Leukotactin-1-induced ERK activation is mediated via Gi/Go protein/PLC/PKCδ/Ras cascades in HOS cells

Kim, In Sik; Ryang, Yong Suk; Kim, Yoon Suk; Jang, Su-Jin; Sung, Ho Joong; Lee, Young Han; Kim, Jiyoung; Na, Doe Sun; Ko, Jesang

doi:10.1016/s0024-3205(03)00312-6

Cited by 19 publications

(17 citation statements)

References 39 publications

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“…Since 9CRA, a lipophilic molecule, freely diffuses across plasma membranes, direct MAPK activation by 9CRA would be rapidly induced. Most of the MAPK phosphorylation by extracellular ligands are elicited within 30 min (Feoktistov et al, 1999;Kim et al, 2003). Our results show that both p38 MAPK and ERK phosphorylation peaked at 2 h after treatment with 100 nM 9CRA.…”

Section: Discussionsupporting

confidence: 52%

p38 MAPK and ERK activation by 9-cis-retinoic acid induces chemokine receptors CCR1 and CCR2 expression in human monocytic THP-1 cells

Yun²,

Lee³

et al. 2007

Exp Mol Med

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9-cis-retinoic acid (9CRA) plays an important role in the immune response; this includes cytokine production and cell migration. We have previously demonstrated that 9CRA increases expression of chemokine receptors CCR1 and CCR2 in human monocytes. To better understand how 9CRA induces CCR1 and CCR2 expression, we examined the contribution of signaling proteins in human monocytic THP-1 cells. The mRNA and surface protein up-regulation of CCR1 and CCR2 in 9CRA-stimulated cells were weakly blocked by the pretreatment of SB202190, a p38 MAPK inhibitor, and PD98059, an upstream ERK inhibitor. Activation of p38 MAPK and ERK1/2 was induced in both a time and dose-dependent manner after 9CRA stimulation. Both p38 MAPK and ERK1/2 phosphorylation peaked at 2 h after a 100 nM 9CRA treatment. 9CRA increased calcium influx and chemotactic activity in response to CCR1-dependent chemokines, Lkn-1/CCL15, MIP-1α/CCL3, and RANTES/ CCL5, and the CCR2-specific chemokine, MCP-1/ CCL2. Both SB202190 and PD98059 pretreatment diminished the increased calcium mobilization and chemotactic ability due to 9CRA. SB202190 inhibited the expression and functional activities of CCR1 and CCR2 more effectively than did PD98059. Therefore, our results demonstrate that 9CRA transduces the signal through p38 MAPK and ERK1/2 for CCR1 and CCR2 up-regulation, and may regulate the pro-inflammatory process through the p38 MAPK and ERKdependent signaling pathways.

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Section: Discussionsupporting

confidence: 52%

p38 MAPK and ERK activation by 9-cis-retinoic acid induces chemokine receptors CCR1 and CCR2 expression in human monocytic THP-1 cells

Yun²,

Lee³

et al. 2007

Exp Mol Med

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“…1). Furthermore, this pattern is highly consistent with the kinetics of ERKs, as they regulate a variety of physiological readouts such as platelet-derived growth factor-induced mitogenesis (31), cellular propagation of influenza (32), leukotactin-1 control of cell cycle progression (33), and effects of phorbol esters and nerve growth factors on cell survival (34,42). Although the data favor 22-HC and 9-cis-RA activation of p42/44 kinase, concurrent activation of p38 kinase, JNK, or p34 cdc2 is also possible, as these enzymes utilize similar minimal recognition motifs ((Ser/Thr)-Pro) for substrate phosphorylation (43,44).…”

Section: Discussionmentioning

confidence: 55%

Oxysterols Inhibit Phosphatidylcholine Synthesis via ERK Docking and Phosphorylation of CTP:Phosphocholine Cytidylyltransferase

Agassandian¹,

Zhou²,

Tephly³

et al. 2005

Journal of Biological Chemistry

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Surfactant deficiency contributes to acute lung injury and may result from the elaboration of bioactive lipids such as oxysterols. We observed that the oxysterol 22-hydroxycholesterol (22-HC) in combination with its obligate partner, 9-cis-retinoic acid (9-cis-RA), decreased surfactant phosphatidylcholine (PtdCho) synthesis by increasing phosphorylation of the regulatory enzyme CTP:phosphocholine cytidylyltransferase-␣ (CCT␣). Phosphorylation of CCT␣ decreased its activity. 22-HC/ 9-cis-RA inhibition of PtdCho synthesis was blocked by PD98059 or dominant-negative ERK (p42 kinase). Overexpression of constitutively active MEK1, the kinase upstream of p42 kinase, increased CCT␣ phosphorylation. Expression of truncated CCT␣ mutants lacking prolinedirected sites within the C-terminal phosphorylation domain partially blocked oxysterol-mediated inhibition of PtdCho synthesis. Mutagenesis of Ser315 within CCT␣ was both required and sufficient to confer significant resistance to 22-HC/9-cis-RA inhibition of PtdCho synthesis. A novel putative ERK-docking domain N-terminal to this phosphoacceptor site was mapped within the CCT␣ membrane-binding domain (residues 287-300). The results are the first demonstration of a physiologically relevant phosphorylation site and docking domain within CCT␣ that serve as targets for ERKs, resulting in inhibition of surfactant synthesis.

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“…To better understand the physiological roles of HBx, it is worthwhile to strive for a better understanding of the signaling pathways associated with HBx-mediated cell growth. ERK-MAPK signaling has been clearly implicated in the regulation of liver cell proliferation [32,33]. However, the molecular mechanism underlying the liver cell proliferation mediated by HBx remained unclear.…”

Section: -Test)mentioning

confidence: 99%

“…It has been reported that Gi/o proteins, which are known to affect a variety of cellular functions, activate p-ERK1/2 and subsequent cell proliferation signals [10,32]. AA metabolites are also able to induce cell growth and have been strongly implicated in tumor development [38,39].…”

Section: -Test)mentioning

confidence: 99%

Hepatitis B virus X protein promotes liver cell proliferation via a positive cascade loop involving arachidonic acid metabolism and p-ERK1/2

Shan

Zhang

et al. 2010

Cell Res

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Leukotactin-1-induced ERK activation is mediated via Gi/Go protein/PLC/PKCδ/Ras cascades in HOS cells

Cited by 19 publications

References 39 publications

p38 MAPK and ERK activation by 9-cis-retinoic acid induces chemokine receptors CCR1 and CCR2 expression in human monocytic THP-1 cells

p38 MAPK and ERK activation by 9-cis-retinoic acid induces chemokine receptors CCR1 and CCR2 expression in human monocytic THP-1 cells

Oxysterols Inhibit Phosphatidylcholine Synthesis via ERK Docking and Phosphorylation of CTP:Phosphocholine Cytidylyltransferase

Hepatitis B virus X protein promotes liver cell proliferation via a positive cascade loop involving arachidonic acid metabolism and p-ERK1/2

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