CAMK4

(redirected from CAMKIV)

CAMK4

A gene on chromosome 5q21.3 that encodes a multifunctional serine/threonine protein kinase, which is part of the calcium-triggered CaMKK-CaMK4 signalling cascade and regulates, mainly by phosphorylation, the activity of transcription activators (e.g., CREB1, MEF2D, JUN and RORA). These activators play key roles in immune response, inflammation and memory consodilation. In the thymus, CAMK4 regulates the CD4/CD8 (double positive thymocytes) selection threshold during T-cell ontogeny; it also play a role in transcriptional regulation in lymphocytes, neurons and male germ cells, and is expressed in the brain, thymus, CD4 T-cells and in epithelial ovarian cancers.
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Evidence of vanillin binding to CAMKIV explains the anti-cancer mechanism in human hepatic carcinoma and neuroblastoma cells.
That is, it was found that importin [alpha] by itself, (88) without importin [beta]1, could transport cargo proteins, such as calcium/calmodulin-dependent protein kinase type IV (CaMKIV) or Vpr from human immunodeficiency virus type 1 (HIV-1).
(2005) Importin a transports CaMKIV to the nucleus without utilizing importin [beta].
Tonegawa, "An important role of neural activity-dependent CaMKIV signaling in the consolidation of long-term memory," Cell, vol.
CREB is activated by several protein kinases such as PKA, CAMKII, CAMKIV, MAPK, MSK1/2, and PKC, while Ser/Thr phosphatases, protein phosphatase 1 (PP1) and PP2A negatively regulate CREB [9].
Illario, "Converging signaling between CaMK II and CaMKIV, two members of the same family," Translational Medicine @ UniSa, vol.
(34,15) The role of calcium/calmodulin-dependent kinase IV (CaMKIV) in blood pressure regulation (through the contro of endothelial nitric oxide synthase activity), increased levels of G protein coupled receptor kinase and action of heparin by acting as a GRK inhibitor was observed (36-38)
A third possibility is suggested by the report that transfection of cortical neurons with constitutively active CaMKIV ([Ca.sup.2+] calmodulin-dependent protein kinase IV) promotes dendritic growth, whereas expres-sion of constitutively active CaMKII ([Ca.sup.2+]/calmodulin-dependent protein kinase H) inhibits dendritic growth (Redmond et al.
Changes in CREB and BDNF in aged and blueberry-supplemented animals were accompanied by increases in the phosphorylation state of extracellular signal-related kinase (ERK1/2), rather than that of calcium calmodulin kinase (CaMKII and CaMKIV) or protein kinase A.
The CREB-mediated response to extracellular stimuli can be modulated by a number of kinases (PKA, CamKII, CamKIV, RSK2 MAPK, and PKC) and phosphatases (PP1 and calcineurin).
Previous results [164] support this dissociation between tag-setting (calcium/calmodulin-dependent protein kinase (CaMK) II signaling pathway) and the availability of PRPs (CaMKIV signaling pathway).
First, high levels of antilymphocytic antibodies in patients with SLE activate calcium/calmodulin-dependent kinase IV (CaMKIV) which enhances CREM activity through phosphorylation [44].