ArticleGenes & development1998
Oncogenic Abl and Src tyrosine kinases elicit the ubiquitin-dependent degradation of target proteins through a Ras-independent pathway.
Article in Genes & development, 1998. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 41 papers.
What it found
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Who cites it
41 citing papers in PubMed, 113 citations in OpenAlex.
- Adaptor protein Abelson interactor 1 in homeostasis and disease.Cell communication and signaling : CCS · 2024Review
- PIM1 phosphorylates ABI2 to enhance actin dynamics and promote tumor invasion.The Journal of cell biology · 2023Article
- CRISPR/CAS9-mediated knockout of Abi1 inhibits p185Journal of hematology & oncology · 2020Article
- The physiological role of Wnt pathway in normal development and cancer.Experimental biology and medicine (Maywood, N.J.) · 2020Review
- Review
- Low expression of Abelson interactor-1 is linked to acquired drug resistance in Bcr-Abl-induced leukemia.Leukemia · 2014Article
- Article
- BRK targets Dok1 for ubiquitin-mediated proteasomal degradation to promote cell proliferation and migration.PloS one · 2014Article
- Phosphoregulation of the WAVE regulatory complex and signal integration.Seminars in cell & developmental biology · 2013Review
- CDK1-mediated phosphorylation of Abi1 attenuates Bcr-Abl-induced F-actin assembly and tyrosine phosphorylation of WAVE complex during mitosis.The Journal of biological chemistry · 2011Article
- SH2-containing inositol 5'-phosphatase inhibits transformation of Abelson murine leukemia virus.Journal of virology · 2011Article
- Pilot study of bortezomib for patients with imatinib-refractory chronic myeloid leukemia in chronic or accelerated phase.Clinical lymphoma, myeloma & leukemia · 2011Article
- Oncogenic tyrosine kinases target Dok-1 for ubiquitin-mediated proteasomal degradation to promote cell transformation.Molecular and cellular biology · 2011Article
- Downregulation of ABI1 expression affects the progression and prognosis of human gastric carcinoma.Medical oncology (Northwood, London, England) · 2010Article
- Abl interactor 1 regulates Src-Id1-matrix metalloproteinase 9 axis and is required for invadopodia formation, extracellular matrix degradation and tumor growth of human breast cancer cells.Carcinogenesis · 2009Article
- Degradation of activated protein kinases by ubiquitination.Annual review of biochemistry · 2009Review
- Abi1 gene silencing by short hairpin RNA impairs Bcr-Abl-induced cell adhesion and migration in vitro and leukemogenesis in vivo.Carcinogenesis · 2008Article
- Abi-1 forms an epidermal growth factor-inducible complex with Cbl: role in receptor endocytosis.Cellular signalling · 2007Article
- Bcr-Abl induces abnormal cytoskeleton remodeling, beta1 integrin clustering and increased cell adhesion to fibronectin through the Abl interactor 1 pathway.Journal of cell science · 2007Article
- Molecular signature of CD34(+) hematopoietic stem and progenitor cells of patients with CML in chronic phase.Leukemia · 2007Article
Corrections and comments
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Authors and funding
7 authors at 2 institutions in 1 country.
Funding
Abstract
Oncogenic forms of the Abl and Src tyrosine kinases trigger the destruction of the Abi proteins, a family of Abl-interacting proteins that antagonize the oncogenic potential of Abl after overexpression in fibroblasts. The destruction of the Abi proteins requires tyrosine kinase activity and is dependent on the ubiquitin-proteasome pathway. We show that degradation of the Abi proteins occurs through a Ras-independent pathway. Significantly, expression of the Abi proteins is lost in cell lines and bone marrow cells isolated from patients with aggressive Bcr-Abl-positive leukemias. These findings suggest that loss of Abi proteins may be a component in the progression of Bcr-Abl-positive leukemias and identify a novel pathway linking activated nonreceptor protein tyrosine kinases to the destruction of specific target proteins through the ubiquitin-proteasome pathway.
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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.