The insulin-like growth factor I receptor is required for Akt activation and suppression of anoikis in cells transformed by the ETV6-NTRK3 chimeric tyrosine kinase.
about
Targeting the insulin growth factor receptor 1MMP13 mediates cell cycle progression in melanocytes and melanoma cells: in vitro studies of migration and proliferation.PTK6 regulates IGF-1-induced anchorage-independent survival.Long-term IGF-I exposure decreases autophagy and cell viability.Can we unlock the potential of IGF-1R inhibition in cancer therapy?Understanding micrometastatic disease and Anoikis resistance in ewing family of tumors and osteosarcoma.The AMPK stress response pathway mediates anoikis resistance through inhibition of mTOR and suppression of protein synthesis.Inhibition of PI3K/mTOR leads to adaptive resistance in matrix-attached cancer cells.Metformin accelerates the growth of BRAF V600E-driven melanoma by upregulating VEGF-A.p66Shc mediates anoikis through RhoAInhibition of IGF-IR tyrosine kinase induces apoptosis and cell cycle arrest in imatinib-resistant chronic myeloid leukaemia cellsAnoikis, initiated by Mcl-1 degradation and Bim induction, is deregulated during oncogenesisMechanisms that link the oncogenic epithelial-mesenchymal transition to suppression of anoikis.Identification of kinase fusion oncogenes in post-Chernobyl radiation-induced thyroid cancers.E-cadherin cell-cell adhesion in ewing tumor cells mediates suppression of anoikis through activation of the ErbB4 tyrosine kinase.Inhibition of c-Src blocks oestrogen-induced apoptosis and restores oestrogen-stimulated growth in long-term oestrogen-deprived breast cancer cells.Targeting the insulin-like growth factor 1 receptor (IGF1R) signaling pathway for cancer therapy.Detecting and targetting oncogenic fusion proteins in the genomic era.JNK-mediated phosphorylation of paxillin in adhesion assembly and tension-induced cell death by the adenovirus death factor E4orf4.Expression of insulin-like growth factor pathway proteins in rhabdomyosarcoma: IGF-2 expression is associated with translocation-negative tumors.Mutation of the salt bridge-forming residues in the ETV6-SAM domain interface blocks ETV6-NTRK3-induced cellular transformation.Areca-treated fibroblasts enhance tumorigenesis of oral epithelial cells.Loss of PRP4K drives anoikis resistance in part by dysregulation of epidermal growth factor receptor endosomal trafficking.IGF2 is highly expressed in pediatric undifferentiated sarcomas and reveals two distinct cytoplasmic trafficking patterns.A tripartite complex composed of ETV6-NTRK3, IRS1 and IGF1R is required for ETV6-NTRK3-mediated membrane localization and transformation.
P2860
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P2860
The insulin-like growth factor I receptor is required for Akt activation and suppression of anoikis in cells transformed by the ETV6-NTRK3 chimeric tyrosine kinase.
description
2006 nî lūn-bûn
@nan
2006年の論文
@ja
2006年学术文章
@wuu
2006年学术文章
@zh
2006年学术文章
@zh-cn
2006年学术文章
@zh-hans
2006年学术文章
@zh-my
2006年学术文章
@zh-sg
2006年學術文章
@yue
2006年學術文章
@zh-hant
name
The insulin-like growth factor ...... TRK3 chimeric tyrosine kinase.
@en
The insulin-like growth factor ...... TRK3 chimeric tyrosine kinase.
@nl
type
label
The insulin-like growth factor ...... TRK3 chimeric tyrosine kinase.
@en
The insulin-like growth factor ...... TRK3 chimeric tyrosine kinase.
@nl
prefLabel
The insulin-like growth factor ...... TRK3 chimeric tyrosine kinase.
@en
The insulin-like growth factor ...... TRK3 chimeric tyrosine kinase.
@nl
P2093
P2860
P1476
The insulin-like growth factor ...... NTRK3 chimeric tyrosine kinase
@en
P2093
Martin Gleave
Mary Bowden
Matthew J Martin
Michelle Pollard
Nataliya Melnyk
Poul H B Sorensen
Thomas J Podor
P2860
P304
P356
10.1128/MCB.26.5.1754-1769.2006
P407
P50
P577
2006-03-01T00:00:00Z