ArticleLeukemia2011
Low expression of PP2A regulatory subunit B55α is associated with T308 phosphorylation of AKT and shorter complete remission duration in acute myeloid leukemia patients.
Article in Leukemia, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 54 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
54 citing papers in PubMed, 81 citations in OpenAlex.
- CUE domain-containing 2 promotes diffuse large B-cell lymphoma progression via PP2A-B55β degradation and shapes macrophage-mediated immune responses.Molecular biomedicine · 2026Article
- PP2A phosphatase regulates Hippo signalling in dual manner.The EMBO journal · 2026Article
- Caloric restriction reprograms skeletal muscle molecular pathways in non-human primates: potential relevance to human aging biology.Skeletal muscle · 2026Article
- DMH1 improves palmitic acid-Induced insulin resistance in cardiomyocytes via PP2A inhibition and AKT/AMPK signaling activation.Scientific reports · 2026Article
- Targeting the UFL1-AKT cascade suppresses triple-negative breast cancer progression.Nature communications · 2026Article
- Phosphatase PP2A promotes RTA dephosphorylation to impair KSHV lytic replication.PLoS pathogens · 2025Article
- Targeting PP2A in cancer: an underrated option.Journal of experimental & clinical cancer research : CR · 2025Review
- Galectin-3 Release in the Bone Marrow Microenvironment Promotes Drug Resistance and Relapse in Acute Myeloid Leukemia.Life (Basel, Switzerland) · 2025Review
- Microcystin-LR activates serine/threonine kinases and alters the phosphoproteome in human HepaRG cells.Toxicon : official journal of the International Society on Toxinology · 2024Article
- Phosphorylation of PP2Ac by PKC is a key regulatory step in the PP2A-switch-dependent AKT dephosphorylation that leads to apoptosis.Cell communication and signaling : CCS · 2024Article
- miR-142: A Master Regulator in Hematological Malignancies and Therapeutic Opportunities.Cells · 2023Review
- JNK Cascade-Induced Apoptosis-A Unique Role in GqPCR Signaling.International journal of molecular sciences · 2023Review
- Review
- Article
- GqPCR-stimulated dephosphorylation of AKT is induced by an IGBP1-mediated PP2A switch.Cell communication and signaling : CCS · 2022Article
- Research progress on the relationship between the TOR signaling pathway regulator, epigenetics, and tumor development.Frontiers in genetics · 2022Review
- Review
- Reverse phase protein arrays in acute leukemia: investigative and methodological challenges.Expert review of proteomics · 2021Review
- PP2A-B55 Holoenzyme Regulation and Cancer.Biomolecules · 2020Review
- A Genome-Wide Pooled shRNA Screen Identifies PPP2R2A as a Predictive Biomarker for the Response to ATR and CHK1 Inhibitors.Cancer research · 2020Article
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 1 institution in 1 country.
Funding
Abstract
The regulation of protein kinase B (AKT) is a dynamic process that depends on the balance between phosphorylation by upstream kinases for activation and inactivation by dephosphorylation by protein phosphatases. Phosphorylated AKT is commonly found in acute myeloid leukemia (AML) and confers an unfavorable prognosis. Understanding the relative importance of upstream kinases and AKT phosphatase in the activation of AKT is relevant for the therapeutic targeting of this signaling axis in AML. The B55α subunit of protein phosphatase 2A (PP2A) has been implicated in AKT dephosphorylation, but its role in regulating AKT in AML is unknown. We examined B55α protein expression in blast cells derived from 511 AML patients using reverse phase protein analysis. B55α protein expression was lower in AML cells compared with normal CD34+ cells. B55α protein levels negatively correlated with threonine 308 phosphorylation levels. Low levels of B55α were associated with shorter complete remission duration, demonstrating that decreased expression is an adverse prognostic factor in AML. These findings suggest that decreased B55α expression in AML is at least partially responsible for increased AKT signaling in AML and suggests that therapeutic targeting of PP2A could counteract this.
Indexed as
Identifiers
What OpenQuestion 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 OpenQuestion graph.