◀ Back to CREB1
CAMK4 — CREB1
Pathways - manually collected, often from reviews:
Text-mined interactions from Literome
Anderson et al., Biometals 1998
:
CaMKIV dependent activation of
CREB is a key event in the expression of genes involved in the processes of T-cell activation and neuronal long term potentiation
Hansen et al., J Neurosci Res 2003
(Calcium Signaling) :
First, that depolarization of SGNs activates CaMKs is evidenced by observation of increased CaMKII phosphorylation and of
CaMK dependent
CREB phosphorylation
Linseman et al., J Biol Chem 2003
:
Selectivity of the CaMKIIalpha antisense was demonstrated by its lack of effect on
CaMKIV mediated
CREB phosphorylation
Ahi et al., Behav Brain Res 2004
:
Inhibition of
CaMK II did not affect fear conditioning and
reduced the phosphorylation of Erk-1/2, Elk-1,
CREB , and p90Rsk-1 only transiently, whereas Mek-1/2 inhibition was ineffective in all experiments
Egan et al., Cell Signal 2004
:
In contrast,
CREB activation induced by depolarization in both neonatal and developed VSM was significantly
reduced by
CaMK inhibition and by ERK1/2 inhibition
Mathieson et al., Br J Pharmacol 2006
:
CREB activation by SPC
required both p38MAPK and
CaMK activation, but not ERK1/2
Blanquet et al., Exp Neurol 2006
(Ischemic Attack, Transient) :
We provide evidence that ischemia triggers activation of a biphasic pathway during the resistance period of dentate neurons : ( 1 )
CaMKIV mediates the early phosphorylation of
CREB which drives a prominent synthesis of BDNF ; ( 2 ) this BDNF synthesis, in turn, induces a second peak of CREB phosphorylation which is required for the maintenance of BDNF synthesis
Bok et al., Mol Cell Neurosci 2007
:
CaMKIV , but not CaMKII,
requires CREB to promote SGN survival, consistent with the exclusively nuclear localization of CaMKIV and indicating that the principal prosurvival function of CaMKIV is activation of CREB
Spencer et al., Mol Cell Neurosci 2008
:
Here, we show that
calcium/calmodulin dependent kinase IV (CaMKIV) is
necessary for the neurotrophin induced phosphorylation of
CREB and the block of myelin mediated inhibition of axonal growth
Francis et al., Am J Physiol Cell Physiol 2008
:
In several cells : 1 ) activation of HRH1 increases intracellular Ca ( 2+ ) concentration levels ; and 2 ) increased [ Ca ( 2+ ) ] ( i ) levels are coupled with calmodulin dependent stimulation of calmodulin dependent protein kinase (
CaMK ) and
activation of cAMP-response element binding protein (
CREB )
Fukushima et al., J Neurosci 2008
(Memory Disorders) :
We generated a transgenic mouse overexpressing CaMKIV in the forebrain and showed that the upregulation of
CaMKIV led to an increase in learning induced
CREB activity, increased learning related hippocampal potentiation, and enhanced consolidation of contextual fear and social memories
Han et al., Brain Res 2009
:
Taken together, in addition to CaMKII, CaMKI and
CaMKIV activation mediated by nefiracetam treatment might
mediate CREB phosphorylation following chronic nefiracetam treatment, thereby eliciting an anti-depressive and cognition enhancing effect on OBX mice
Kokubo et al., J Neurosci 2009
(Calcium Signaling) :
Here, we demonstrate that
CaMKK2/CaMKIV dependent phosphorylation of cAMP response element binding protein (
CREB ) correlates with Bdnf transcription, which is required for normal development of cerebellar granule cell neurons ... Furthermore, loss of CaMKK2 or
CaMKIV results in decreased
CREB phosphorylation ( pCREB ), Bdnf exon I and IV-containing mRNAs, and brain derived neurotrophic factor (BDNF) protein in cerebellar granule cell neurons
Sasaki et al., Neuron 2011
:
These findings suggest that SIK2 plays critical roles in neuronal survival, is modulated by
CaMK I/IV , and
regulates CREB via TORC1
Song et al., Int J Neuropsychopharmacol 2013
:
Phosphorylation of
CaMKIV was up-regulated in WT mice and phosphorylation of
CREB was
impaired in CaMKIV KO mice after FLX treatment
Liu et al., PloS one 2012
(Diabetes Mellitus, Type 2) :
Our results indicate that
CaMK4 regulates ß-cell proliferation and apoptosis in a
CREB dependent manner and that CaMK4 induced IRS-2 expression is important in these processes
Jackson et al., PloS one 2012
(Substance Withdrawal Syndrome...) :
Given the proposed
role of
CaMKIV in
CREB activation, we hypothesized that CaMKIV might be a crucial molecular component in the development of nicotine dependence
Sun et al., Genes Dev 1994
:
Because both CaMKII and CaMKIV can phosphorylate CREB, we pursued further the mechanism by which CaMKII and
CaMKIV differentially
regulate CREB activity ... When Ser142 was mutated to alanine,
CREB was
activated by CaMKII, as well as by
CaMKIV
Houglum et al., J Clin Invest 1997
:
Moreover, the phosphorylation of
CREB on Ser133 was
stimulated in activated cells by inducing the activity of PKA or
CAMK-II