PKCα induces differentiation through ERK1/2 phosphorylation in mouse keratinocytes

Seo, Haeng Ran; Kwan, Yoo-Wook; Cho, Chul-Koo; Bae, Sangwoo; Lee, Su‐Jae; Soh, Jae-Won; Chung, Hee-Yong; Lee, Yun‐Sil

doi:10.1038/emm.2004.40

Cited by 39 publications

(33 citation statements)

References 16 publications

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“…Despite several previous reports demonstrating direct phosphorylation of MAPK by PKCα (Mauro et al, 2002;Seo et al, 2004), we found no evidence that the PKC and MAPK pathways interact during neural induction other than indirectly, through Syn4. Neuralisation by PKCα is evidently MAPK-independent and PKCα does not affect MAPK activity.…”

Section: Discussioncontrasting

confidence: 99%

“…What is the link between the MAPK and PKCα activities? PKCα is known to activate MAPKs, including p38-MAPK, ERK and JNK (Mauro et al, 2002;Rucci et al, 2005;Seo et al, 2004;Skaletzrorowski et al, 2005;Wensheng, 2006). However, we found no evidence that neural induction by PKCα depends on MAPK.…”

Section: Pkcδ and Pkcα As Downstream Effectors Of Syn4 During Neural mentioning

confidence: 99%

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A role for Syndecan-4 in neural induction involving ERK- and PKC-dependent pathways

Kuriyama

Mayor

2009

Development

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Syndecan-4 (Syn4) is a heparan sulphate proteoglycan that is able to bind to some growth factors, including FGF, and can control cell migration. Here we describe a new role for Syn4 in neural induction in Xenopus. Syn4 is expressed in dorsal ectoderm and becomes restricted to the neural plate. Knockdown with antisense morpholino oligonucleotides reveals that Syn4 is required for the expression of neural markers in the neural plate and in neuralised animal caps. Injection of Syn4 mRNA induces the cellautonomous expression of neural, but not mesodermal, markers. We show that two parallel pathways are involved in the neuralising activity of Syn4: FGF/ERK, which is sensitive to dominant-negative FGF receptor and to the inhibitors SU5402 and U0126, and a PKC pathway, which is dependent on the intracellular domain of Syn4. Neural induction by Syn4 through the PKC pathway requires inhibition of PKCδ and activation of PKCα. We show that PKCα inhibits Rac GTPase and that c-Jun is a target of Rac. These findings might account for previous reports implicating PKC in neural induction and allow us to propose a link between FGF and PKC signalling pathways during neural induction.

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Section: Discussioncontrasting

confidence: 99%

Section: Pkcδ and Pkcα As Downstream Effectors Of Syn4 During Neural mentioning

confidence: 99%

A role for Syndecan-4 in neural induction involving ERK- and PKC-dependent pathways

Kuriyama

Mayor

2009

Development

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“…PKC family of serine/ threonine kinases is thought to play roles in a variety of tissues and cell types Seo et al, 2004). Among these, PKC is expressed predominantly in skeletal muscle and lymphoid organs (Osada et al, 1992;Baier et al, 1993).…”

Section: Menin Represses Jund Transcriptional Activity In Protein Kinmentioning

confidence: 99%

Menin represses JunD transcriptional activity in protein kinase Cθ-mediated Nur77 expression

Kim¹,

Lee²,

Kim³

et al. 2005

Exp Mol Med

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TCR signaling leading to thymocyte apoptosis is mediated through the expression of the Nur77 family of orphan nuclear receptors. It has been shown that the Nur77 promoter is activated by at least two signaling pathways, one mediated by calcium and the other by protein kinase C (PKC). MEF2D has been known to regulate Nur77 expression in a calciumdependent manner. The mechanism by which calcium regulates MEF2D is through dissociation of calcium-sensitive MEF2 corepressors (Cabin1/ HDACs, HDAC4/5) and the association with calcineurin-activated transcription factor NF-AT and the coactivator p300. However, little is known about how PKC activates the Nur77 promoter. Herein, we report that PKC targets AP-1 like response element in the Nur77 promoter where JunD constitutively binds. PKCθ triggers mitogen-activated protein kinaseinediated phosphorylation of JunD, and increases transcriptional activity of JunD, cooperatively with p300. Menin is identified as the transcriptional corepressor for JunD via recruitment of mSin3-istone deacetylases. In fact, Menin represses PKCθ/ p300-mediated transcriptional activity of JunD in T cell. Its dynamic regulation of histone modifiers with JunD is responsible for PKCθ-synergistic effect on Nur77 expression in T cell.

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“…Western blots were performed as described previously (Seo et al, 2004). Cells were homogenized with extraction buffer (10 mM PBS [pH 7.4], 0.5% sodium dodecyl sulfate [SDS], 10 mM phenylmethylsulfonyl fluoride, and 10 g/ml leu-…”

Section: Fluorescence-activated Cell Sorter (Facs) Analysismentioning

confidence: 99%

Downregulation of neurotrophic factors in the brain of a mouse model of Gaucher disease: implications for neuronal loss in Gaucher disease

Kim

Hong²,

Go³

et al. 2006

Exp Mol Med

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Gaucher disease is a glycosphingolipid storage disease caused by deficiency of glucocerebrosidase, resulting in the accumulation of glucosylceramide in lysosomes. The neuronopathic forms of this disease are associated with neuronal loss and neurodegeneration. However, the pathophysiological mechanisms leading to prenatal and neonatal death remain uncharacterized. To investigate brain dysfunction in Gaucher disease, we studied the effects of neurotrophic factors during development in a mouse model of Gaucher disease. The expression of brain-derived neurotrophic factor and nerve growth factor was reduced in the cerebral cortex, brainstem, and cerebellum of Gaucher mice, compared with that in wild-type mice. Extracellular signal-regulated kinase (ERK) 1/2 expression was downregulated in neurons from Gaucher mice and correlated with a decreased number of neurons. These results suggest that a reduction in neurotrophic factors could be involved in neuronal loss in Gaucher disease.

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PKCα induces differentiation through ERK1/2 phosphorylation in mouse keratinocytes

Cited by 39 publications

References 16 publications

A role for Syndecan-4 in neural induction involving ERK- and PKC-dependent pathways

A role for Syndecan-4 in neural induction involving ERK- and PKC-dependent pathways

Menin represses JunD transcriptional activity in protein kinase Cθ-mediated Nur77 expression

Downregulation of neurotrophic factors in the brain of a mouse model of Gaucher disease: implications for neuronal loss in Gaucher disease

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