Signal transduction through atypical PKCs, but not the EGF receptor, is necessary for UVC-induced AP-1 activation in immortal murine cells

Huang, Chuanshu; Ma, Weiya; Dong, Zigang

doi:10.1038/sj.onc.1201056

Cited by 36 publications

(38 citation statements)

References 30 publications

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“…38 Overexpression of PKC-z in rat mesangial cells enhanced COX-2 expression and inducible nitric oxide synthase. 39 PKC-i overexpression has been shown to protect cells from UV-induced cell death, 40 as well as, okadaic acid-and taxol-induced apoptosis. 37 Moreover, overexpression of atypical PKC in NIH3T3 cells has been shown to block PAR4-induced apoptosis.…”

Section: Discussionmentioning

confidence: 99%

Overexpression of atypical PKC in PC12 cells enhances NGF-responsiveness and survival through an NF-κB dependent pathway

et al. 1999

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Removal of atypical PKC blocks NGF-induced differentiation of PC12 cells. 1 We now examine the consequences that overexpression of atypical PKCs had upon NGF responses. PC12 cells were stably transfected with either PKC-i or PKC-z. Overexpression of atypical PKCs markedly enhanced NGFinduced neurite outgrowth as well as enhanced NGFstimulated JNK kinase. Cotransfection of HA-JNK1 along with increasing concentrations of PKC-i, resulted in dosedependent phosphorylation of GST c-Jun (1 ± 79). NGF treatment of PC12 cells resulted in activation of NF-kB. In comparison, overexpression of atypical PKC-i was by itself sufficient to activate NF-kB and shift the kinetics of NGFinduced kB activity. Furthermore, transfection of full-length antisense PKC-i blocked basal and NGF-stimulated NF-kB. Differentiated and undifferentiated PC12 cells overexpressing atypical PKC-i were protected from serum deprivationinduced cell death. Collectively, these findings demonstrate that atypical PKC-i lies in a pathway that regulates NF-kB and contributes to both neurotrophin-mediated differentiation and survival signaling.

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Section: Discussionmentioning

confidence: 99%

Overexpression of atypical PKC in PC12 cells enhances NGF-responsiveness and survival through an NF-κB dependent pathway

et al. 1999

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“…Generally, this UV response serves to protect the cells (44). The initial signal triggering the UV response is in large part independent of DNA damage, but rather appears to be mediated by a membrane-associated component of the Ras pathway with activation of mitogen-activated protein kinases (45)(46)(47)(48)(49). This idea is supported by our findings that atypical protein kinase C is a mediator of UV-induced activation of extracellular signal-regulated kinases and AP-1 activity (48) and that sphingomyelinase is required for UV-induced c-Jun NH 2 -terminal kinase activation (33).…”

Section: Discussionmentioning

confidence: 99%

Involvement of Nuclear Factor of Activated T Cells Activation in UV Response

Huang

Mattjus

et al. 2000

Journal of Biological Chemistry

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Mammalian cells respond to UV radiation by signaling cascades leading to activation of transcription factors, such as activated protein 1, NFB, and p53, a process known as the "UV response." Nuclear factor of activated T cells (NFAT) was first identified as an inducible nuclear factor in immune response and subsequently found to be expressed in other tissues and cells. To date, however, the regulation and function of NFAT in tissues and cells, other than the immune system, are not well understood. In this study, we demonstrate that UV radiation activates NFAT-dependent transcription through a calcium-dependent mechanism in mouse epidermal JB6 cell lines, as well as in the skin of NFAT-luciferase reporter transgenic mice. Exposure of JB6 cells to UV radiation leads to the transactivation of NFAT in a dosedependent manner. A23187 had a synergistic effect with UV for NFAT induction, whereas pretreatment of cells with nifedipine, a calcium channel blocker, dramatically impaired the NFAT activity induced by either UV or UV plus A23187. Calcium-dependent activation of NFAT by UV was further confirmed by an in vivo study using NFAT-luciferase reporter transgenic mice. These results demonstrated that UV radiation is a strong activator for skin NFAT transactivation through calciumdependent pathways, suggesting that NFAT activation may be a part of the UV response. The nuclear factor of activated T cells (NFAT)1 was originally described as a transcriptional factor expressed in activated T cells but not resting T cells (1-4). The induction of NFAT in T cells required a calcium-activated signaling pathway and was blocked by cyclosporin A (CsA) and FK506 (5-11). Over the last decade, studies from several laboratories have indicated that the preexisting/cytoplasmic component of NFAT was a mixture of proteins belonging to a novel family of transcription factors (12)(13)(14). The first member of the family (NFATp, later renamed NFAT 1 ) was purified from cytoplasmic extracts of a murine T cell cloned by affinity chromatography using the distal NFAT site of murine IL-2 promoter (9, 15) and cloned from murine (Ar-5) and human (Jurkat) T cell cDNA libraries (15,16). Other distinct proteins belonging to the same family, such as NFATc, NFAT 3 , and NFAT 4 , were isolated and cloned (17-20). There are three functional domains in NFAT family proteins: the Rel similarity domain, which is responsible for the DNA binding activity and interaction with AP-1; the NFAT homology region, which regulates the intracellular localization; and the transcriptional activation domain (21). The activation of NFAT in T cells includes dephosphorylation, nuclear translocation, and increase in affinity for DNA binding (5). Stimuli that elicit calcium mobilization result in rapid dephosphorylation of NFAT proteins and their translocation to the nucleus; the dephosphorylated proteins show increased affinity for DNA binding (5).Growing evidence indicates that NFAT is not only a T cellspecific transcriptional factor but is also expressed in a variety of lympho...

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“…Mouse fibroblast B82, B82L and B82M721, as well as their AP-1-lucifrase stable transfectants, were cultured in 10% fetal bovine serum (FBS) DMEM supplemented with 2 mm l-glutamine, and 25 mg of gentamicin/ml as described previously (Huang et al, 1996b;1997c). B82 is a mouse fibroblast cell line that is devoid of EGF receptor expression (Lin et al, 1986;Chen et al, 1987).…”

Section: Methodsmentioning

confidence: 99%

Signal transduction through atypical PKCs, but not the EGF receptor, is necessary for UVC-induced AP-1 activation in immortal murine cells

Cited by 36 publications

References 30 publications

Overexpression of atypical PKC in PC12 cells enhances NGF-responsiveness and survival through an NF-κB dependent pathway

Overexpression of atypical PKC in PC12 cells enhances NGF-responsiveness and survival through an NF-κB dependent pathway

Involvement of Nuclear Factor of Activated T Cells Activation in UV Response

Differential requirement of EGF receptor and its tyrosine kinase for AP-1 transactivation induced by EGF and TPA

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