PLCγ2 Activates CREB-dependent Transcription in PC12 Cells Through Phosphorylation of CREB at Serine 133

Iwamoto, Toschitake; Mamiya, Nori; Masushige, Shoichi; Kida, Satoshi

doi:10.1007/s10616-005-3763-6

Cited by 10 publications

(12 citation statements)

References 64 publications

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“…Regulatory pathways that modulate bone metabolism are, therefore, likely to be key in determining whether cancer cells can home to the bone and establish metastatic lesions. In support of this idea, de novo production of L-serine, an essential factor for differentiation of mesenchymal bone marrow precursors into osteoclasts (Iwamoto et al, 2005), has been observed in osteotropic breast cancer cells (Pollari et al, 2011) (Figure 4). Specifically, expression of the three enzymes required for de novo serine synthesis, phosphoglycerate dehydrogenase (PHGDH), phosphoserine aminotransferase 1 (PSAT1), and phosphoserine phosphatase (PSPH), as well as the serine transporter SLC1A4, was observed to be significantly higher in bone-metastatic variants of breast tumors (Pollari et al, 2011).…”

Section: Bone Metastases: Undercover Agents To Destroy and Invade Bonementioning

confidence: 69%

Unique Metabolic Adaptations Dictate Distal Organ-Specific Metastatic Colonization

et al. 2018

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Summary Metastases arising from tumors have the proclivity to colonize specific organs, suggesting that they must rewire their biology to meet the demands of the organ colonized, thus altering their primary properties. Each metastatic site presents distinct metabolic challenges to a colonizing cancer cell, ranging from fuel and oxygen availability to oxidative stress. Here, we discuss the organ-specific metabolic adaptations cancer cells must undergo, which provide the ability to overcome the unique barriers to colonization in foreign tissues and establish the metastatic tissue tropism phenotype.

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Section: Bone Metastases: Undercover Agents To Destroy and Invade Bonementioning

confidence: 69%

Unique Metabolic Adaptations Dictate Distal Organ-Specific Metastatic Colonization

et al. 2018

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“…The GAL4-dependent luciferase reporter plasmid (pGAL4RE-Luc) was generated as described previously (Iwamoto et al 2005). The ␤-galactosidase expression plasmid (pCMV-␤-gal) and PKA catalytic subunit expression plasmid (pCMV-PKA) were purchased from Clontech or Stratagene, respectively.…”

Section: Methodsmentioning

confidence: 99%

“…COS-1 and PC12 cells were maintained and transiently transfected as described previously (Hosoda et al, 2004(Hosoda et al, , 2009Iwamoto et al, 2005). Luciferase and ␤-galactosidase activities were measured as described previously (Hosoda et al, 2004(Hosoda et al, , 2009Iwamoto et al, 2005).…”

Section: Methodsmentioning

confidence: 99%

Upregulation of CREB-Mediated Transcription Enhances Both Short- and Long-Term Memory

Suzuki¹,

Fukushima²,

Mukawa³

et al. 2011

Journal of Neuroscience

232

206

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Unraveling the mechanisms by which the molecular manipulation of genes of interest enhances cognitive function is important to establish genetic therapies for cognitive disorders. Although CREB is thought to positively regulate formation of long-term memory (LTM), gain-of-function effects of CREB remain poorly understood, especially at the behavioral level. To address this, we generated four lines of transgenic mice expressing dominant active CREB mutants (CREB-Y134F or CREB-DIEDML) in the forebrain that exhibited moderate upregulation of CREB activity. These transgenic lines improved not only LTM but also long-lasting long-term potentiation in the CA1 area in the hippocampus. However, we also observed enhanced short-term memory (STM) in contextual fear-conditioning and social recognition tasks. Enhanced LTM and STM could be dissociated behaviorally in these four lines of transgenic mice, suggesting that the underlying mechanism for enhanced STM and LTM are distinct. LTM enhancement seems to be attributable to the improvement of memory consolidation by the upregulation of CREB transcriptional activity, whereas higher basal levels of BDNF, a CREB target gene, predicted enhanced shorter-term memory. The importance of BDNF in STM was verified by microinfusing BDNF or BDNF inhibitors into the hippocampus of wild-type or transgenic mice. Additionally, increasing BDNF further enhanced LTM in one of the lines of transgenic mice that displayed a normal BDNF level but enhanced LTM, suggesting that upregulation of BDNF and CREB activity cooperatively enhances LTM formation. Our findings suggest that CREB positively regulates memory consolidation and affects memory performance by regulating BDNF expression.

