Hydrogen peroxide mediates Rac1 activation of S6K1

Bae, Gyu‐Un; Kim, Yong Kee; Kwon, Hyoung-Keun; Park, Jong Woo; Lee, Eun Kyung; Paek, Se Jin; Choi, Wahn Soo; Jung, In Duk; Lee, Hoi Young; Cho, Eun Jung; Lee, Hyang Woo; Han, Jeung‐Whan

doi:10.1016/j.yexcr.2004.07.013

Cited by 7 publications

(2 citation statements)

References 53 publications

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“…Also we previously reported various signaling molecules including Rac1 and PI3K mediate mitogen activation of S6K1 which plays an important role in cell proliferation and growth (Bae et al ., 1999; Jung et al ., 2003; Bae et al ., 2004). However, little is known about signaling molecules involved in S6K1 activation followed by FcεRI aggregation.…”

Section: Resultsmentioning

confidence: 99%

Destabilization of TNF-α mRNA by Rapamycin

Park¹,

Jeon²,

Lee³

et al. 2012

Biomolecules and Therapeutics

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Stimulation of mast cells through the high affinity IgE receptor (FcεRI) induces degranulation, lipid mediator release, and cytokine secretion leading to allergic reactions. Although various signaling pathways have been characterized to be involved in the FcεRI-mediated responses, little is known about the precious mechanism for the expression of tumor necrosis factor-α (TNF-α) in mast cells. Here, we report that rapamycin, a specific inhibitor of mammalian target of rapamycin (mTOR), reduces the expression of TNF-α in rat basophilic leukemia (RBL-2H3) cells. IgE or specific antigen stimulation of RBL-2H3 cells increases the expression of TNF-α and activates various signaling molecules including S6K1, Akt and p38 MAPK. Rapamycin specifically inhibits antigen-induced TNF-α mRNA level, while other kinase inhibitors have no effect on TNF-α mRNA level. These data indicate that mTOR signaling pathway is the main regulation mechanism for antigen-induced TNF-α expression. TNF-α mRNA stability analysis using reporter construct containing TNF-α adenylate/uridylate-rich elements (AREs) shows that rapamycin destabilizes TNF-α mRNA via regulating the AU-rich element of TNF-α mRNA. The antigen-induced activation of S6K1 is inhibited by specific kinase inhibitors including mTOR, PI3K, PKC and Ca2+chelator inhibitor, while TNF-α mRNA level is reduced only by rapamycin treatment. These data suggest that the effects of rapamycin on the expression of TNF-α mRNA are not mediated by S6K1 but regulated by mTOR. Taken together, our results reveal that mTOR signaling pathway is a novel regulation mechanism for antigen-induced TNF-α expression in RBL-2H3 cells.

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Section: Resultsmentioning

confidence: 99%

Destabilization of TNF-α mRNA by Rapamycin

Park¹,

Jeon²,

Lee³

et al. 2012

Biomolecules and Therapeutics

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“…Several MAPkinases, signal transducers and activators of transcription, Akt/protein kinase B and phospholipase D-signaling pathways are all activated by ROS [48,49] but in some cases, activation is indirect [50].…”

Section: Transduction Signals and Oncogene Expressionmentioning

confidence: 99%

Cancer induction pathways and HF-EMF irradiation

Ledoigt¹,

Belpomme²

2013

ABC

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The response of cells to different types of electromagnetic fields can be induced by low-level (athermal) high frequency (HF) electromagnetic field (EMF) exposure associated with mobile phone technologies. There are many examples of biological effects involving the epigenome. EMF could trigger protein activation mediated by ligands, such as Ca²⁺, that alter the conformation of binding proteins, especially the NADPH plasmic membrane oxidase, so inducing increased formation of reactive oxygen species (ROS) that may alter proteomic functions. Classical antiapoptotic and procarcinogenic signaling mechanisms that are commonly found activated in human malignancies and in inflammation mainly involve the transcription factor NF-κB. The microenvironment that exists during chronic inflammation can contribute to cancer progression. The data support the proposition that long term HF-EMF exposure caused by improper use of cell phones may potentially cause cancer.

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