ArticleThe Journal of biological chemistry2015
Protein-tyrosine Phosphatase and Kinase Specificity in Regulation of SRC and Breast Tumor Kinase.
Article in The Journal of biological chemistry, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers.
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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
28 citing papers in PubMed, 40 citations in OpenAlex.
- CCR4-NOT Transcription Complex Subunit 7 (CNOT7) Protein and Leukocyte-Associated Immunoglobulin-like Receptor-1 in Breast Cancer Progression: Clinical Mechanistic Insights and In Silico Therapeutic Potential.International journal of molecular sciences · 2025Article
- Targeting Shp2 as a therapeutic strategy for neurodegenerative diseases.Translational psychiatry · 2025Review
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- Combination Approaches to Target PD-1 Signaling in Cancer.Frontiers in immunology · 2022Review
- Protein Tyrosine Phosphatase Receptor Type R (PTPRR) Reduces AChR Clustering by Dephosphorylating MuSK.Disease markers · 2022Article
- The possible role of SRMS in colorectal cancer by bioinformatics analysis.World journal of surgical oncology · 2021Article
- TRAF3 in T Cells Restrains Negative Regulators of LAT to Promote TCR/CD28 Signaling.Journal of immunology (Baltimore, Md. : 1950) · 2021Article
- The nonreceptor tyrosine kinase SRMS inhibits autophagy and promotes tumor growth by phosphorylating the scaffolding protein FKBP51.PLoS biology · 2021Article
- A functional variant on 20q13.33 related to glioma risk alters enhancer activity and modulates expression of multiple genes.Human mutation · 2021Article
- Protein Tyrosine Phosphatases: A new paradigm in an old signaling system?Advances in cancer research · 2021Review
- Targeting protein tyrosine kinase 6 in cancer.Biochimica et biophysica acta. Reviews on cancer · 2020Review
- Structure, Function, and Regulation of the SRMS Tyrosine Kinase.International journal of molecular sciences · 2020Review
- Nuclear Functions of the Tyrosine Kinase Src.International journal of molecular sciences · 2020Review
- Study on the Antibreast Cancer Mechanism and Bioactive Components ofEvidence-based complementary and alternative medicine : eCAM · 2020Article
- Protein tyrosine kinase 6 signaling in prostate cancer.American journal of clinical and experimental urology · 2020Review
- Spatial regulation of signaling by the coordinated action of the protein tyrosine kinases MET and FER.Cellular signalling · 2018Article
- Palbociclib resistance confers dependence on an FGFR-MAP kinase-mTOR-driven pathway inOncotarget · 2018Article
- Phosphoproteomics Analysis Identifies Novel Candidate Substrates of the Nonreceptor Tyrosine Kinase,Molecular & cellular proteomics : MCP · 2018Article
Corrections and comments
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Authors and funding
5 authors at 2 institutions in 1 country.
Funding
Abstract
Despite significant evidence to the contrary, the view that phosphatases are "nonspecific" still pervades the field. Systems biology approaches to defining how signal transduction pathways are integrated at the level of whole organisms also often downplay the contribution of phosphatases, defining them as "erasers" that serve merely to restore the system to its basal state. Here, we present a study that counteracts the idea of "nonspecific phosphatases." We have characterized two structurally similar and functionally related kinases, BRK and SRC, which are regulated by combinations of activating autophosphorylation and inhibitory C-terminal sites of tyrosine phosphorylation. We demonstrated specificity at the level of the kinases in that SRMS phosphorylated the C terminus of BRK, but not SRC; in contrast, CSK is the kinase responsible for C-terminal phosphorylation of SRC, but not BRK. For the phosphatases, we observed that RNAi-mediated suppression of PTP1B resulted in opposing effects on the activity of BRK and SRC and have defined the mechanisms underlying this specificity. PTP1B inhibited BRK by directly dephosphorylating the Tyr-342 autophosphorylation site. In contrast, PTP1B potentiated SRC activity, but not by dephosphorylating SRC itself directly; instead, PTP1B regulated the interaction between CBP/PAG and CSK. SRC associated with, and phosphorylated, the transmembrane protein CBP/PAG at Tyr-317, resulting in CSK recruitment. We identified PAG as a substrate of PTP1B, and dephosphorylation abolished recruitment of the inhibitory kinase CSK. Overall, these findings illustrate how the combinatorial effects of PTKs and PTPs may be integrated to regulate signaling, with both classes of enzymes displaying exquisite specificity.
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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.