Activating transcription factor 3 up-regulated by c-Jun NH2-terminal kinase/c-Jun contributes to apoptosis induced by potassium deprivation in cerebellar granule neurons

Mei, Yuping; Zhang, Yuan; Song, Bin; Li, D.; Ma, Chi; Hu, Chih‐Chi Andrew; Ching, Yick–Pang; Li, M.

doi:10.1016/j.neuroscience.2007.10.057

Cited by 38 publications

(31 citation statements)

References 41 publications

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“…In addition, we could show that inhibition of JNK attenuated stimulus-induced ATF3 expression and up-regulation of caspase-3/7 activity as well. The connection between JNK activation, ATF3 biosynthesis, and programmed cell death has also been reported to occur in K ϩ -deprived cerebellar granule cells (Mei et al, 2008).…”

Section: Downloaded Frommentioning

confidence: 91%

Thapsigargin Induces Expression of Activating Transcription Factor 3 in Human Keratinocytes Involving Ca²⁺ Ions and c-Jun N-Terminal Protein Kinase

Spohn

Rößler²,

Philipp³

et al. 2010

Mol Pharmacol

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Thapsigargin is a specific inhibitor of the sarco/endoplasmic reticulum Ca 2ϩ ATPase of the endoplasmic reticulum. Here, we show that stimulation of human HaCaT keratinocytes with nanomolar concentrations of thapsigargin triggers expression of activating transcription factor (ATF) 3, a basic-region leucin zipper transcription factor. ATF3 expression was also up-regulated in thapsigargin-stimulated glioma cells, hepatoma cells, retinal pigment epithelial cells, and airway epithelial cells. Thapsigargin-induced up-regulation of ATF3 expression in keratinocytes was attenuated by BAPTA-acetoxymethyl ester or by expression of the Ca 2ϩ -binding protein parvalbumin in the cytosol of HaCaT cells but not by a panel of pharmacological agents that chelate extracellular Ca 2ϩ (EGTA) or inhibit either ryanodine receptors (dantrolene) or voltage-gated Ca 2ϩ channels (nifedipine). Hence, elevated levels of intracellular Ca 2ϩ , released from intracellular stores, are essential for the effect of thapsigargin on the biosynthesis of ATF3. The thapsigargininduced signaling pathway was blocked by expression of either mitogen-activated protein kinase phosphatase-1 or -5. Experiments involving pharmacological and genetic tools revealed the importance of c-Jun N-terminal protein kinase (JNK) within the signaling cascade, whereas inhibition of extracellular signal-regulated protein kinase or p38 protein kinase did not attenuate thapsigargin-induced expression of ATF3. Functional studies showed that treatment of HaCaT keratinocytes with thapsigargin led to a 2-fold induction of caspase-3/7 activity. The up-regulation of caspase-3/7 activity in thapsigargin-stimulated HaCaT cells was attenuated by inhibition of JNK. Together, these data show that stimulation of HaCaT cells with thapsigargin induces a specific signaling pathway in keratinocytes involving activation of JNK, biosynthesis of ATF3, and up-regulation of caspase-3/7 activity.

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Section: Downloaded Frommentioning

confidence: 91%

Thapsigargin Induces Expression of Activating Transcription Factor 3 in Human Keratinocytes Involving Ca²⁺ Ions and c-Jun N-Terminal Protein Kinase

Spohn

Rößler²,

Philipp³

et al. 2010

Mol Pharmacol

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“…JUN is a known positive regulator of ATF3 transcription (44)(45)(46)(47), and there is also implication that ATF3 may control JUN expression (48). Furthermore, a recent report described ATF2 as a positive regulator of JUN expression in human T cells (49).…”

Section: Atf3 Is a Positive Regulator Of Ifn-g Production And T-bet Amentioning

confidence: 99%

Activating Transcription Factor 3 Is a Positive Regulator of Human IFNG Gene Expression

