(Q34980977)

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Transient inhibition of the ERK pathway prevents cerebellar developmental defects and improves long-term motor functions in murine models of neurofibromatosis type 1.

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Europe PubMed Central

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5 August 2017

Transient inhibition of the ERK pathway prevents cerebellar developmental defects and improves long-term motor functions in murine models of neurofibromatosis type 1. (English)

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Europe PubMed Central

PubMed publication ID

5 August 2017

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Edward Kim

1

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5 August 2017

Yuan Wang

2

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5 August 2017

Sun-Jung Kim

3

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5 August 2017

Miriam Bornhorst

4

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5 August 2017

Emmanuelle S Jecrois

5

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5 August 2017

Todd E Anthony

6

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5 August 2017

Chenran Wang

7

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5 August 2017

Yi E Li

8

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5 August 2017

Jun-Lin Guan

9

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5 August 2017

Geoffrey G Murphy

10

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5 August 2017

Yuan Zhu

11

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5 August 2017

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23 December 2014

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5 August 2017

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5 August 2017

3

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5 August 2017

describes a project that uses

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Europe PubMed Central

11 June 2022

https://www.ebi.ac.uk/europepmc/webservices/rest/PMC4297949/fullTextXML

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FGF/FGFR2 signaling regulates the generation and correct positioning of Bergmann glia cells in the developing mouse cerebellum

1 reference

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Shp2-dependent ERK signaling is essential for induction of Bergmann glia and foliation of the cerebellum

1 reference

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1 reference

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ERK inhibition rescues defects in fate specification of Nf1-deficient neural progenitors and brain abnormalities

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Sprouty genes prevent excessive FGF signalling in multiple cell types throughout development of the cerebellum.

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Evidence for and against regional differences in neural stem and progenitor cells of the CNS.

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Motor Learning in Children with Neurofibromatosis Type I

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Neuron-derived FGF9 is essential for scaffold formation of Bergmann radial fibers and migration of granule neurons in the cerebellum

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1 reference

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12 December 2020

based on heuristic

inferred from PubMed ID database lookup

Identifiers

10.7554/ELIFE.05151

1 reference

Europe PubMed Central

PubMed publication ID

5 August 2017

PMC publication ID

1 reference

Europe PubMed Central

PubMed publication ID

5 August 2017

PubMed publication ID

1 reference

Europe PubMed Central

PubMed publication ID

5 August 2017

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