ArticleMolecular and cellular biology2006
The adaptor protein Tom1L1 is a negative regulator of Src mitogenic signaling induced by growth factors.
Article in Molecular and cellular biology, 2006. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.
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Who cites it
23 citing papers in PubMed, 41 citations in OpenAlex.
- Genetic determinants of drug-induced gingival overgrowth.Scientific reports · 2026Article
- Genetic Variant Overlap Analysis Identifies Established and Putative Genes Involved in Pulmonary Fibrosis.International journal of molecular sciences · 2023Article
- Protein Trafficking or Cell Signaling: A Dilemma for the Adaptor Protein TOM1.Frontiers in cell and developmental biology · 2021Review
- Cellular Aging Characteristics and Their Association with Age-Related Disorders.Antioxidants (Basel, Switzerland) · 2020Review
- Proteomic Identification of Heat Shock-Induced Danger Signals in a Melanoma Cell Lysate Used in Dendritic Cell-Based Cancer Immunotherapy.Journal of immunology research · 2018Article
- Temporal Profiling of Astrocyte Precursors Reveals Parallel Roles for Asef during Development and after Injury.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2016Article
- Vesicular trafficking regulators are new players in breast cancer progression: Role of TOM1L1 in ERBB2-dependent invasion.Molecular & cellular oncology · 2016Article
- TOM1L1 drives membrane delivery of MT1-MMP to promote ERBB2-induced breast cancer cell invasion.Nature communications · 2016Article
- Quantitative analysis of the TNF-α-induced phosphoproteome reveals AEG-1/MTDH/LYRIC as an IKKβ substrate.Nature communications · 2015Article
- Identification of novel regulatory genes in development of the avian reproductive tracts.PloS one · 2014Article
- MicroRNA-124 suppresses the transactivation of nuclear factor of activated T cells by targeting multiple genes and inhibits the proliferation of pulmonary artery smooth muscle cells.The Journal of biological chemistry · 2013Article
- Analysis of SRC oncogenic signaling in colorectal cancer by stable isotope labeling with heavy amino acids in mouse xenografts.Molecular & cellular proteomics : MCP · 2012Article
- Endosomal-sorting complexes required for transport (ESCRT) pathway-dependent endosomal traffic regulates the localization of active Src at focal adhesions.Proceedings of the National Academy of Sciences of the United States of America · 2010Article
- Article
- Multiple myeloma phosphotyrosine proteomic profile associated with FGFR3 expression, ligand activation, and drug inhibition.Proceedings of the National Academy of Sciences of the United States of America · 2009Article
- Participation of Tom1L1 in EGF-stimulated endocytosis of EGF receptor.The EMBO journal · 2009Article
- TOM1L is involved in a novel signaling pathway important for the IL-2 production in Jurkat T cells stimulated by CD3/CD28 co-ligation.Mediators of inflammation · 2009Article
- The Csk-binding protein PAG regulates PDGF-induced Src mitogenic signaling via GM1.The Journal of cell biology · 2008Article
- Tom1l2 hypomorphic mice exhibit increased incidence of infections and tumors and abnormal immunologic response.Mammalian genome : official journal of the International Mammalian Genome Society · 2008Article
- The tyrosine kinase Abl is required for Src-transforming activity in mouse fibroblasts and human breast cancer cells.Oncogene · 2007Article
Corrections and comments
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Authors and funding
6 authors at 2 institutions in 3 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The Src family of protein-tyrosine kinases (SFK) play important roles in mitogenesis and morphological changes induced by growth factors. The involved substrates are, however, ill defined. Using an antiphosphotyrosine antibody to screen tyrosine-phosphorylated cDNA expression library, we have identified Tom1L1, an adaptor protein of the Tom1 family and a novel substrate and activator of the SFK. Surprisingly, we found that Tom1L1 does not promote DNA synthesis induced by Src. Furthermore, we report that Tom1L1 negatively regulates SFK mitogenic signaling induced by platelet-derived growth factor (PDGF) through modulation of SFK-receptor association: (i) Tom1L1 inhibits DNA synthesis induced by PDGF; (ii) inhibition is overcome by c-myc expression or p53 inactivation, two regulators of SFK mitogenic function; (iii) Src or Fyn coexpression overrides Tom1L1 mitogenic activity; (iv) overexpression of the adaptor reduces Src association with the receptor; and (v) protein inactivation potentiates receptor complex formation, allowing increased SFK activation and DNA synthesis. However, Tom1L1 affects neither DNA synthesis induced by the constitutively active allele SrcY527F nor SFK-regulated actin assembly induced by PDGF. Finally, overexpressed Tom1 and Tom1L2 also associate with Src and affected mitogenic signaling in agreement with some redundancy among members of the Tom1 family. We concluded that Tom1L1 defines a novel mechanism for regulation of SFK mitogenic signaling induced by growth factors.
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