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==Model retinoic acid extracellular signal-regulated kinase and Wnt pathway interactions==
==Model retinoic acid extracellular signal-regulated kinase and Wnt pathway interactions==


A. Interaction between retinoic acid (RA) and the extracellular signal-regulated kinase (ERK) pathway during promoted neural specification. FGF receptor tyrosine kinase inhibitor SU5402 and MEK1/2 inhibitors PD184352 and PD0325901, respectively suppresses neural differentiation of ESCs. In RA-treated cultures, PD184352, PD0325901 and RARα-selective antagonist Ro 41–5253 could inhibit the neural specification of ESCs, while SU5402 shows weak neural inhibition effect. RA probably enhances ERK phosphorylation via MEK1/2 or its upstream but not in a manner that is dependent on FGF signaling, and activated ERK1/2 mediates phosphorylation of the MAPK sites of Smad1 (pSmad1MAPK), which inhibits the inhibitory function of the bone morphogenetic proteins (BMPs)-Smad1 pathway on neural differentiation. Blockade of RA signaling might affect the activation of the upstream of ERK1/2, which leads to failure of neural specification of ESCs even with the stimulation of FGF signaling.  
'''A.''' Interaction between retinoic acid (RA) and the extracellular signal-regulated kinase (ERK) pathway during promoted neural specification. FGF receptor tyrosine kinase inhibitor SU5402 and MEK1/2 inhibitors PD184352 and PD0325901, respectively suppresses neural differentiation of ESCs. In RA-treated cultures, PD184352, PD0325901 and RARα-selective antagonist Ro 41–5253 could inhibit the neural specification of ESCs, while SU5402 shows weak neural inhibition effect. RA probably enhances ERK phosphorylation via MEK1/2 or its upstream but not in a manner that is dependent on FGF signaling, and activated ERK1/2 mediates phosphorylation of the MAPK sites of Smad1 (pSmad1MAPK), which inhibits the inhibitory function of the bone morphogenetic proteins (BMPs)-Smad1 pathway on neural differentiation. Blockade of RA signaling might affect the activation of the upstream of ERK1/2, which leads to failure of neural specification of ESCs even with the stimulation of FGF signaling.  


B. Possible roles of Wnt signaling in RA-promoted neural differentiation. RA promotes neural specification probably by up-regulating Sfrp2, which inhibits the Wnt-β-catenin anti-neural pathway. Upon adding LiCl or CHIR99021, which stimulates the β-catenin signaling and/or BMP signaling through inhibition of GSK3, the suppression effects on neural specification of β-catenin pathway can be passed down even with the stimuli of RA. RA also may promote neural differentiation by up-regulating RAR, which may decrease β-catenin/LEF/TCF mediated transactivation. There exists a possibility that RA may suppress the inhibition effects on neural differentiation of Wnt-β-catenin pathway by sequestration of β-catenin. pSmad1GSK3 indicates phosphorylation of the GSK3 sites of Smad1.
'''B.''' Possible roles of Wnt signaling in RA-promoted neural differentiation. RA promotes neural specification probably by up-regulating Sfrp2, which inhibits the Wnt-β-catenin anti-neural pathway. Upon adding LiCl or CHIR99021, which stimulates the β-catenin signaling and/or BMP signaling through inhibition of GSK3, the suppression effects on neural specification of β-catenin pathway can be passed down even with the stimuli of RA. RA also may promote neural differentiation by up-regulating RAR, which may decrease β-catenin/LEF/TCF mediated transactivation. There exists a possibility that RA may suppress the inhibition effects on neural differentiation of Wnt-β-catenin pathway by sequestration of β-catenin. pSmad1GSK3 indicates phosphorylation of the GSK3 sites of Smad1.




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Original file name: Figure 6. 1471-2121-10-57-6-l.jpg
:'''Links:''' [[Developmental_Signals_-_Retinoic_acid|Retinoic acid]]


===Reference===
===Reference===
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This is an Open Access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/2.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.
This is an Open Access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/2.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.
Original file name: Figure 6. 1471-2121-10-57-6-l.jpg
[[Category:Retinoic acid]]

Revision as of 12:27, 31 August 2014

Model retinoic acid extracellular signal-regulated kinase and Wnt pathway interactions

A. Interaction between retinoic acid (RA) and the extracellular signal-regulated kinase (ERK) pathway during promoted neural specification. FGF receptor tyrosine kinase inhibitor SU5402 and MEK1/2 inhibitors PD184352 and PD0325901, respectively suppresses neural differentiation of ESCs. In RA-treated cultures, PD184352, PD0325901 and RARα-selective antagonist Ro 41–5253 could inhibit the neural specification of ESCs, while SU5402 shows weak neural inhibition effect. RA probably enhances ERK phosphorylation via MEK1/2 or its upstream but not in a manner that is dependent on FGF signaling, and activated ERK1/2 mediates phosphorylation of the MAPK sites of Smad1 (pSmad1MAPK), which inhibits the inhibitory function of the bone morphogenetic proteins (BMPs)-Smad1 pathway on neural differentiation. Blockade of RA signaling might affect the activation of the upstream of ERK1/2, which leads to failure of neural specification of ESCs even with the stimulation of FGF signaling.

B. Possible roles of Wnt signaling in RA-promoted neural differentiation. RA promotes neural specification probably by up-regulating Sfrp2, which inhibits the Wnt-β-catenin anti-neural pathway. Upon adding LiCl or CHIR99021, which stimulates the β-catenin signaling and/or BMP signaling through inhibition of GSK3, the suppression effects on neural specification of β-catenin pathway can be passed down even with the stimuli of RA. RA also may promote neural differentiation by up-regulating RAR, which may decrease β-catenin/LEF/TCF mediated transactivation. There exists a possibility that RA may suppress the inhibition effects on neural differentiation of Wnt-β-catenin pathway by sequestration of β-catenin. pSmad1GSK3 indicates phosphorylation of the GSK3 sites of Smad1.


extracellular signal-regulated kinase (ERK)


Links: Retinoic acid

Reference

<pubmed>19642999</pubmed>


Lu et al. BMC Cell Biology 2009 10:57 doi:10.1186/1471-2121-10-57

© 2009 Lu et al; licensee BioMed Central Ltd.

This is an Open Access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/2.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.


Original file name: Figure 6. 1471-2121-10-57-6-l.jpg

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