(Q40618620)

English

Insulin-like Growth Factor-1 Rescues the Mutated FGF Receptor 3 (G380R) Expressing ATDC5 Cells From Apoptosis Through Phosphatidylinositol 3-Kinase and MAPK

scientific article published on November 1, 2003

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scholarly article

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Europe PubMed Central

PubMed publication ID

22 September 2017

Insulin-like Growth Factor-1 Rescues the Mutated FGF Receptor 3 (G380R) Expressing ATDC5 Cells From Apoptosis Through Phosphatidylinositol 3-Kinase and MAPK (English)

1 reference

10.1359/JBMR.2003.18.11.2043

https://api.crossref.org/works/10.1359/JBMR.2003.18.11.2043

30 March 2024

Orthopedics and sports medicine

1 reference

10.1359/JBMR.2003.18.11.2043

https://api.crossref.org/works/10.1359/JBMR.2003.18.11.2043

30 March 2024

5

object named as

Riko Nishimura

1 reference

Europe PubMed Central

PubMed publication ID

https://www.ebi.ac.uk/europepmc/webservices/rest/search?resulttype=core&format=json&query=SRC%3AMED%20AND%20EXT_ID%3A14606518

30 March 2024

author name string

Mio Koike

1

1 reference

Europe PubMed Central

PubMed publication ID

22 September 2017

Yoshitaka Yamanaka

2

1 reference

Europe PubMed Central

PubMed publication ID

22 September 2017

Masaru Inoue

3

1 reference

Europe PubMed Central

PubMed publication ID

22 September 2017

Hiroyuki Tanaka

4

1 reference

Europe PubMed Central

PubMed publication ID

22 September 2017

Yoshiki Seino

6

1 reference

Europe PubMed Central

PubMed publication ID

22 September 2017

language of work or name

1 reference

National Center for Biotechnology Information

PubMed publication ID

https://eutils.ncbi.nlm.nih.gov/entrez/eutils/esummary.fcgi?db=pubmed&retmode=json&id=14606518

30 March 2024

publication date

1 November 2003

1 reference

Europe PubMed Central

PubMed publication ID

22 September 2017

full work available at URL

https://onlinelibrary.wiley.com/doi/pdfdirect/10.1359/jbmr.2003.18.11.2043

Portable Document Format

online access status

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Europe PubMed Central

PubMed publication ID

https://www.ebi.ac.uk/europepmc/webservices/rest/search?resulttype=core&format=json&query=SRC%3AMED%20AND%20EXT_ID%3A14606518

30 March 2024

https://api.wiley.com/onlinelibrary/tdm/v1/articles/10.1359%2Fjbmr.2003.18.11.2043

1 reference

10.1359/JBMR.2003.18.11.2043

https://api.crossref.org/works/10.1359/JBMR.2003.18.11.2043

30 March 2024

https://academic.oup.com/jbmr/article-pdf/18/11/2043/56469320/5650181116.pdf

Portable Document Format

1 reference

10.1359/JBMR.2003.18.11.2043

https://api.crossref.org/works/10.1359/JBMR.2003.18.11.2043

30 March 2024

Journal of Bone and Mineral Research

1 reference

Europe PubMed Central

PubMed publication ID

22 September 2017

18

1 reference

Europe PubMed Central

PubMed publication ID

22 September 2017

11

1 reference

Europe PubMed Central

PubMed publication ID

22 September 2017

2043-2051

1 reference

Europe PubMed Central

PubMed publication ID

22 September 2017

Profound ligand-independent kinase activation of fibroblast growth factor receptor 3 by the activation loop mutation responsible for a lethal skeletal dysplasia, thanatophoric dysplasia type II

1 reference

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Enhanced signaling and morphological transformation by a membrane-localized derivative of the fibroblast growth factor receptor 3 kinase domain

1 reference

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Cell death signal transduction and Bcl-2 function

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Fibroblast growth factor receptor 3 is a negative regulator of bone growth

1 reference

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Control of Bone Growth by Fibroblast Growth Factors

1

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30 March 2024

Mutations in the gene encoding fibroblast growth factor receptor-3 in achondroplasia

2

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Mutations in the transmembrane domain of FGFR3 cause the most common genetic form of dwarfism, achondroplasia

3

1 reference

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Thanatophoric dysplasia (types I and II) caused by distinct mutations in fibroblast growth factor receptor 3.

