CAMK1

(redirected from CAMKI)

CAMK1

A gene on chromosome 3p25.3 that encodes the alpha subunit of a calcium/calmodulin-dependent protein kinase, which is part of the calcium-triggered CaMKK-CaMK1 signalling cascade and, upon calcium influx, regulates transcription activation, cell cycling, hormone production, cell differentiation, actin filament organisation and neurite outgrowth.
Mentioned in ?
References in periodicals archive ?
Phosphorylation of Ser600 by Pka [15,52, 53], CamkII [48], or Ampk [55] induces mitochondrial fusion, and its dephosphorylation by calcineurin (CaN) [53, 54] induces mitochondrial fission, but, in some circumstances, phosphorylation of Ser600 by CamkI [50] or Rockl [51] can induce mitochondrial fission.
Activity-dependent dendritic growth, which is a critical determinant of neuronal connectivity in the developing brain, is mediated by calcium ion ([Ca.sup.2+])-dependent activation of [Ca.sup.2+]/calmodulin kinase-I (CaMKI), which triggers cAMP response element binding protein (CREB)-dependent Wnt2 transcription.
KEY WORDS: autism, [Ca.sup.2+], CaMKI, CREB, dendrites, developmental neurotoxicity, hippocampal MEK, neuronal connectivity, neurons, non-dioxin-like PCBs, ryanodine receptor, Wnt2.
We previously identified an NMDA (N-methyl-D-aspartate) receptor-mediated [Ca.sup.2+]-dependent signaling pathway that couples neuronal activity to dendritic arborization via sequential activation of [Ca.sup.2+]/calmodulin-dependent protein kinase kinase (CaMKK), [Ca.sup.2+]/calmodulin kinase-I (CaMKI), and extracellular signal-regulated kinase kinase (MEK/ERK) to enhance the CAMP response element binding protein (CREB)-mediated transcription of Wnt2 [wingless-type mouse mammary tumor virus (MMTV) integration site family member 2] (Wayman et al.
A subset of cultures was simultaneously transfected with plasmids encoding dominant negative (dn) CaMKI (dnCaMKI), dnCREB (also referred to as ACREB), or Wnt inhibitory factor (Wif).
Previous reports demonstrated that treatment of cultured hippocampal neurons with the CaMK kinase inhibitor STO-609 (2-5 [micro]M) inhibits CaMKI but not CaMKII (Wayman et al.
To probe downstream effectors of CaMKI, we first determined whether PCB-95-induced dendritic growth requires MEK/ERK signaling.
We previously demonstrated that activity-dependent dendritic growth in hippocampal neurons is mediated by sequential activation of NMDA receptors, CaMKK, CaMKI, Ras, MEK/ERK, and CREB-dependent transcription of Wnt2 (Wayman et al.