α-thrombin activates Akt via a nonreceptor tyrosine kinase in IIC9 cells

Polly J. Phillips-Mason; Reema Goel; Joseph J. Baldassare

doi:10.1111/j.1749-6632.2002.tb04623.x

α-thrombin activates Akt via a nonreceptor tyrosine kinase in IIC9 cells

Polly J. Phillips-Mason, Reema Goel, Joseph J. Baldassare

Department of Public Health Sciences

Research output: Contribution to journal › Article › peer-review

4 Scopus citations

Abstract

Previous data from our laboratory show that PI 3-kinase is required for α-thrombin-stimulated G₁ progression in IIC9 cells. In IIC9 cells, PI 3-kinase acts downstream of Ras to activate Akt, in a pathway parallel to ERK1. Here we show that α-thrombin does not transactivate either the EGF receptor or the PDGF receptor as measured by tyrosine phosphorylation, suggesting that activation of PI 3-kinase by α-thrombin is not the result of an RTK. Interestingly, both genistein and PP1 block α-thrombin-stimulated Akt phosphorylation, suggesting the involvement of a member of the Src family of non-receptor tyrosine kinases.

Original language	English (US)
Pages (from-to)	142-144
Number of pages	3
Journal	Annals of the New York Academy of Sciences
Volume	973
DOIs	https://doi.org/10.1111/j.1749-6632.2002.tb04623.x
State	Published - 2002

All Science Journal Classification (ASJC) codes

General Neuroscience
General Biochemistry, Genetics and Molecular Biology
History and Philosophy of Science

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title = "α-thrombin activates Akt via a nonreceptor tyrosine kinase in IIC9 cells",

abstract = "Previous data from our laboratory show that PI 3-kinase is required for α-thrombin-stimulated G1 progression in IIC9 cells. In IIC9 cells, PI 3-kinase acts downstream of Ras to activate Akt, in a pathway parallel to ERK1. Here we show that α-thrombin does not transactivate either the EGF receptor or the PDGF receptor as measured by tyrosine phosphorylation, suggesting that activation of PI 3-kinase by α-thrombin is not the result of an RTK. Interestingly, both genistein and PP1 block α-thrombin-stimulated Akt phosphorylation, suggesting the involvement of a member of the Src family of non-receptor tyrosine kinases.",

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doi = "10.1111/j.1749-6632.2002.tb04623.x",

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T1 - α-thrombin activates Akt via a nonreceptor tyrosine kinase in IIC9 cells

AU - Phillips-Mason, Polly J.

AU - Goel, Reema

AU - Baldassare, Joseph J.

PY - 2002

Y1 - 2002

N2 - Previous data from our laboratory show that PI 3-kinase is required for α-thrombin-stimulated G1 progression in IIC9 cells. In IIC9 cells, PI 3-kinase acts downstream of Ras to activate Akt, in a pathway parallel to ERK1. Here we show that α-thrombin does not transactivate either the EGF receptor or the PDGF receptor as measured by tyrosine phosphorylation, suggesting that activation of PI 3-kinase by α-thrombin is not the result of an RTK. Interestingly, both genistein and PP1 block α-thrombin-stimulated Akt phosphorylation, suggesting the involvement of a member of the Src family of non-receptor tyrosine kinases.

AB - Previous data from our laboratory show that PI 3-kinase is required for α-thrombin-stimulated G1 progression in IIC9 cells. In IIC9 cells, PI 3-kinase acts downstream of Ras to activate Akt, in a pathway parallel to ERK1. Here we show that α-thrombin does not transactivate either the EGF receptor or the PDGF receptor as measured by tyrosine phosphorylation, suggesting that activation of PI 3-kinase by α-thrombin is not the result of an RTK. Interestingly, both genistein and PP1 block α-thrombin-stimulated Akt phosphorylation, suggesting the involvement of a member of the Src family of non-receptor tyrosine kinases.

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AN - SCOPUS:0036961974

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JO - Annals of the New York Academy of Sciences

JF - Annals of the New York Academy of Sciences

ER -

α-thrombin activates Akt via a nonreceptor tyrosine kinase in IIC9 cells

Abstract

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