein kinase II delta subunit
, Ca++/calmodulin-dependent protein kinase II, delta subunit
, calcium/calmodulin-dependent protein kinase II delta 2-subunit
, CaMK II