ArticleOncogene2007
Recruitment of insulin receptor substrate-1 and activation of NF-kappaB essential for midkine growth signaling through anaplastic lymphoma kinase.
Article in Oncogene, 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 37 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.
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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
37 citing papers in PubMed, 63 citations in OpenAlex.
- Three decades of anaplastic lymphoma kinase: from physiological roles to cancer and immune evasion.Cancer metastasis reviews · 2026Review
- Significance of Midkine Signaling in Women's Cancers: Novel Biomarker and Therapeutic Target.International journal of molecular sciences · 2025Review
- Association between autoimmune disease and neurodevelopmental disorder: a Mendelian randomization analysis.Italian journal of pediatrics · 2025Article
- Article
- Population pharmacokinetics and exposure-response analyses of SAF-189s in Chinese patients with ALK+/ROS1+ non-small cell lung cancer.Frontiers in pharmacology · 2024Article
- The role of midkine in health and disease.Frontiers in immunology · 2023Review
- Obesity and Risk for Lymphoma: Possible Role of Leptin.International journal of molecular sciences · 2022Review
- The PI3K/AKT signaling pathway: How does it regulate development of Sertoli cells and spermatogenic cells?Histology and histopathology · 2022Review
- Midkine promotes breast cancer cell proliferation and migration by upregulating NR3C1 expression and activating the NF-κB pathway.Molecular biology reports · 2022Article
- Midkine-A novel player in cardiovascular diseases.Frontiers in cardiovascular medicine · 2022Review
- Defining Pathological Activities of ALK in Neuroblastoma, a Neural Crest-Derived Cancer.International journal of molecular sciences · 2021Review
- Aberrant role of ALK in tau proteinopathy through autophagosomal dysregulation.Molecular psychiatry · 2021Article
- Cystic Fibrosis-Related Diabetes (CFRD): Overview of Associated Genetic Factors.Diagnostics (Basel, Switzerland) · 2021Review
- Pulmonary midkine inhibition ameliorates sepsis induced lung injury.Journal of translational medicine · 2021Article
- Midkine: The Who, What, Where, and When of a Promising Neurotrophic Therapy for Perinatal Brain Injury.Frontiers in neurology · 2020Review
- Dual inhibition of IGF-IR and ALK as an effective strategy to eradicate NPM-ALKJournal of hematology & oncology · 2019Article
- Exome-wide search and functional annotation of genes associated in patients with severe tick-borne encephalitis in a Russian population.BMC medical genomics · 2019Article
- Insulin Receptor Substrate-1 (IRS-1) and IRS-2 expression levels are associated with prognosis in non-small cell lung cancer (NSCLC).PloS one · 2019Article
- Integrated proximal proteomics reveals IRS2 as a determinant of cell survival in ALK-driven neuroblastoma.Science signaling · 2018Article
- Spotlight on the treatment ofLung cancer management · 2017Article
Corrections and comments
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Authors and funding
4 authors at 2 institutions in 1 country.
Funding
Abstract
Anaplastic lymphoma kinase (ALK) is a transmembrane receptor tyrosine kinase in the insulin receptor superfamily. We recently demonstrated that the growth factors pleiotrophin (PTN) and midkine (MK) are ligands for ALK and that upon ALK activation, insulin receptor substrate-1 (IRS-1) and other substrates are phosphorylated. Here, the role of IRS-1 in ligand-mediated ALK signaling is investigated in interleukin-3 (IL-3)-dependent 32D murine myeloid cells. These cells do not express ALK and IRS family members, and do not respond to exogenously added PTN or MK. We show that expression of ALK plus IRS-1 renders these cells independent of IL-3 owing to the activation of ALK by endogenous MK. Mutational analysis reveals that this transformed phenotype of 32D cells requires kinase-active ALK as well as the interaction of ALK with IRS-1. Furthermore, 32D/IRS-1/ALK cells display an enhanced activation of mitogen-activated protein kinase and PI3-kinase pathways, and a selective transcriptional activation of nuclear factor (NF)-kappaB. Small interfering RNA-mediated knockdown of the endogenous MK or p65/NF-kappaB revealed that both these are rate limiting for the transformed phenotype induced by ALK plus IRS-1. We conclude that the recruitment of IRS-1 to activated ALK and the activation of NF-kappaB are essential for the autocrine growth and survival signaling of MK.
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What OpenQuestion holds
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.