ArticleThe Journal of experimental medicine2003
Bruton's tyrosine kinase cooperates with the B cell linker protein SLP-65 as a tumor suppressor in Pre-B cells.
Article in The Journal of experimental medicine, 2003. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 42 papers.
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Who cites it
42 citing papers in PubMed, 112 citations in OpenAlex.
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- Enzyme Is the Name-Adapter Is the Game.Cells · 2024Review
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- Niche-expressed Galectin-1 is involved in pre-B acute lymphoblastic leukemia relapse through pre-B cell receptor activation.iScience · 2023Article
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- Current Perspectives: Evidence to Date on BTK Inhibitors in the Management of Multiple Sclerosis.Drug design, development and therapy · 2022Review
- Kinomics platform using GBM tissue identifies BTK as being associated with higher patient survival.Life science alliance · 2021Article
- Deciphering intratumoral heterogeneity using integrated clonal tracking and single-cell transcriptome analyses.Nature communications · 2021Article
- Developmental partitioning of SYK and ZAP70 prevents autoimmunity and cancer.Molecular cell · 2021Article
- Functional Antibody Responses Following Allogeneic Stem Cell Transplantation forFrontiers in immunology · 2019Article
- Role of Bruton's tyrosine kinase in B cells and malignancies.Molecular cancer · 2018Review
- Autoimmunity checkpoints as therapeutic targets in B cell malignancies.Nature reviews. Cancer · 2018Review
- BTK modulates p73 activity to induce apoptosis independently of p53.Cell death discovery · 2018Article
- BTK blocks the inhibitory effects of MDM2 on p53 activity.Oncotarget · 2017Article
- Review
- Review
- Rationale for targeting the pre-B-cell receptor signaling pathway in acute lymphoblastic leukemia.Blood · 2015Review
- Are patients with X-linked agammaglobulinemia at increased risk of developing acute lymphoblastic leukemia?Journal of clinical immunology · 2015Article
- Bruton's tyrosine kinase: from X-linked agammaglobulinemia toward targeted therapy for B-cell malignancies.Journal of clinical oncology : official journal of the American Society of Clinical Oncology · 2014Article
Corrections and comments
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Authors and funding
7 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Expression of the pre-B cell receptor (pre-BCR) leads to activation of the adaptor molecule SLP-65 and the cytoplasmic kinase Btk. Mice deficient for one of these signaling proteins have an incomplete block in B cell development at the stage of large cycling pre-BCR+CD43+ pre-B cells. Our recent findings of defective SLP-65 expression in approximately 50% of childhood pre-B acute lymphoblastic leukemias and spontaneous pre-B cell lymphoma development in SLP-65-/- mice demonstrate that SLP-65 acts as a tumor suppressor. To investigate cooperation between Btk and SLP-65, we characterized the pre-B cell compartment in single and double mutant mice, and found that the two proteins have a synergistic role in the developmental progression of large cycling into small resting pre-B cells. We show that Btk/SLP-65 double mutant mice have a dramatically increased pre-B cell tumor incidence ( approximately 75% at 16 wk of age), as compared with SLP-65 single deficient mice (<10%). These findings demonstrate that Btk cooperates with SLP-65 as a tumor suppressor in pre-B cells. Furthermore, transgenic low-level expression of a constitutive active form of Btk, the E41K-Y223F mutant, prevented tumor formation in Btk/SLP-65 double mutant mice, indicating that constitutive active Btk can substitute for SLP-65 as a tumor suppressor.
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