Soluble form of FGFR2 with S252W partially prevents craniosynostosis of the apert mouse model. (Q54395469)

http://europepmc.org/abstract/MED/24259495

29 May 2018

title

Soluble form of FGFR2 with S252W partially prevents craniosynostosis of the apert mouse model. (English)

1 reference

http://europepmc.org/abstract/MED/24259495

29 May 2018

0 references

5

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8 June 2020

author name string

Jumpei Morita

1

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8 June 2020

Masataka Nakamura

2

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8 June 2020

Yukiho Kobayashi

3

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8 June 2020

Chu-Xia Deng

4

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https://www.ebi.ac.uk/europepmc/webservices/rest/search?query=EXT_ID:24259495%20AND%20SRC:MED&resulttype=core&format=json

8 June 2020

Keiji Moriyama

6

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8 June 2020

publication date

19 December 2013

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http://europepmc.org/abstract/MED/24259495

29 May 2018

published in

Developmental Dynamics

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8 June 2020

volume

243

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8 June 2020

issue

4

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8 June 2020

page(s)

560-567

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Apert syndrome mutations in fibroblast growth factor receptor 2 exhibit increased affinity for FGF ligand

8 June 2020

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Apert syndrome mutant FGFR2 and its soluble form reciprocally alter osteogenesis of primary calvarial osteoblasts

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A soluble form of fibroblast growth factor receptor 2 (FGFR2) with S252W mutation acts as an efficient inhibitor for the enhanced osteoblastic differentiation caused by FGFR2 activation in Apert syndrome

21 January 2018

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Abnormalities in cartilage and bone development in the Apert syndrome FGFR2(+/S252W) mouse.

21 January 2018

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Activation of p38 MAPK pathway in the skull abnormalities of Apert syndrome Fgfr2(+P253R) mice

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Apert syndrome results from localized mutations of FGFR2 and is allelic with Crouzon syndrome

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A Pro253Arg mutation in fibroblast growth factor receptor 2 (Fgfr2) causes skeleton malformation mimicking human Apert syndrome by affecting both chondrogenesis and osteogenesis

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