The cAMP Response Element Binding protein (CREB) is activated by Insulin-like Growth Factor-1 (IGF-1) and regulates myostatin gene expression in skeletal myoblast

Zuloaga, Rodrigo; Fuentes, Eduardo N.; Molina, Alfredo; Valdés, Juan Antonio

doi:10.1016/j.bbrc.2013.09.067

Cited by 27 publications

(21 citation statements)

References 34 publications

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“…31, 32 Crucially, T98G and U118 differ in PTEN status (T98G PTEN + and U118 PTEN − ), which may account for the differential CREB-mediated regulation of cell cycle factors via interaction with the MAPK and PI3K pathways. 33, 34 Treatment of T98G cells with siCREB resulted in an almost complete block of AKT activation, which was not rescued by the addition of serum (Figure 6a).…”

Section: Resultsmentioning

confidence: 99%

Selective CREB-dependent cyclin expression mediated by the PI3K and MAPK pathways supports glioma cell proliferation

et al. 2014

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The cyclic-AMP response element binding (CREB) protein has been shown to have a pivotal role in cell survival and cell proliferation. Transgenic rodent models have revealed a role for CREB in higher-order brain functions, such as memory and drug addiction behaviors. CREB overexpression in transgenic animals imparts oncogenic properties on cells in various tissues, and aberrant CREB expression is associated with tumours. It is the central position of CREB, downstream from key developmental and growth signalling pathways, which gives CREB this ability to influence a spectrum of cellular activities, such as cell survival, growth and differentiation, in both normal and cancer cells. We show that CREB is highly expressed and constitutively activated in patient glioma tissue and that this activation closely correlates with tumour grade. The mechanism by which CREB regulates glioblastoma (GBM) tumour cell proliferation involves activities downstream from both the mitogen-activated protein kinase and phosphoinositide 3-kinase (PI3K) pathways that then modulate the expression of three key cell cycle factors, cyclin B, D and proliferating cell nuclear antigen (PCNA). Cyclin D1 is highly CREB-dependent, whereas cyclin B1 and PCNA are co-regulated by both CREB-dependent and -independent mechanisms. The precise regulatory network involved appears to differ depending on the tumour-suppressor phosphatase and tensin homolog status of the GBM cells, which in turn allows CREB to regulate the activity of the PI3K itself. Given that CREB sits at the hub of key cancer cell signalling pathways, understanding the role of glioma-specific CREB function may lead to improved novel combinatorial anti-tumour therapies, which can complement existing PI3K-specific drugs undergoing early phase clinical trials.

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Section: Resultsmentioning

confidence: 99%

Selective CREB-dependent cyclin expression mediated by the PI3K and MAPK pathways supports glioma cell proliferation

et al. 2014

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“…Moreover, CREB, a key downstream marker of both CaMK (Zuloaga et al . ) and PKA (Bruno et al . ), and MEF2, a CnA‐associated transcription factor (Dunn et al .…”

Section: Discussionmentioning

confidence: 99%

Protein composition of the muscle mitochondrial reticulum during postnatal development

Kim

Yang

Katti

2019

The Journal of Physiology

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Key pointsr Muscle mitochondrial networks changed from a longitudinal, fibre parallel orientation to a perpendicular configuration during postnatal development.r Mitochondrial dynamics, mitophagy and calcium uptake proteins were abundant during early postnatal development.r Mitochondrial biogenesis and oxidative phosphorylation proteins were upregulated throughout muscle development.r Postnatal muscle mitochondrial network formation is accompanied by a change in protein expression profile from mitochondria designed for co-ordinated cellular assembly to mitochondria highly specialized for cellular energy metabolism.Abstract Striated muscle mitochondria form connected networks capable of rapid cellular energy distribution. However, the mitochondrial reticulum is not formed at birth and the mechanisms driving network development remain unclear. In the present study, we aimed to establish the network formation timecourse and protein expression profile during postnatal development of the murine muscle mitochondrial reticulum. Two-photon microscopy was used to observe mitochondrial network orientation in tibialis anterior (TA) muscles of live mice at postnatal days (P) 1, 7, 14, 21 and 42, respectively. All muscle fibres maintained a longitudinal, fibre parallel mitochondrial network orientation early in development (P1-7). Mixed networks were most common at P14 but, by P21, almost all fibres had developed the perpendicular mitochondrial orientation observed in mature, glycolytic fibres. Tandem mass tag proteomics were then applied to examine changes in 6869 protein abundances in developing TA muscles. Mitochondrial proteins increased by 32% from P1 to P42. In addition, both nuclear-and mitochondrial-DNA encoded oxidative phosphorylation (OxPhos) components were increased during development, whereas OxPhos assembly factors decreased. Although mitochondrial dynamics and mitophagy were induced at P1-7, mitochondrial biogenesis was enhanced after P14. Moreover, calcium signalling Y. Kim and others J Physiol 597.10 proteins and the mitochondrial calcium uniporter had the highest expression early in postnatal development. In conclusion, mitochondrial networks transform from a fibre parallel to perpendicular orientation during the second and third weeks after birth in murine glycolytic skeletal muscle. This structural transition is accompanied by a change in protein expression profile from mitochondria designed for co-ordinated cellular assembly to mitochondria highly specialized for cellular energy metabolism.

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“…CREB responds to cAMP, intracellular Ca2 + , various growth factors, such as nerve growth factor (NGF), fibroblast growth factor (FGF) and the insulin growth factor 1 as well as cytokines, like IL-4, IL-10, IL-13 and transforming growth factor (TGF)-β thereby activating gene transcription [39–41]. The FGF- and stress-mediated regulation of CREB occurs via the MAPK kinase pathway [9, 42].…”

Section: Molecular Basis Of Creb Regulationmentioning

confidence: 99%

Control of CREB expression in tumors: from molecular mechanisms and signal transduction pathways to therapeutic target

2016

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The cyclic AMP response element binding (CREB) protein has pleiotropic activities in physiologic processes. Due to its central position downstream of many growth signaling pathways CREB has the ability to influence cell survival, growth and differentiation of normal, but also of tumor cells suggesting an oncogenic potential of CREB. Indeed, increased CREB expression and activation is associated with tumor progression, chemotherapy resistance and reduced patients' survival. We summarize here the different cellular functions of CREB in tumors of distinct histology as well as its use as potential prognostic marker. In addition, the underlying molecular mechanisms to achieve constitutive activation of CREB including structural alterations, such as gene amplification and chromosomal translocation, and deregulation, which could occur at the transcriptional, post-transcriptional and post-translational level, will be described. Since downregulation of CREB by different strategies resulted in inhibition of cell proliferation, invasion and induction of apoptosis, the role of CREB as a promising target for cancer therapy will be also discussed.

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The cAMP Response Element Binding protein (CREB) is activated by Insulin-like Growth Factor-1 (IGF-1) and regulates myostatin gene expression in skeletal myoblast

Cited by 27 publications

References 34 publications

Selective CREB-dependent cyclin expression mediated by the PI3K and MAPK pathways supports glioma cell proliferation

Selective CREB-dependent cyclin expression mediated by the PI3K and MAPK pathways supports glioma cell proliferation

Protein composition of the muscle mitochondrial reticulum during postnatal development

Control of CREB expression in tumors: from molecular mechanisms and signal transduction pathways to therapeutic target

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