Sequence analysis and DNA-protein interactions within the 5' flanking region of the Ca2+/calmodulin-dependent protein kinase II alpha-subunit gene.

Sunyer, Teresa; Sahyoun, Naji

doi:10.1073/pnas.87.1.278

Cited by 21 publications

(6 citation statements)

References 52 publications

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“…6A). The length of this protected fragment corresponds to TIS ϩ1 in rat forebrain and is consistent with previous results (Sunyer and Sahyoun, 1990;Olson et al, 1995). Surprisingly, however, mRNA from PC12 cells protected only a 62 nt fragment from the ␣5Ј probe (Fig.…”

Section: Analysis Of Transcription Initiation Sites Of ␣-Camkii Gene supporting

confidence: 91%

Retinoic Acid Stimulates α-CAMKII Gene Expression in PC12 Cells at a Distinct Transcription Initiation Site

Chen¹,

Kelly²

1996

J. Neurosci.

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The promoter region of the alpha-subunit of the calcium/calmodulin-dependent protein kinase II (alpha-CaMKII) gene was inserted into a beta-galactosidase (beta-gal) reporter plasmid, and beta-gal activities were examined in neuroblastoma (NB2a) and pheochromocytoma (PC12) cells after transient or stable transfections. The alpha-CaMKII promoter was 12- to 45-fold more active in NB2a compared with PC12 cells after transient or stable transfections. All-trans retinoic acid (RA) stimulated reporter gene expression at both protein and mRNA levels in transfected PC12 cells. RA increased the level of endogenous alpha-CaMKII mRNA in untransfected PC12 cells by 4.4-fold. The transcription initiation site(s) (TIS) of the alpha-CaMKII gene in PC12 cells and rat brain was examined by RNase protection assays (RPA) and reverse transcriptase PCRs. The TIS for the alpha-CaMKII/beta-gal reporter gene in transfected PC12 cells was indistinguishable from the TIS+1 in rat hippocampus. In contrast, the only detectable TIS for the alpha-CaMKII gene in untransfected PC12 cells was located near the ATG translation start codon, 147 nucleotides 3' to TIS+1 in hippocampus. This unusual TIS was also the predominant TIS in rat cerebellum. These results suggest that the alpha-CaMKII promoter may contain sequences that respond directly or indirectly to RA. In addition, the unusual TIS of the alpha-CaMKII gene in PC12 cells and rat cerebellum may contribute to the very low expression of this gene compared with that in hippocampus.

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Section: Analysis Of Transcription Initiation Sites Of ␣-Camkii Gene supporting

confidence: 91%

Retinoic Acid Stimulates α-CAMKII Gene Expression in PC12 Cells at a Distinct Transcription Initiation Site

Chen¹,

Kelly²

1996

J. Neurosci.

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“…In regards to CaMKII, TNFα may play a role in modulating CaMKII expression, through regulation of the transcription factor Myb (Schachner et al. 1988), for which there are two putative binding sites within the CaMKII promoter (Sunyer and Sahyoun 1990). As well, TNFα is known to promote CaMKII activity (Lee et al.…”

Section: Discussionmentioning

confidence: 99%

A novel role for calcium/calmodulin kinase II within the brainstem pedunculopontine tegmentum for the regulation of wakefulness and rapid eye movement sleep

