ArticleMolecular and cellular biology1998
Direct interaction of Jak1 and v-Abl is required for v-Abl-induced activation of STATs and proliferation.
Article in Molecular and cellular biology, 1998. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 34 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
34 citing papers in PubMed, 64 citations in OpenAlex.
- Pathological Mechanisms Involved in HIV-Associated Lymphomagenesis: Novel Targeted Therapeutic Approaches.Cells · 2025Review
- B-cell clonogenic activity of HIV-1 p17 variants is driven by PAR1-mediated EGF transactivation.Cancer gene therapy · 2021Article
- The tyrosine kinase c-Abl potentiates interferon-mediated antiviral immunity by STAT1 phosphorylation.iScience · 2021Article
- Role of the JAK/STAT Pathway in Cervical Cancer: Its Relationship with HPV E6/E7 Oncoproteins.Cells · 2020Review
- The role of Tyk2 in regulation of breast cancer growth.Journal of interferon & cytokine research : the official journal of the International Society for Interferon and Cytokine Research · 2011Article
- Jak/STAT pathways in cytokine signaling and myeloproliferative disorders: approaches for targeted therapies.Genes & cancer · 2010Article
- Aggressive breast cancer cells are dependent on activated Abl kinases for proliferation, anchorage-independent growth and survival.Oncogene · 2008Article
- Hematopoietic cytokine receptor signaling.Oncogene · 2007Review
- Article
- TYK2 is a key regulator of the surveillance of B lymphoid tumors.The Journal of clinical investigation · 2004Article
- The extreme carboxyl terminus of v-Abl is required for lymphoid cell transformation by Abelson virus.Journal of virology · 2003Article
- Review
- Jak2 is involved in c-Myc induction by Bcr-Abl.Oncogene · 2002Article
- NF-kappaB1 can inhibit v-Abl-induced lymphoid transformation by functioning as a negative regulator of cyclin D1 expression.Molecular and cellular biology · 2002Article
- The tumor suppressor activity of SOCS-1.Oncogene · 2002Article
- JAKs, STATs and Src kinases in hematopoiesis.Oncogene · 2002Review
- Pim serine/threonine kinases regulate the stability of Socs-1 protein.Proceedings of the National Academy of Sciences of the United States of America · 2002Article
- Article
- Inhibition of v-Abl transformation in 3T3 cells overexpressing different forms of the Abelson interactor protein Abi-1.Oncogene · 2001Article
- Molecular biology of chronic myeloid leukemia.International journal of hematology · 2001Review
Corrections and comments
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Authors and funding
9 authors at 3 institutions in 3 countries.
Funding
Abstract
In Abelson murine leukemia virus (A-MuLV)-transformed cells, members of the Janus kinase (Jak) family of non-receptor tyrosine kinases and the signal transducers and activators of transcription (STAT) family of signaling proteins are constitutively activated. In these cells, the v-Abl oncoprotein and the Jak proteins physically associate. To define the molecular mechanism of constitutive Jak-STAT signaling in these cells, the functional significance of the v-Abl-Jak association was examined. Mapping the Jak1 interaction domain in v-Abl demonstrates that amino acids 858 to 1080 within the carboxyl-terminal region of v-Abl bind Jak1 through a direct interaction. A mutant of v-Abl lacking this region exhibits a significant defect in Jak1 binding in vivo, fails to activate Jak1 and STAT proteins, and does not support either the proliferation or the survival of BAF/3 cells in the absence of cytokine. Cells expressing this v-Abl mutant show extended latency and decreased frequency in generating tumors in nude mice. In addition, inducible expression of a kinase-inactive mutant of Jak1 protein inhibits the ability of v-Abl to activate STATs and to induce cytokine-independent proliferation, indicating that an active Jak1 is required for these v-Abl-induced signaling pathways in vivo. We propose that Jak1 is a mediator of v-Abl-induced STAT activation and v-Abl induced proliferation in BAF/3 cells, and may be important for efficient transformation of immature B cells by the v-abl oncogene.
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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.