The insulin receptor substrate (IRS)-1 recruits phosphatidylinositol 3-kinase to Ret: evidence for a competition between Shc and IRS-1 for the binding to Ret. (Q42829672)

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scientific article published on January 2001

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English	The insulin receptor substrate (IRS)-1 recruits phosphatidylinositol 3-kinase to Ret: evidence for a competition between Shc and IRS-1 for the binding to Ret.	scientific article published on January 2001

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6 November 2019

The insulin receptor substrate (IRS)-1 recruits phosphatidylinositol 3-kinase to Ret: evidence for a competition between Shc and IRS-1 for the binding to Ret (English)

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6 November 2019

Gabriella De Vita

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6 November 2019

Pietro Formisano

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6 November 2019

Rosa Marina Melillo

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6 November 2019

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F Carlomagno

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6 November 2019

G Vecchio

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6 November 2019

M Billaud

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6 November 2019

M Santoro

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6 November 2019

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1 January 2001

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6 November 2019

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6 November 2019

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6 November 2019

209-218

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6 November 2019

2

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6 November 2019

https://scigraph.springernature.com/pub.10.1038/sj.onc.1204049

0 references

GDNF family neurotrophic factor signaling: four masters, one servant?

1 reference

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Grb2 binding to the different isoforms of Ret tyrosine kinase.

1 reference

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Identification of Shc docking site on Ret tyrosine kinase

1 reference

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A mutation at tyrosine 1062 in MEN2A-Ret and MEN2B-Ret impairs their transforming activity and association with shc adaptor proteins

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Akt activation by growth factors is a multiple-step process: the role of the PH domain

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Cell survival promoted by the Ras-MAPK signaling pathway by transcription-dependent and -independent mechanisms

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The full oncogenic activity of Ret/ptc2 depends on tyrosine 539, a docking site for phospholipase Cgamma

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21 January 2018

Glial cell line-derived neurotrophic factor differentially stimulates ret mutants associated with the multiple endocrine neoplasia type 2 syndromes and Hirschsprung's disease.

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Cellular survival: a play in three Akts

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Shc and Enigma are both required for mitogenic signaling by Ret/ptc2.

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Two distinct mutations of the RET receptor causing Hirschsprung's disease impair the binding of signalling effectors to a multifunctional docking site

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Interleukins 2, 4, 7, and 15 stimulate tyrosine phosphorylation of insulin receptor substrates 1 and 2 in T cells. Potential role of JAK kinases

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Characterization of intracellular signals via tyrosine 1062 in RET activated by glial cell line-derived neurotrophic factor

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Oncogenic RET receptors display different autophosphorylation sites and substrate binding specificities

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Specificity of receptor tyrosine kinase signaling: transient versus sustained extracellular signal-regulated kinase activation

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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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Rho-dependent and -independent tyrosine phosphorylation of focal adhesion kinase, paxillin and p130Cas mediated by Ret kinase

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Enhanced phosphatidylinositol 3-kinase activity and high phosphorylation state of its downstream signalling molecules mediated by ret with the MEN 2B mutation

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YMXM motifs and signaling by an insulin receptor substrate 1 molecule without tyrosine phosphorylation sites

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The Ret receptor protein tyrosine kinase associates with the SH2-containing adapter protein Grb10

1 reference

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Direct association between the Ret receptor tyrosine kinase and the Src homology 2-containing adapter protein Grb7

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RET mutations in human disease

1 reference

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Signaling through scaffold, anchoring, and adaptor proteins

1 reference

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A novel transforming protein (SHC) with an SH2 domain is implicated in mitogenic signal transduction

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The role of phosphoinositide 3-kinase lipid products in cell function

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The GDNF protein family: gene ablation studies reveal what they really do and how.

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Activation of RET as a dominant transforming gene by germline mutations of MEN2A and MEN2B

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An epidermal growth factor receptor/ret chimera generates mitogenic and transforming signals: evidence for a ret-specific signaling pathway

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How receptor tyrosine kinases activate Ras.

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SH2/SH3 signaling proteins

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Transforming ability of MEN2A-RET requires activation of the phosphatidylinositol 3-kinase/AKT signaling pathway.

1 reference

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The function of GRB2 in linking the insulin receptor to Ras signaling pathways

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Ret-dependent and -independent mechanisms of glial cell line-derived neurotrophic factor signaling in neuronal cells

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Interferon-alpha engages the insulin receptor substrate-1 to associate with the phosphatidylinositol 3'-kinase

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Re-engineering the target specificity of the insulin receptor by modification of a PTB domain binding site

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Tyrosine phosphorylation of insulin receptor substrate-1 in vivo depends upon the presence of its pleckstrin homology region

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IRS-1: essential for insulin- and IL-4-stimulated mitogenesis in hematopoietic cells

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PTB domains of IRS-1 and Shc have distinct but overlapping binding specificities

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Insulin receptor substrate (IRS)-1 and IRS-2 are tyrosine-phosphorylated and associated with phosphatidylinositol 3-kinase in response to brain-derived neurotrophic factor in cultured cerebral cortical neurons.

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Structural basis for IL-4 receptor phosphopeptide recognition by the IRS-1 PTB domain

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An IL-4 receptor region containing an insulin receptor motif is important for IL-4-mediated IRS-1 phosphorylation and cell growth

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7 January 2021

based on heuristic

inferred from DOI database lookup

RET alternate splicing influences the interaction of activated RET with the SH2 and PTB domains of Shc, and the SH2 domain of Grb2

1 reference

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7 January 2021

based on heuristic

inferred from DOI database lookup

The surprisingly flexible PTB domain

1 reference

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7 January 2021

based on heuristic

inferred from DOI database lookup

Protein kinase B activation and lamellipodium formation are independent phosphoinositide 3-kinase-mediated events differentially regulated by endogenous Ras.

1 reference

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7 January 2021

based on heuristic

inferred from DOI database lookup

Identifiers

10.1038/SJ.ONC.1204049

1 reference

Europe PubMed Central

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6 November 2019

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6 November 2019

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