4

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Another mutation that results in the substitution of an unpaired cysteine residue in the extracellular domain of FGFR3 in thanatophoric dysplasia type I

5

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A recurrent mutation in the tyrosine kinase domain of fibroblast growth factor receptor 3 causes hypochondroplasia

6

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A novel skeletal dysplasia with developmental delay and acanthosis nigricans is caused by a Lys650Met mutation in the fibroblast growth factor receptor 3 gene

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The molecular and genetic basis of fibroblast growth factor receptor 3 disorders: the achondroplasia family of skeletal dysplasias, Muenke craniosynostosis, and Crouzon syndrome with acanthosis nigricans

9

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Skeletal overgrowth and deafness in mice lacking fibroblast growth factor receptor 3.

11

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Graded activation of fibroblast growth factor receptor 3 by mutations causing achondroplasia and thanatophoric dysplasia

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Constitutive activation of fibroblast growth factor receptor 3 by the transmembrane domain point mutation found in achondroplasia

13

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A mouse model for achondroplasia produced by targeting fibroblast growth factor receptor 3.

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Gly369Cys mutation in mouse FGFR3 causes achondroplasia by affecting both chondrogenesis and osteogenesis

17

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Fibroblast growth factor receptor 3 mutations promote apoptosis but do not alter chondrocyte proliferation in thanatophoric dysplasia

18

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PTHrP rescues ATDC5 cells from apoptosis induced by FGF receptor 3 mutation

19

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Cellular hypertrophy and calcification of embryonal carcinoma-derived chondrogenic cell line ATDC5 in vitro

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Growth hormone therapy in achondroplasia

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Effect of growth hormone therapy in children with achondroplasia: growth pattern, hypothalamic-pituitary function, and genotype

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Molecular defects in achondroplasia and the effects of growth hormone treatment

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Somatomedin: Proposed Designation for Sulphation Factor

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Liver-derived insulin-like growth factor I (IGF-I) is the principal source of IGF-I in blood but is not required for postnatal body growth in mice

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Normal growth and development in the absence of hepatic insulin-like growth factor I

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Insulin-like growth factors I and II. Peptide, messenger ribonucleic acid and gene structures, serum, and tissue concentrations

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The mitogenic and myogenic actions of insulin-like growth factors utilize distinct signaling pathways.

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Insulin-like Growth Factor-I Rapidly Activates Multiple Signal Transduction Pathways in Cultured Rat Cardiac Myocytes

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Insulin-like Growth Factor 1 Inhibits Apoptosis Using the Phosphatidylinositol 3′-Kinase and Mitogen-activated Protein Kinase Pathways

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Comparison of the insulin and insulin-like growth factor 1 mitogenic intracellular signaling pathways

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Interaction of the molecular weight 85K regulatory subunit of the phosphatidylinositol 3-kinase with the insulin receptor and the insulin-like growth factor-1 (IGF- I) receptor: comparative study using the yeast two-hybrid system

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The synergistic effect of PDGF-AA and IGF-1 on VSMC proliferation might be explained by the differential activation of their intracellular signaling pathways

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Isolation of an additional member of the fibroblast growth factor receptor family, FGFR-3

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Signal transduction pathway of human fibroblast growth factor receptor 3. Identification of a novel 66-kDa phosphoprotein

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Mitochondria and apoptosis

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Insulin receptor substrate-4 enhances insulin-like growth factor-I-induced cell proliferation

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Identification and inhibition of the ICE/CED-3 protease necessary for mammalian apoptosis

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Insulin-like growth factor-1 inhibition of apoptosis is associated with increased expression of the bcl-xL gene product

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Identifiers

10.1359/JBMR.2003.18.11.2043

1 reference

Europe PubMed Central

PubMed publication ID

22 September 2017

PubMed publication ID

1 reference

Europe PubMed Central

PubMed publication ID

22 September 2017

ResearchGate publication ID

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