ArticleJournal of hematology & oncology2015
Alteration of gene expression profile following PPP2R5C knockdown may be associated with proliferation suppression and increased apoptosis of K562 cells.
Article in Journal of hematology & oncology, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 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.
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Who cites it
4 citing papers in PubMed, 6 citations in OpenAlex.
- Integrated Genomic-Metabolomic Analysis for Tri-Categorical Classification of Type 2 Diabetes Status in the Korean Ansan-Ansung Cohort.International journal of molecular sciences · 2025Article
- Analysis of the Association of Two SNPs in the Promoter Regions of theAnimals : an open access journal from MDPI · 2022Article
- Prognostic Impact of PPP2R5C Gene Expression in Adult Acute Myeloid Leukemia Patients with Normal Cytogenetics.Indian journal of hematology & blood transfusion : an official journal of Indian Society of Hematology and Blood Transfusion · 2020Article
- Alteration of gene expression profile in CD3ImmunoTargets and therapy · 2018Article
Corrections and comments
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Authors and funding
10 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
We reported that knockdown of PPP2R5C by siRNA led to proliferation inhibition and apoptosis induction in K562 cells. In this study, we further characterized the gene expression profiles after PPP2R5C suppression by microarray analysis. Genes which participate in the MAPK, PI3K/AKT, and JAK/STAT pathways, were mainly altered in the K562 cells. We propose that the mechanism for proliferation inhibition and increased apoptosis of K562 cells following PPP2R5C suppression may be related to the alteration of expression profiles of BRAF, AKT2, AKT3, NFKB2 and STAT3 genes.
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Registered trials
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