ArticleOncogene2000
p95(vav) associates with the type I interferon (IFN) receptor and contributes to the antiproliferative effect of IFN-alpha in megakaryocytic cell lines.
Article in Oncogene, 2000. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 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
9 citing papers in PubMed, 26 citations in OpenAlex.
- Differential Regulation of Type I and Type III Interferon Signaling.International journal of molecular sciences · 2019Review
- IFNs-signaling effects on lung cancer: an up-to-date pathways-specific review.Clinical and experimental medicine · 2017Review
- CD25 and CD69 induction by α4β1 outside-in signalling requires TCR early signalling complex proteins.The Biochemical journal · 2013Article
- Filamin B serves as a molecular scaffold for type I interferon-induced c-Jun NH2-terminal kinase signaling pathway.Molecular biology of the cell · 2008Article
- Mechanisms of type-I- and type-II-interferon-mediated signalling.Nature reviews. Immunology · 2005Review
- Altered transcription of the stem cell leukemia gene in myelofibrosis with myeloid metaplasia.Leukemia · 2003Article
- The therapy of myelofibrosis: targeting pathogenesis.International journal of hematology · 2002Review
- Clinical and scientific advances in the Philadelphia-chromosome negative chronic myeloproliferative disorders.International journal of hematology · 2002Review
- IFN-zeta/ limitin: a member of type I IFN with mild lympho-myelosuppression.Journal of cellular and molecular medicineReview
Corrections and comments
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Authors and funding
4 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The vav proto-oncogene product is a 95 kDa protein predominantly expressed in hematopoietic cells. Vav presents a wide range of functional domains, including structural domains known to be involved in signal transduction. Triggering of various cytokine receptors among which type I interferon receptor induces a rapid and transient tyrosine phosphorylation of p95(vav). Nevertheless, the biological functions of p95(vav) are still unclear. This report is the first documentation on the physical association of p95(vav) with both alpha and beta type I interferon receptor chains, as demonstrated by co-immunoprecipitation and Western blot analysis in megakaryocytic cells (Dami and UT7). This interaction is increased by interferon-alpha/beta stimulation. Moreover, p95(vav) phosphorylated subsequently to type I interferon treatment, is translocated in the nucleus; a concomitant increase of its association with the regulatory subunit of the nuclear DNA-dependent protein kinase, KU-70 is observed in the nucleus. To determine whether p95(vav) participates in the biological response to type I interferons, we studied the effects of non modified Vav oligodeoxynucleotides on the antiproliferative effect of interferon-alpha on megakaryocytic cells. By this oligodeoxynucleotide strategy, we show that p95(vav) contributes greatly to the cell proliferation inhibition induced by type I IFN.
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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.