Sustained phosphorylation of mutated FGFR3 is a crucial feature of genetic dwarfism and induces apoptosis in the ATDC5 chondrogenic cell line via PLCgamma-activated STAT1 (Q24309328)

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English	Sustained phosphorylation of mutated FGFR3 is a crucial feature of genetic dwarfism and induces apoptosis in the ATDC5 chondrogenic cell line via PLCgamma-activated STAT1	scientific article

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scholarly article

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Sustained phosphorylation of mutated FGFR3 is a crucial feature of genetic dwarfism and induces apoptosis in the ATDC5 chondrogenic cell line via PLCgamma-activated STAT1 (English)

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apoptotic process

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fibroblast growth factor receptor apoptotic signaling pathway

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Gene Ontology release 2020-05-02

Gene Ontology ID

GOA release 2020-03-11

fibroblast growth factor receptor 3

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GOA release 2020-03-11

phosphorylation

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based on heuristic

inferred from title

author name string

Daisuke Harada

1

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Yoshitaka Yamanaka

2

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Koso Ueda

3

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Riko Nishimura

4

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Tsuneo Morishima

5

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Yoshiki Seino

6

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Hiroyuki Tanaka

7

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language of work or name

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publication date

August 2007

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41

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2

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273-81

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Thanatophoric dysplasia: fetal manifestations and prenatal diagnosis

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A new neonatal short limbed dwarfism.

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Immunohistochemical localization of fibroblast growth factor receptors in the rat mandibular condylar cartilage and tibial cartilage

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

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Overexpression of FGFR3, Stat1, Stat5 and p21Cip1 correlates with phenotypic severity and defective chondrocyte differentiation in FGFR3-related chondrodysplasias

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FGF signaling in the developing endochondral skeleton

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K644E/M FGFR3 mutants activate Erk1/2 from the endoplasmic reticulum through FRS2 alpha and PLC gamma-independent pathways

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Cell responses to FGFR3 signalling: growth, differentiation and apoptosis

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Stat3 as an oncogene

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Control of Bone Growth by Fibroblast Growth Factors

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

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Activation of Stat1 by mutant fibroblast growth-factor receptor in thanatophoric dysplasia type II dwarfism

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

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Stop codon FGFR3 mutations in thanatophoric dwarfism type 1.

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

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

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FGF signaling activates STAT1 and p21 and inhibits the estrogen response and proliferation of MCF-7 cells.

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Transformation and Stat activation by derivatives of FGFR1, FGFR3, and FGFR4

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https://api.crossref.org/works/10.1016%2FJ.BONE.2006.11.030

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based on heuristic

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The thanatophoric dysplasia type II mutation hampers complete maturation of fibroblast growth factor receptor 3 (FGFR3), which activates signal transducer and activator of transcription 1 (STAT1) from the endoplasmic reticulum

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https://api.crossref.org/works/10.1016%2FJ.BONE.2006.11.030

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Activation of the ERK1/2 and p38 mitogen-activated protein kinase pathways mediates fibroblast growth factor-induced growth arrest of chondrocytes

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https://api.crossref.org/works/10.1016%2FJ.BONE.2006.11.030

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The kinase activity of fibroblast growth factor receptor 3 with activation loop mutations affects receptor trafficking and signaling

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Chondrogenic differentiation of clonal mouse embryonic cell line ATDC5 in vitro: differentiation-dependent gene expression of parathyroid hormone (PTH)/PTH-related peptide receptor

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based on heuristic

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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

1 reference

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based on heuristic

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Distinct missense mutations of the FGFR3 lys650 codon modulate receptor kinase activation and the severity of the skeletal dysplasia phenotype

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based on heuristic

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Identification of tyrosine residues in constitutively activated fibroblast growth factor receptor 3 involved in mitogenesis, Stat activation, and phosphatidylinositol 3-kinase activation

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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

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https://api.crossref.org/works/10.1016%2FJ.BONE.2006.11.030

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based on heuristic

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A Lys644Glu substitution in fibroblast growth factor receptor 3 (FGFR3) causes dwarfism in mice by activation of STATs and ink4 cell cycle inhibitors

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https://api.crossref.org/works/10.1016%2FJ.BONE.2006.11.030

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based on heuristic

inferred from DOI database lookup

FGF signaling inhibits chondrocyte proliferation and regulates bone development through the STAT-1 pathway

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based on heuristic

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Phospholipase C-gamma1: a phospholipase and guanine nucleotide exchange factor

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Differential role of Janus family kinases (JAKs) in interferon-gamma-induced lung epithelial ICAM-1 expression: involving protein interactions between JAKs, phospholipase Cgamma, c-Src, and STAT1.

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Defective TNF-alpha-induced apoptosis in STAT1-null cells due to low constitutive levels of caspases

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A tyrosine-phosphorylated carboxy-terminal peptide of the fibroblast growth factor receptor (Flg) is a binding site for the SH2 domain of phospholipase C-gamma 1

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based on heuristic

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Activation of the STAT signaling pathway can cause expression of caspase 1 and apoptosis

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STAT1: a modulator of chemotherapy-induced apoptosis

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Constitutively activated FGFR3 mutants signal through PLCgamma-dependent and -independent pathways for hematopoietic transformation.

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Differential activation of cysteine-substitution mutants of fibroblast growth factor receptor 3 is determined by cysteine localization

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

1 reference

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

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10.1016/J.BONE.2006.11.030

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