Stack¹,

Desarnaud²,

Siwek³

et al. 2009

Journal of Neurochemistry

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Considerable evidence suggests that the brainstem pedunculopontine tegmentum (PPT) neurons are critically involved in the regulation of rapid eye movement (REM) sleep and wakefulness (W); however, the molecular mechanisms operating within the PPT to regulate these two behavioral states remain relatively unknown. Here we demonstrate that the levels of calcium/calmodulin kinase II (CaMKII) and phosphorylated CaMKII expression in the PPT decreased and increased with 'low W with high REM sleep' and 'high W/ low REM sleep' periods, respectively. These state-specific expression changes were not observed in the cortex, or in the immediately adjacent medial pontine reticular formation. Next, we demonstrate that CaMKII activity in the PPT is negatively and positively correlated with the 'low W with high REM sleep' and 'high W/low REM sleep' periods, respectively. These differences in correlations were not seen in the medial pontine reticular formation CaMKII activity. Finally, we demonstrate that with increased PPT CaMKII activity observed during high W/low REM sleep, there were marked shifts in the expression of genes that are involved in components of various signal transduction pathways. Collectively, these results for the first time suggest that the increased CaMKII activity within PPT neurons is associated with increased W at the expense of REM sleep, and this process is accomplished through the activation of a specific gene expression profile.

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“…After hybridization with a 290‐bp RsaI‐DraI fragment from CREBM1 (Gonzalez & Montminy, 1989), DNA of the transgenic CaMKIIα‐CREB A133 animals contained a 1250‐bp fragment. The following primers were used for genotyping transgenic animals by PCR: forward primer 5′‐AAG CTC GTC AAT CAA GCT GGT TCT‐3′ at position −139 of first ATG in the CaMKIIα gene (Sunyer & Sahyoun, 1990); reverse primer 5′‐TAA GGT TAC AGT GGG AGC AGA TGA‐3′ at position 204 of rat CREB (accession number), resulting in an ∼ 700‐bp band. Using the same two primers on cDNA results in an ∼ 560 bp due to the intron in pNN265 (see above).…”

Section: Methodsmentioning

confidence: 99%

Synaptic plasticity in the basolateral amygdala in transgenic mice expressing dominant‐negative cAMP response element‐binding protein (CREB) in forebrain

Rammes

Steckler

Kresse

et al. 2000

Eur J of Neuroscience

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Electrophysiological and behavioural experiments were performed in transgenic mice expressing a dominant-negative form of cAMP response element-binding protein (CREBA133) in the limbic system. In control littermate in vitro slice preparation, tetanizing the lateral amygdala-basolateral amygdala (BLA) pathway with a single train (100 Hz for 1 s) produced short-term potentiation (STP) in the BLA. Five trains (10-s interstimulus interval) induced long-term potentiation (LTP), which was completely blocked by the N-methyl-D-aspartate (NMDA) receptor antagonist D(-)-2-amino-5-phosphonopentanoic acid (AP5; 50 microM). When GABAergic (gamma-aminobutyric acid) inhibition was blocked by picrotoxin (10 microM), LTP became more pronounced. Low-frequency stimulation (1 Hz for 15 min) induced either long-term depression (LTD) or depotentiation. LTD remained unaffected by AP5 (50 microM) or by the L- and T-type Ca2+-channel blockers nifedipine (20 microM) and Ni2+ (50 microM), but was prevented by picrotoxin (10 microM), indicating a GABAergic link in the expression of LTD in the BLA. When conditioned fear was tested, a mild impairment was seen in one of three transgenic lines only. Although high levels of mRNA encoding CREBA133 lead to downregulation of endogenous CREB, expression of LTP and depotentiation were unaltered in BLA of these transgenic animals. These results could suggest that residual CREB activity was still present or that CREB per se is dispensable. Alternatively, other CREB-like proteins were able to compensate for impaired CREB function.

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Sequence analysis and DNA-protein interactions within the 5' flanking region of the Ca2+/calmodulin-dependent protein kinase II alpha-subunit gene.

Cited by 21 publications

References 52 publications

Retinoic Acid Stimulates α-CAMKII Gene Expression in PC12 Cells at a Distinct Transcription Initiation Site

Retinoic Acid Stimulates α-CAMKII Gene Expression in PC12 Cells at a Distinct Transcription Initiation Site

A novel role for calcium/calmodulin kinase II within the brainstem pedunculopontine tegmentum for the regulation of wakefulness and rapid eye movement sleep

Synaptic plasticity in the basolateral amygdala in transgenic mice expressing dominant‐negative cAMP response element‐binding protein (CREB) in forebrain

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