TrkA alternative splicing: a regulated tumor-promoting switch in human neuroblastoma (Q24307374)

Phosphoinositide-3-kinase regulatory subunit 1

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Growth factor receptor bound protein 2

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Fibroblast growth factor receptor substrate 2

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Neurotrophic receptor tyrosine kinase 1

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Phospholipase C gamma 1

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neurotrophin TRKA receptor binding

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alternative mRNA splicing, via spliceosome

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Antonella Tacconelli

1

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Antonietta R Farina

2

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Lucia Cappabianca

3

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Giuseppina Desantis

4

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Alessandra Tessitore

5

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Antonella Vetuschi

6

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Roberta Sferra

7

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Nadia Rucci

8

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Beatrice Argenti

9

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Isabella Screpanti

10

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Alberto Gulino

11

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Andrew R Mackay

Neuronal differentiation signals are controlled by nerve growth factor receptor/Trk binding sites for SHC and PLC gamma.

12

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language of work or name

English

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publication date

October 2004

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published in

Cancer Cell

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volume

6

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issue

4

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page(s)

347-60

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cites work

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TrkA glycosylation regulates receptor localization and activity

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EGF regulates a complex pattern of gene expression and represses smooth muscle differentiation during the neurotypic conversion of the neural-crest-derived TC-1S cell line

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A sequence analysis of the genomic regions involved in the rearrangements between TPM3 and NTRK1 genes producing TRK oncogenes in papillary thyroid carcinomas

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The trk proto-oncogene encodes a receptor for nerve growth factor

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The protein kinase encoded by the Akt proto-oncogene is a target of the PDGF-activated phosphatidylinositol 3-kinase

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Deletion of a conserved juxtamembrane sequence in Trk abolishes NGF-promoted neuritogenesis

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Early events in neurotrophin signalling via Trk and p75 receptors

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Angiogenesis extent and expression of matrix metalloproteinase-2 and -9 correlate with progression in human neuroblastoma

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Trk receptor tyrosine kinases: a bridge between cancer and neural development

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Activation of trk-A but not trk-B signal transduction pathway inhibits growth of neuroblastoma cells.

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Hypoxia promotes invasive growth by transcriptional activation of the met protooncogene

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A human oncogene formed by the fusion of truncated tropomyosin and protein tyrosine kinase sequences

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Tyrosine phosphorylation and tyrosine kinase activity of the trk proto-oncogene product induced by NGF.

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Matrix metalloproteinase-9 triggers the angiogenic switch during carcinogenesis

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High-affinity NGF binding requires coexpression of the trk proto-oncogene and the low-affinity NGF receptor

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NF-kappaB activation by tumour necrosis factor requires the Akt serine-threonine kinase

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Hypoxia--a key regulatory factor in tumour growth

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Nerve growth factor induced stimulation of Ras requires Trk interaction with Shc but does not involve phosphoinositide 3-OH kinase

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A novel mutation within the extracellular domain of TrkA causes constitutive receptor activation

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Meaningful relationships: the regulation of the Ras/Raf/MEK/ERK pathway by protein interactions

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Upregulation of vascular endothelial growth factor receptors is associated with advanced neuroblastoma.

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Activation of Trk neurotrophin receptors in the absence of neurotrophins

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Hypoxia alters gene expression in human neuroblastoma cells toward an immature and neural crest-like phenotype

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Thrombospondin-1 suppresses spontaneous tumor growth and inhibits activation of matrix metalloproteinase-9 and mobilization of vascular endothelial growth factor

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Frequent generation of oncogenes by in vitro recombination of TRK protooncogene sequences

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Tyrosine kinase activity coupled to the high-affinity nerve growth factor-receptor complex

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Nerve growth factor binding site on TrkA mapped to a single 24-amino acid leucine-rich motif.

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Autophosphorylation of activation loop tyrosines regulates signaling by the TRK nerve growth factor receptor

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The signaling adapter FRS-2 competes with Shc for binding to the nerve growth factor receptor TrkA. A model for discriminating proliferation and differentiation

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Regulation of Raf-Akt Cross-talk

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Identification of functional hypoxia response elements in the promoter region of the DEC1 and DEC2 genes

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Neurotrophins: key regulators of cell fate and cell shape in the vertebrate nervous system

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Signal transduction pathways through TRK-A and TRK-B receptors in human neuroblastoma cells

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Human trk oncogenes activated by point mutation, in-frame deletion, and duplication of the tyrosine kinase domain

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Nerve growth factor (NGF) induces neuronal differentiation in neuroblastoma cells transfected with the NGF receptor cDNA.

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The DNA rearrangement that generates the TRK-T3 oncogene involves a novel gene on chromosome 3 whose product has a potential coiled-coil domain

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TrkA immunoglobulin-like ligand binding domains inhibit spontaneous activation of the receptor

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Identification and characterization of an activating TrkA deletion mutation in acute myeloid leukemia

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NGF stimulation of erk phosphorylation is impaired by a point mutation in the transmembrane domain of trkA receptor

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Neuroendocrine tumours

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