Activation mechanism of c‐Jun amino‐terminal kinase in the course of endodermal differentiation of P19 embryonic carcinoma cells

Kudo, Tada Aki; Sakamoto, Yoshiyuki; Tamura, Shinji; Kobayashi, Toshihide

doi:10.1016/s0014-5793(03)00179-0

Cited by 2 publications

(3 citation statements)

References 21 publications

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“…We have also shown that MKK4 but not MKK7 was activated in the course of the RA-induced primitive endodermal differentiation of P19 cells (26). These observations suggest that the activation of MKK4 but not MKK7 serves as the common mechanism of JNK activation in both the neural and the primitive endodermal differentiation of P19 cells.…”

Section: Discussionsupporting

confidence: 53%

Activation Mechanism of c-Jun Amino-terminal Kinase in the Course of Neural Differentiation of P19 Embryonic Carcinoma Cells

Akiyama

Yonezawa

Kudo

et al. 2004

Journal of Biological Chemistry

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P19 embryonic carcinoma cells, a model system for studying early development and differentiation, can differentiate into neurons and primitive endoderm-like cells depending on the culture conditions. We have previously reported that the activation of c-Jun amino-terminal kinase (JNK) is required for the retinoic acidinduced neural differentiation of P19 cells. However, the signaling pathway(s) responsible for the activation of JNK has not been known. In this study, we demonstrated that activities of MAPK kinase 4 (MKK4) and TAK1, one of the upstream kinases of MKK4, were enhanced in the neurally differentiating cells. Inhibition of the neural differentiation by an overexpression of protein phosphatase 2C⑀, an inactivator of TAK1, suggested a critical role of the TAK1 signaling pathway during the differentiation. Confocal microscopic analysis indicated that TAK1, phospho-MKK4, and phospho-JNK were colocalized with tubulin in the neurites and localized also in the nuclei of the differentiating cells. In contrast, two TAK1-binding proteins, TAB1 and TAB2, which are involved in the activation of TAK1, were localized in the neurites and the nuclei of the differentiating cells, respectively. These results suggest that two distinct TAK1-MKK4-JNK signaling pathways are independently activated at the different intracellular locations and may participate in the regulation of the neural differentiation of P19 cells.

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Section: Discussionsupporting

confidence: 53%

Activation Mechanism of c-Jun Amino-terminal Kinase in the Course of Neural Differentiation of P19 Embryonic Carcinoma Cells

Akiyama

Yonezawa

Kudo

et al. 2004

Journal of Biological Chemistry

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“…While phospho-MAP2K3/MAP2K6 proteins were detected in the cytoplasm and the nucleus, phospho-MAP2K4 proteins were confined to the nuclei, suggesting that p38 MAPK phosphorylation by MAP2K4 may occur predominantly in the nucleus. This nuclear localization is supported by studies that investigated the activation of JNK/SAPK in P19 embryonic carcinoma cells [28]. MAP2K4 was detected in both the nucleus and cytoplasm of differentiated P19 cells, but only in the nucleus of undifferentiated P19 cells [28].…”

Section: Discussionmentioning

confidence: 60%

“…This nuclear localization is supported by studies that investigated the activation of JNK/SAPK in P19 embryonic carcinoma cells [28]. MAP2K4 was detected in both the nucleus and cytoplasm of differentiated P19 cells, but only in the nucleus of undifferentiated P19 cells [28]. Other studies have established that JNK/SAPK and MAP2K4 are activated and translocated into the nucleus in response to cellular stress [29,30].…”

Section: Discussionmentioning

confidence: 64%

Mouse preimplantation embryo responses to culture medium osmolarity include increased expression of CCM2 and p38 MAPK activation

Fong

Watson

2007

BMC Dev Biol

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Background: Mechanisms that confer an ability to respond positively to environmental osmolarity are fundamental to ensuring embryo survival during the preimplantation period. Activation of p38 mitogen-activated protein kinase (MAPK) occurs following exposure to hyperosmotic treatment. Recently, a novel scaffolding protein called Osmosensing Scaffold for MEKK3 (OSM) was linked to p38 MAPK activation in response to sorbitol-induced hypertonicity. The human ortholog of OSM is cerebral cavernous malformation 2 (CCM2). The present study was conducted to investigate whether CCM2 is expressed during mouse preimplantation development and to determine whether this scaffolding protein is associated with p38 MAPK activation following exposure of preimplantation embryos to hyperosmotic environments.

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Activation mechanism of c‐Jun amino‐terminal kinase in the course of endodermal differentiation of P19 embryonic carcinoma cells

Cited by 2 publications

References 21 publications

Activation Mechanism of c-Jun Amino-terminal Kinase in the Course of Neural Differentiation of P19 Embryonic Carcinoma Cells

Activation Mechanism of c-Jun Amino-terminal Kinase in the Course of Neural Differentiation of P19 Embryonic Carcinoma Cells

Mouse preimplantation embryo responses to culture medium osmolarity include increased expression of CCM2 and p38 MAPK activation

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