ReviewBiochemical Society transactions2016
Regulatory mechanisms of phosphatase of regenerating liver (PRL)-3.
Review in Biochemical Society transactions, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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
16 citing papers in PubMed.
- Targeting PTP4A3 with KVX-053 mitigates alcohol-amplified SARS-CoV-2 spike protein-induced acute lung injury.Frontiers in pharmacology · 2026Article
- PRL-3 as a metastasis-associated phosphatase in colorectal cancer: Mechanisms and therapeutic strategies.Clinical & experimental metastasis · 2025Review
- Targeting of PTP4A3 overexpression sensitises HGSOC cells towards chemotherapeutic drugs.Molecular oncology · 2025Article
- Article
- HSC70 mediated autophagic degradation of oxidized PRL2 is responsible for osteoclastogenesis and inflammatory bone destruction.Cell death and differentiation · 2023Article
- Article
- The Tyrosine Phosphatase PRL Regulates Attachment of Toxoplasma gondii to Host Cells and Is Essential for Virulence.mSphere · 2022Article
- The phosphatase PRL-3 affects intestinal homeostasis by altering the crypt cell composition.Journal of molecular medicine (Berlin, Germany) · 2021Article
- PRL3 pseudophosphatase activity is necessary and sufficient to promote metastatic growth.The Journal of biological chemistry · 2020Article
- Fast Diffusion Sustains Plasma Membrane Accumulation of Phosphatase of Regenerating Liver-1.Frontiers in cell and developmental biology · 2020Article
- Targeting phosphatases of regenerating liver (PRLs) in cancer.Pharmacology & therapeutics · 2018Review
- Review
- A loss-of-function genetic screening reveals synergistic targeting of AKT/mTOR and WTN/β-catenin pathways for treatment of AML with high PRL-3 phosphatase.Journal of hematology & oncology · 2018Article
- Targeting ovarian cancer and endothelium with an allosteric PTP4A3 phosphatase inhibitor.Oncotarget · 2018Article
- Covalent inhibition of protein tyrosine phosphatases.Molecular bioSystems · 2017Review
- Article
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.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The phosphatase of regenerating liver (PRL)-3 is overexpressed in many human cancer types and tumor metastases when compared with healthy tissues. Different pathways and mechanisms have been suggested to modulate PRL-3 expression levels and activity, giving some valuable insights but still leaving an incomplete picture. Investigating these mechanisms could provide new targets for therapeutic drug development. Here, we present an updated overview and summarize recent findings concerning the different PRL-3 expression regulatory mechanisms and posttranslational modifications suggested to modulate the activity, localization, or stability of this phosphatase.
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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.