ArticleThe Journal of cell biology2009
Reversion-induced LIM interaction with Src reveals a novel Src inactivation cycle.
Article in The Journal of cell biology, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
23 citing papers in PubMed, 41 citations in OpenAlex.
- PDLIM4 promotes dephosphorylation of STAT transcription factors by recruiting PTP-BL and inhibits Th1, Th2, and Th17 cell differentiation.International immunology · 2026Article
- BRD4-mediated transcriptional activation of PDLIM4 enhances p21 stability and chemosensitivity in lung adenocarcinoma independent of p53.BMC biology · 2026Article
- Enhanced Anti-Lung Cancer Effects of SteamedInternational journal of molecular sciences · 2025Article
- Protein tyrosine phosphatase PTPL1 suppresses lung cancer through Src/ERK/YAP1 signaling.Thoracic cancer · 2022Article
- Circular RNA hsa_circ_0002360 Promotes Proliferation and Invasion and Inhibits Oxidative Stress in Gastric Cancer by Sponging miR-629-3p and Regulating the PDLIM4 Expression.Oxidative medicine and cellular longevity · 2022Article
- Epigenetic modification and BRAF gene mutation in thyroid carcinoma.Cancer cell international · 2021Review
- Novel Majeed Syndrome-Causing LPIN2 Mutations Link Bone Inflammation to Inflammatory M2 Macrophages and Accelerated Osteoclastogenesis.Arthritis & rheumatology (Hoboken, N.J.) · 2021Article
- Dual Role of the PTPN13 Tyrosine Phosphatase in Cancer.Biomolecules · 2020Review
- Regulation of Src Family Kinases during Colorectal Cancer Development and Its Clinical Implications.Cancers · 2020Review
- PDLIM4/RIL-mediated regulation of Src and malignant properties of breast cancer cells.Oncotarget · 2020Article
- Analysis of EYA3 Phosphorylation by Src Kinase Identifies Residues Involved in Cell Proliferation.International journal of molecular sciences · 2019Article
- Methylation of tumour suppressor genes associated with thyroid cancer.Cancer biomarkers : section A of Disease markers · 2019Article
- Genomic rearrangements in sporadic lymphangioleiomyomatosis: an evolving genetic story.Modern pathology : an official journal of the United States and Canadian Academy of Pathology, Inc · 2017Article
- Hematopoietic cell kinase (HCK) as a therapeutic target in immune and cancer cells.Oncotarget · 2015Review
- Oncogenic signaling by tyrosine kinases of the SRC family in advanced colorectal cancer.American journal of cancer research · 2012Article
- Discovery of cellular substrates for protein kinase A using a peptide array screening protocol.The Biochemical journal · 2011Article
- Actin cytoskeleton remodeling by the alternatively spliced isoform of PDLIM4/RIL protein.The Journal of biological chemistry · 2011Article
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- PTPN13/PTPL1: an important regulator of tumor aggressiveness.Anti-cancer agents in medicinal chemistry · 2011Review
Corrections and comments
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
Abstract
Aberrant Src activation plays prominent roles in cancer progression. However, how Src is activated in cancer cells is largely unknown. Genetic Src-activating mutations are rare and, therefore, are insufficient to account for Src activation commonly found in human cancers. In this study, we show that reversion-induced LIM (RIL), which is frequently lost in colon and other cancers as a result of epigenetic silencing, suppresses Src activation. Mechanistically, RIL suppresses Src activation through interacting with Src and PTPL1, allowing PTPL1-dependent dephosphorylation of Src at the activation loop. Importantly, the binding of RIL to Src is drastically reduced upon Src inactivation. Our results reveal a novel Src inactivation cycle in which RIL preferentially recognizes active Src and facilitates PTPL1-mediated inactivation of Src. Inactivation of Src, in turn, promotes dissociation of RIL from Src, allowing the initiation of a new Src inactivation cycle. Epigenetic silencing of RIL breaks this Src inactivation cycle and thereby contributes to aberrant Src activation in human cancers.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.