Tyrosine-phosphorylated low density lipoprotein receptor-related protein 1 (Lrp1) associates with the adaptor protein SHC in SRC-transformed cells
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Updated: Oct 9, 2026

Development and Application of Rapamycin-regulated Tyrosine Phosphatases
Published on: September 6, 2024
1Department of Chemistry and Biochemistry, University of California, San Diego, La Jolla, California 92093-0359, USA.
Abstract:
v-Src transforms fibroblasts in vitro and causes tumor formation in the animal by tyrosine phosphorylation of critical cellular substrates. Exactly how v-Src interacts with these substrates remains unknown. One of its substrates, the adaptor protein Shc, is thought to play a crucial role during cellular transformation by v-Src by linking v-Src to Ras. We used Shc proteins with mutations in either the phosphotyrosine binding (PTB) or Src homology 2 domain to determine that phosphorylation of Shc in v-Src-expressing cells depends on the presence of a functional PTB domain. We purified a 100-kDa Shc PTB-binding protein from Src-transformed cells that was identified as the beta chain of the low density lipoprotein receptor-related protein LRP1. LRP1 acts as an import receptor for a variety of proteins and is involved in clearance of the beta-amyloid precursor protein. This study shows that LRP1 is tyrosine-phosphorylated in v-Src-transformed cells and that tyrosine-phosphorylated LRP1 binds in vivo and in vitro to Shc. The association between Shc and LRP1 may provide a mechanism for recruitment of Shc to the plasma membrane where it is phosphorylated by v-Src. It is at the membrane that Shc is thought to be involved in Ras activation. These observations further suggest that LRP1 could function as a signaling receptor and may provide new avenues to investigate its possible role during embryonal development and the onset of Alzheimer's disease.
Insights
v-Src transformation involves tyrosine phosphorylation of substrates like Shc. This study identifies the low-density lipoprotein receptor-related protein 1 (LRP1) as a key binding partner for Shc, potentially mediating its membrane recruitment and phosphorylation by v-Src.
Area of Science:
- Cellular Biology
- Molecular Oncology
- Signal Transduction
Background:
- v-Src oncoprotein drives cellular transformation and tumor formation via tyrosine phosphorylation.
- The adaptor protein Shc is a critical substrate linking v-Src to downstream signaling pathways like Ras.
- The precise mechanism of Shc interaction and phosphorylation by v-Src remains incompletely understood.
Purpose of the Study:
- To elucidate the interaction mechanism between v-Src and its substrate Shc.
- To identify the protein responsible for binding Shc and mediating its phosphorylation.
- To explore the role of LRP1 in v-Src-induced cellular transformation.
Main Methods:
- Utilized mutant Shc proteins (PTB and SH2 domains) to assess phosphorylation dependency.
- Purified Shc PTB-binding proteins from v-Src-transformed cells.
- Performed in vivo and in vitro binding assays to confirm LRP1-Shc interaction.
Main Results:
- Shc phosphorylation by v-Src requires a functional PTB domain.
- Identified the beta chain of LRP1 as a 100-kDa Shc PTB-binding protein.
- Demonstrated tyrosine phosphorylation of LRP1 in v-Src-transformed cells and its binding to Shc.
Conclusions:
- LRP1 is tyrosine-phosphorylated and binds to Shc in v-Src-transformed cells.
- LRP1 may recruit Shc to the plasma membrane for v-Src-mediated phosphorylation and subsequent Ras activation.
- LRP1 may function as a signaling receptor, with implications for embryonal development and Alzheimer's disease.
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