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PMID |
Sentence |
1 |
7499194
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PTB domains of IRS-1 and Shc have distinct but overlapping binding specificities.
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2 |
7499194
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By serial truncation, we show that a 174-residue region of Shc p52 (33-206) has full PTB activity.
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3 |
7499194
|
Phosphopeptide assays developed to compare PTB domain specificities show that the Shc PTB domain binds with highest affinity to psi XN beta 1 beta 2 pY motifs derived from middle T (mT), TrkA, ErbB4, or epidermal growth factor receptors (psi = hydrophobic, beta = beta-turn forming); the IRS-1 PTB domain does not bind with this motif.
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4 |
7499194
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In contrast, both the Shc and IRS-1 PTB domains bind psi psi psi XXN beta 1 beta 2pY sequences derived from insulin and interleukin 4 receptors, although specificities vary in detail.
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5 |
7499194
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Shc and IRS-1 are phosphorylated by distinct but overlapping sets of receptor-linked tyrosine kinases.
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6 |
19608732
|
Previously, we found that overexpression of the growth factor heparin-binding epidermal growth factor-like growth factor (HB-EGF) in pancreatic islets led to intraislet fibrosis.
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7 |
19608732
|
HB-EGF binds to and activates two receptors, epidermal growth factor receptor (EGFR) and ErbB4, as well as heparin moieties and CD9/DRAP27.
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8 |
19608732
|
To understand the mechanism underlying the induction of fibrogenesis by HB-EGF, we utilized a hypomorphic allele of Egfr, the Waved-2 allele, to demonstrate that EGFR signaling regulates fibrogenesis in vivo.
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9 |
19608732
|
Using an in vitro cell migration assay, we show that HB-EGF regulates both chemoattraction and stimulation of proliferation of PSCs via EGFR activation.
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