Filén

Ylikoski

Tripathi

et al. 2010

The Journal of Immunology

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IL-12 and IL-18 are essential for Th1 differentiation, whereas the role of IFN-α in Th1 development is less understood. In this microarray-based study, we searched for genes that are regulated by IFN-α, IL-12, or the combination of IL-12 plus IL-18 during the early differentiation of human umbilical cord blood CD4+ Th cells. Twenty-six genes were similarly regulated in response to treatment with IL-12, IFN-α, or the combination of IL-12 plus IL-18. These genes could therefore play a role in Th1 lineage decision. Transcription factor activating transcription factor (ATF) 3 was upregulated by these cytokines and selected for further study. Ectopic expression of ATF3 in CD4+ T cells enhanced the production of IFN-γ, the hallmark cytokine of Th1 cells, whereas small interfering RNA knockdown of ATF3 reduced IFN-γ production. Furthermore, ATF3 formed an endogenous complex with JUN in CD4+ T cells induced to Th1. Chromatin immunoprecipitation and luciferase reporter assays showed that both ATF3 and JUN are recruited to and transactivate the IFNG promoter during early Th1 differentiation. Collectively, these data indicate that ATF3 promotes human Th1 differentiation.

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“…Stable clones expressing HA-tagged 14-3-3, namely HA-14-3-3-1 and HA-14-3-3-2, and the respective vector control (vector) clones were generated in HCT116 14-3-3 Ϫ/Ϫ cells, and clones were selected in medium containing 1 g/ml puromycin. Published shRNA sequences for slug (sh-1Slug and sh-2Slug) and c-Jun (sh1-c-Jun and sh2-c-Jun) (64,65) cloned in pLKO.1 vector were used to generate viral particles in HEK293FT as described previously (66). The viral particles were used to transduce 14-3-3 Ϫ/Ϫ cells to generate stable knockdown clones.…”

Section: Methodsmentioning

confidence: 99%

“…Primers used for both RT-PCR and quantitative real time PCR for PKP3, CK8, CK18, vimentin, c-Jun, and different 14-3-3 isoforms were described previously (65,72,73). Primer sequences are listed in supplemental Table 3.…”

Section: Methodsmentioning

confidence: 99%

14-3-3σ Gene Loss Leads to Activation of the Epithelial to Mesenchymal Transition Due to the Stabilization of c-Jun Protein

Raychaudhuri

Chaudhary

Gurjar

et al. 2016

Journal of Biological Chemistry

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Activating transcription factor 3 up-regulated by c-Jun NH2-terminal kinase/c-Jun contributes to apoptosis induced by potassium deprivation in cerebellar granule neurons

Cited by 38 publications

References 41 publications

Thapsigargin Induces Expression of Activating Transcription Factor 3 in Human Keratinocytes Involving Ca²⁺ Ions and c-Jun N-Terminal Protein Kinase

Thapsigargin Induces Expression of Activating Transcription Factor 3 in Human Keratinocytes Involving Ca²⁺ Ions and c-Jun N-Terminal Protein Kinase

Activating Transcription Factor 3 Is a Positive Regulator of Human IFNG Gene Expression

14-3-3σ Gene Loss Leads to Activation of the Epithelial to Mesenchymal Transition Due to the Stabilization of c-Jun Protein

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Activating transcription factor 3 up-regulated by c-Jun NH2-terminal kinase/c-Jun contributes to apoptosis induced by potassium deprivation in cerebellar granule neurons

Cited by 38 publications

References 41 publications

Thapsigargin Induces Expression of Activating Transcription Factor 3 in Human Keratinocytes Involving Ca2+ Ions and c-Jun N-Terminal Protein Kinase

Thapsigargin Induces Expression of Activating Transcription Factor 3 in Human Keratinocytes Involving Ca2+ Ions and c-Jun N-Terminal Protein Kinase

Activating Transcription Factor 3 Is a Positive Regulator of Human IFNG Gene Expression

14-3-3σ Gene Loss Leads to Activation of the Epithelial to Mesenchymal Transition Due to the Stabilization of c-Jun Protein

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Thapsigargin Induces Expression of Activating Transcription Factor 3 in Human Keratinocytes Involving Ca²⁺ Ions and c-Jun N-Terminal Protein Kinase

Thapsigargin Induces Expression of Activating Transcription Factor 3 in Human Keratinocytes Involving Ca²⁺ Ions and c-Jun N-Terminal Protein Kinase