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“…As described previously [38,39], cultured cells were maintained at 37°C in 95% O 2 5% CO 2 in Dulbecco’s modified Eagle’s medium (DMEM, NISSUI) supplemented with penicillin (100 U/ml) streptomycin (100 mg/ml) and 5% (HeLa cells and COS-1 cells) or 10 % (SH-SY5Y cells) fetal bovine serum (FBS, JRH BIOSCIENCE), respectively, and transiently transfected. Similarly, rat brain cortical neurons (CAMBREX) were maintained in Neuro basal medium (Invitrogen) supplemented with Penicillin-Streptomycin Mixture (TaKaRa), 200 mM L-Glutamine and B27 Supplement (Invitrogen).…”

Section: Methodsmentioning

confidence: 99%

Interactions between αCaMKII and calmodulin in living cells: conformational changes arising from CaM -dependent and -independent relationships

2013

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BackgroundαCaMKII plays central and essential roles in long-term potentiation (LTP), learning and memory. αCaMKII is activated via binding with Ca2+/CaM in response to elevated Ca2+ concentration. Furthermore, prolonged increase in Ca2+ concentration leads to the auto-phosphorylation of αCaMKII at T286, maintaining the activation of αCaMKII even after Ca2+/CaM dissociation. Importantly, the active form of αCaMKII is thought to exhibit conformational change. In order to elucidate the relationships between the interaction of αCaMKII with CaM and the conformational change of αCaMKII, we generated molecular probes (YFP-αCaMKII with CFP-CaM and YFP-αCaMKII-CFP) and performed time-lapse imaging of the interaction with CaM and the conformational change, respectively, in living cells using FRET.ResultsThe interaction of YFP-αCaMKII with CFP-CaM and the conformational change of YFP-αCaMKII-CFP were induced simultaneously in response to increased concentrations of Ca2+. Consistent with previous predictions, high levels of Ca2+ signaling maintained the conformational change of YFP-αCaMKII-CFP at the time when CFP-CaM was released from YFP-αCaMKII. These observations indicated the transfer of αCaMKII conformational change from CaM-dependence to CaM-independence. Furthermore, analyses using αCaMKII mutants showed that phosphorylation at T286 and T305/306 played positive and negative roles, respectively, during in vivo interaction with CaM and further suggested that CaM-dependent and CaM-independent conformational changed forms displays similar but distinct structures.ConclusionsImportantly, these structual differences between CaM-dependent and -independent forms of αCaMKII may exhibit differential functions for αCaMKII, such as interactions with other molecules required for LTP and memory. Our molecular probes could thus be used to identify therapeutic targets for cognitive disorders that are associated with the misregulation of αCaMKII.

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PLCγ2 Activates CREB-dependent Transcription in PC12 Cells Through Phosphorylation of CREB at Serine 133

Cited by 10 publications

References 64 publications

Unique Metabolic Adaptations Dictate Distal Organ-Specific Metastatic Colonization

Unique Metabolic Adaptations Dictate Distal Organ-Specific Metastatic Colonization

Upregulation of CREB-Mediated Transcription Enhances Both Short- and Long-Term Memory

Interactions between αCaMKII and calmodulin in living cells: conformational changes arising from CaM -dependent and -independent relationships

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