ArticleCancer research2010
A specific need for CRKL in p210BCR-ABL-induced transformation of mouse hematopoietic progenitors.
Article in Cancer research, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
24 citing papers in PubMed, 44 citations in OpenAlex.
- Advancements and Future Prospects in Molecular Targeted and siRNA Therapies for Chronic Myeloid Leukemia.Biomolecules · 2024Review
- Article
- circCRKL, a circRNA derived from CRKL, regulates BCR-ABL via sponging miR-877-5p to promote chronic myeloid leukemia cell proliferation.Journal of translational medicine · 2022Article
- Response and Resistance to BCR-ABL1-Targeted Therapies.Cancer cell · 2020Review
- The Crk adapter protein is essential forMolecular biology of the cell · 2019Article
- IL-7-induced phosphorylation of the adaptor Crk-like and other targets.Cellular signalling · 2018Article
- Structure-guided design of a potent peptide inhibitor targeting the interaction between CRK and ABL kinase.MedChemComm · 2018Article
- The long noncoding RNAThe Journal of biological chemistry · 2017Article
- A pre-metazoan origin of the CRK gene family and co-opted signaling network.Scientific reports · 2016Article
- The chimeric ubiquitin ligase SH2-U-box inhibits the growth of imatinib-sensitive and resistant CML by targeting the native and T315I-mutant BCR-ABL.Scientific reports · 2016Article
- Somatically mutated ABL1 is an actionable and essential NSCLC survival gene.EMBO molecular medicine · 2016Article
- Oncogenic Signaling Adaptor Proteins.Journal of genetics and genomics = Yi chuan xue bao · 2015Review
- Drug target optimization in chronic myeloid leukemia using innovative computational platform.Scientific reports · 2015Article
- Antibody-based detection of protein phosphorylation status to track the efficacy of novel therapies using nanogram protein quantities from stem cells and cell lines.Nature protocols · 2015Article
- The Role of Crk Adaptor Proteins in T-Cell Adhesion and Migration.Frontiers in immunology · 2015Review
- Regulation of the interferon regulatory factor-8 (IRF-8) tumor suppressor gene by the signal transducer and activator of transcription 5 (STAT5) transcription factor in chronic myeloid leukemia.The Journal of biological chemistry · 2014Article
- Article
- Structural biology: CrkL is not Crk-like.Nature chemical biology · 2012Article
- Domain organization differences explain Bcr-Abl's preference for CrkL over CrkII.Nature chemical biology · 2012Article
- Models of crk adaptor proteins in cancer.Genes & cancer · 2012Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
9 authors at 2 institutions in 1 country.
Funding
Abstract
CRKL (CRK-like) is an adapter protein predominantly phosphorylated in cells that express the tyrosine kinase p210(BCR-ABL), the fusion product of a (9;22) chromosomal translocation causative for chronic myeloid leukemia. It has been unclear, however, whether CRKL plays a functional role in p210(BCR-ABL) transformation. Here, we show that CRKL is required for p210(BCR-ABL) to support interleukin-3-independent growth of myeloid progenitor cells and long-term outgrowth of B-lymphoid cells from fetal liver-derived hematopoietic progenitor cells. Furthermore, a synthetic phosphotyrosyl peptide that binds to the CRKL SH2 domain with high affinity blocks association of endogenous CRKL with the p210(BCR-ABL) complex and reduces c-MYC levels in K562 human leukemic cells as well as in mouse hematopoietic cells transformed by p210(BCR-ABL) or the imatinib-resistant mutant T315I. These results indicate that the function of CRKL as an adapter protein is essential for p210(BCR-ABL)-induced transformation.
Indexed as
Identifiers
What Socratic 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 Socratic graph.