The complexity of mitogen-activated protein kinases (MAPKs) made simple

Krishna, M. Bala; Narang, Himanshi

doi:10.1007/s00018-008-8170-7

Cited by 360 publications

(333 citation statements)

References 224 publications

(216 reference statements)

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“…The MAPK pathways are classically divided into the ERK, JNK, and p38 pathways (48). To determine which MAPK signaling pathway may be involved in the regulation of integrin ␤8 expression through AP-1, primary adult lung fibroblasts were treated with chemical inhibitors to each of these pathways then analyzed for surface expression of integrin ␤8 using flow cytometry (Fig.…”

Section: Ap-1 Complexes Bind To the Putative Cre Binding Site In The mentioning

confidence: 99%

Transcription of the Transforming Growth Factor β Activating Integrin β8 Subunit Is Regulated by SP3, AP-1, and the p38 Pathway

Markovics

Araya

Cambier

et al. 2010

Journal of Biological Chemistry

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We show that a SP binding site and a cyclic AMP response element (CRE) in the ITGB8 core promoter are required for its expression and that Sp1, Sp3, and several AP-1 transcription factors form a complex that binds to these sites in a p38-dependent manner. Furthermore, we demonstrate the requirement for Sp3, ATF-2, and p38 for the transcription and protein expression of integrin ␤8. Additionally, reduction of SP3 or inhibition of p38 blocks ␣v␤8-mediated transforming growth factor ␤ activation. These results place integrin ␤8 expression and activity under the control of ubiquitous transcription factors in a stress-activated and pro-inflammatory pathway.

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Section: Ap-1 Complexes Bind To the Putative Cre Binding Site In The mentioning

confidence: 99%

Transcription of the Transforming Growth Factor β Activating Integrin β8 Subunit Is Regulated by SP3, AP-1, and the p38 Pathway

Markovics

Araya

Cambier

et al. 2010

Journal of Biological Chemistry

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“…It is widely believed that activation of MAPK pathways, in particular the extracellular signal-regulated kinase (ERK) 1 and 2 (p44 and p42 MAPKs), contributes to cell proliferation [27] . We previously showed that ERK activation is one of the prerequisites for continuous proliferation of the C2C12 myoblasts [18] .…”

Section: Bupivacaine Inhibits Proliferation Via Erk Pathwaymentioning

confidence: 99%

“…Multiple MAPK signaling cascades can be activated by a variety of stimuli, allowing the cells to respond coordinately to multiple and divergent inputs [27] . The ERK pathway has been believed to be a central regulator of cell proliferation by controlling cell growth and cell cycle progression [27,39] . In the muscle cell model system (C2C12), we previously reported that activation of ERKs is one of the prerequisites for continuous myoblast cell growth [18] .…”

Section: Wwwnaturecom/aps Maurice Jm Et Almentioning

confidence: 99%

Bupivacaine causes cytotoxicity in mouse C2C12 myoblast cells: involvement of ERK and Akt signaling pathways

Maurice

Gan

et al. 2010

Acta Pharmacol Sin

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Aim:The adverse effects of local anesthetics (LAs) on wound healing at surgical sites have been suggested, and may be related to their cytotoxicity. This study was aimed to compare the cellular toxicity of bupivacaine and lidocaine (two well-known LAs), and to explore the molecular mechanism(s). Methods: Toxicity of bupivacaine and lidocaine was assessed in cultured mouse C2C12 myoblasts by cell viability and apoptosis assays. effects of LAs on extracellular signal-regulated kinase (erK) and protein kinase b (Akt) activation, which are essential for cell proliferation and survival, were evaluated by immunoblotting. Results: both LAs, especially bupivacaine, prevented cell growth and caused cell death in a dose-dependent manner. The half maximal inhibitory concentrations (IC 50 ) for bupivacaine and lidocaine were 0.49±0.04 and 3.37±0.53 mmol/L, respectively. When applied at the same dilutions of commercially available preparations, the apoptotic effect induced by bupivacaine was more severe than that of lidocaine in C2C12 cells. Furthermore, bupivacaine significantly diminished the ERK activation, which may underlie its anti-proliferative actions. both LAs suppressed Akt activation, which correlated with their effects on apoptosis. Conclusion: Our study demonstrated that, when used at the same dilutions from clinically relevant concentrations, bupivacaine is more cytotoxic than lidocaine in vitro. Anti-proliferation and cell death with concomitant apoptosis mediated by bupivacaine may offer an explanation for its adverse effects in vivo (eg slowing wound healing at the surgical sites). A less toxic, long-acting anesthetic may be needed.

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“…Once activated, MAPK can affect a number of cytosolic components through its proline-directed serine/threonine activity, or it can translocate to the nucleus where it can phosphorylate and activate a number of transcription factors involved in immediate early gene expression (29)(30)(31). MAPKs are inactivated by a variety of dual-specificity phosphatases called MAP kinase phosphatases or MKPs.…”

Section: Mapk Family Treementioning

confidence: 99%

“…In addition, activated ERK1 and ERK2 can translocate to the nucleus, where they can phosphorylate transcription factors such as Elk-1, SAP-1, c-Myc, and ATF-2 (29)(30)(31)39).…”

Section: Mapk Family Treementioning

confidence: 99%

A Journey Through Mitogen-Activated Protein Kinase and Ochratoxin A Interactions

Rumora

Grubišić

2009

Archives of Industrial Hygiene and Toxicology

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A Journey Through Mitogen-Activated Protein Kinase and Ochratoxin A InteractionsOchratoxin A (OTA) is a ubiquitous mycotoxin with potential nephrotoxic, carcinogenic, and cytotoxic action. It has been proposed that OTA might be involved in the development of Balkan endemic nephropathy, which is associated with an increased risk of urinary tract tumours, and of other forms of interstitial nephritis. Cell susceptibility to OTA mainly depends on mycotoxin concentrations, duration of exposure, and intracellular molecular and genetic context. OTA can affect a cell by stimulating or inhibiting certain signalling pathways such as mitogen-activated protein kinase (MAPK). Three major mammalian MAPKs have been described: extracellular signal-regulated protein kinase (ERK), c-Jun N-terminal kinase (JNK), and p38 MAPK. All MAPKs regulate diverse cellular programmes, but in most cases ERKs have been linked to cell survival, while JNKs, and p38 MAPKs have been implicated in cell death by apoptosis. This review looks into OTA-mediated MAPK activation and its effects.

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The complexity of mitogen-activated protein kinases (MAPKs) made simple

Cited by 360 publications

References 224 publications

Transcription of the Transforming Growth Factor β Activating Integrin β8 Subunit Is Regulated by SP3, AP-1, and the p38 Pathway

Transcription of the Transforming Growth Factor β Activating Integrin β8 Subunit Is Regulated by SP3, AP-1, and the p38 Pathway

Bupivacaine causes cytotoxicity in mouse C2C12 myoblast cells: involvement of ERK and Akt signaling pathways

A Journey Through Mitogen-Activated Protein Kinase and Ochratoxin A Interactions

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