ArticleGenes & cancer2012
Models of crk adaptor proteins in cancer.
Article in Genes & cancer, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 36 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
36 citing papers in PubMed, 52 citations in OpenAlex.
- CRKL but not CRKII contributes to hemin-induced erythroid differentiation of CML.Journal of cellular and molecular medicine · 2024Article
- Article
- Silencing of the CrkL gene reverses the doxorubicin resistance of K562/ADR cells through regulating PI3K/Akt/MRP1 signaling.Journal of clinical laboratory analysis · 2021Article
- Epigenetic Silencing of MicroRNA-126 Promotes Cell Growth in Marek's Disease.Microorganisms · 2021Article
- Review
- CRKL promotes hepatocarcinoma through enhancing glucose metabolism of cancer cells via activating PI3K/Akt.Journal of cellular and molecular medicine · 2021Article
- microRNA-132 inhibits the proliferation, migration, and invasion of ovarian cancer cells by regulating CT10 oncogenic gene homolog II-related signaling pathways.Translational cancer research · 2020Article
- miR-124-3p Suppresses the Invasiveness and Metastasis of Hepatocarcinoma CellsFrontiers in molecular biosciences · 2020Article
- Stromal integrin α11 regulates PDGFR-β signaling and promotes breast cancer progression.The Journal of clinical investigation · 2019Article
- CRKII overexpression promotes theOncology letters · 2019Article
- The Tumor Suppressor SASH1 Interacts With the Signal Adaptor CRKL to Inhibit Epithelial-Mesenchymal Transition and Metastasis in Colorectal Cancer.Cellular and molecular gastroenterology and hepatology · 2019Article
- Secretome profiling of PC3/nKR cells, a novel highly migrating prostate cancer subline derived from PC3 cells.PloS one · 2019Article
- Article
- Structure-guided design of a potent peptide inhibitor targeting the interaction between CRK and ABL kinase.MedChemComm · 2018Article
- CRKL Mediates p110β-Dependent PI3K Signaling in PTEN-Deficient Cancer Cells.Cell reports · 2017Article
- Fibroblast Growth Requires CT10 Regulator of Kinase (Crk) and Crk-like (CrkL).The Journal of biological chemistry · 2016Article
- Abelson kinase acts as a robust, multifunctional scaffold in regulating embryonic morphogenesis.Molecular biology of the cell · 2016Article
- Up-Regulation of Oligodendrocyte Lineage Markers in the Cerebellum of Autistic Patients: Evidence from Network Analysis of Gene Expression.Molecular neurobiology · 2016Article
- MicroRNAs mediated regulation of MAPK signaling pathways in chronic myeloid leukemia.Oncotarget · 2016Review
- Cyclophilin A promotes cell migration via the Abl-Crk signaling pathway.Nature chemical biology · 2016Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
2 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The Crk family of adaptor proteins (CrkI, CrkII, and CrkL), originally discovered as the oncogene fusion product, v-Crk, of the CT10 chicken retrovirus, lacks catalytic activity but engages with multiple signaling pathways through their SH2 and SH3 domains. Crk proteins link upstream tyrosine kinase and integrin-dependent signals to downstream effectors, acting as adaptors in diverse signaling pathways and cellular processes. Crk proteins are now recognized to play a role in the malignancy of many human cancers, stimulating renewed interest in their mechanism of action in cancer progression. The contribution of Crk signaling to malignancy has been predominantly studied in fibroblasts and in hematopoietic models and more recently in epithelial models. A mechanistic understanding of Crk proteins in cancer progression in vivo is still poorly understood in part due to the highly pleiotropic nature of Crk signaling. Recent advances in the structural organization of Crk domains, new roles in kinase regulation, and increased knowledge of the mechanisms and frequency of Crk overexpression in human cancers have provided an incentive for further study in in vivo models. An understanding of the mechanisms through which Crk proteins act as oncogenic drivers could have important implications in therapeutic targeting.
Indexed as
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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 Socratic graph.