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GENE:

RPS16 (Ribosomal Protein S16)

i
Other names: RPS16, Ribosomal Protein S16, 40S Ribosomal Protein S16, S16, Small Ribosomal Subunit Protein US9
Associations
Trials
1m
MRPS16 Regulates NFATC2 Through the Wnt/β-Catenin Pathway to Promote Glioma Proliferation. (PubMed, J Cell Mol Med)
The Wnt/β-Catenin/NFATC2 pathway plays a role in promoting glioma cell proliferation by MRPS16, which is shown in our experimental data. Inhibition of MRPS16 may be a promising and effective treatment option for gliomas.
Journal
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RPS16 (Ribosomal Protein S16)
3ms
CircEPHB4 binds to YBX1 to upregulate MRPS16 and promotes glioma progression. (PubMed, Cell Mol Life Sci)
circEPHB4 bound to YBX1 to inhibit RBBP6-mediated degradation and increase its expression, thus enhancing MRPS16 mRNA stability via m5C modification, and ultimately promoting glioma progression.
Journal
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YBX1 (Y-Box Binding Protein 1) • RPS16 (Ribosomal Protein S16)
8ms
FTO inhibition represses B-cell acute lymphoblastic leukemia progression by inducing nucleolar stress and mitochondrial dysfunction. (PubMed, Free Radic Biol Med)
Furthermore, we found that the FTO inhibitor FB23-2 combined with Doxorubicin markedly repressed B-ALL progression in vivo, accompanied by nucleolar stress-like changes and mitochondrial dysfunction. In summary, our data suggest that FTO is a critical RNA epigenetic promotor of B-ALL, and targeted FTO blockade synergizing with Doxorubicin could be a potential therapy for B-ALL, likely by inhibiting cytoplasmic and mitochondrial ribosome biogenesis.
Journal
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FTO (Alpha-Ketoglutarate-Dependent Dioxygenase FTO) • RPS16 (Ribosomal Protein S16) • YTHDF2 (YTH N6-Methyladenosine RNA Binding Protein 2)
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doxorubicin hydrochloride
almost2years
MRPS16 promotes lung adenocarcinoma growth via the PI3K/AKT/Frataxin signalling axis. (PubMed, J Cell Mol Med)
Moreover, MRPS16-knockdown-mediated Frataxin overexpression was shown to restore the reduction in tumour cells proliferation, migration and invasion. Our results revealed that MRPS16 caused an aggressive phenotype to LAUD and was a poor prognosticator; thus, targeting MRPS16 may be effectual in LAUD treatment.
Journal
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RPS16 (Ribosomal Protein S16)
over2years
Potential prognostic biomarkers of hepatocellular carcinoma based on 4D label-free quantitative proteomics analysis pilot investigation. (PubMed, Int J Biol Markers)
These data suggest that RPL27 and TARS2 play an important role in hepatocellular carcinoma progression and may be potential prognostic biomarkers of overall survival in hepatocellular carcinoma patients.
Journal
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RPS16 (Ribosomal Protein S16) • RPL27A (Ribosomal Protein L27a)
over2years
Establishment of a primary renal lymphoma model and its clinical relevance. (PubMed, Front Oncol)
These findings suggested that the MA-K cell line had strong clinical relevance with human aggressive B-cell lymphoma. Moreover, the MA-K primary renal lymphoma model, as a novel syngenetic mouse model, will be greatly useful for both basic research on lymphoma dissemination and preclinical efficacy evaluation of chemotherapy and immunotherapy.
Journal • IO biomarker
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CDKN2A (Cyclin Dependent Kinase Inhibitor 2A) • MYD88 (MYD88 Innate Immune Signal Transduction Adaptor) • CD52 (CD52 Molecule) • RPS16 (Ribosomal Protein S16)
almost3years
Hyper-expression of GFP-fused active hFGF21 in tobacco chloroplasts. (PubMed, Protein Expr Purif)
GFP-hFGF21 promoted the proliferation of hepatoma cell line HepG2, inducing the expression of glucose transporter 1 in hepatoma HepG2 cells and improving glucose uptake. These results suggested that a chloroplast expression is a promising approach for the production of bioactive recombinant hFGF21.
Journal
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FGF21 (Fibroblast Growth Factor 21) • RPS16 (Ribosomal Protein S16) • TRPS1 (Transcriptional Repressor GATA Binding 1)
almost3years
DNA methylation and mutation spectrum among pediatric acute lymphoblastic leukemia patients by Hispanic/Latinx ethnicity (AACR 2023)
Few of the candidate genes observed in HSP (ITPA, MBP, PPP4R12, and SPOCK3) have been previously implicated in leukemia. The findings suggest that the methylation signatures and mutation spectrum for HSP and NHW pediatric acute ALL patients might differ and further studies among HSP, a group with the highest prevalence of acute pediatric ALL, could potentially identify new genetic and epigenetic markers for acute pediatric ALL.
Clinical • Epigenetic controller
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KRAS (KRAS proto-oncogene GTPase) • FLT3 (Fms-related tyrosine kinase 3) • NRAS (Neuroblastoma RAS viral oncogene homolog) • JARID2 (Jumonji And AT-Rich Interaction Domain Containing 2) • TMPRSS11E (Transmembrane Serine Protease 11E) • YTHDC1 (YTH Domain Containing 1) • GSTT1 (Glutathione S-transferase theta 1) • HTRA1 (HtrA Serine Peptidase 1) • ITPA (Inosine Triphosphatase) • RPS16 (Ribosomal Protein S16) • TEX26 (Testis Expressed 26) • ZFP36 (ZFP36 Ring Finger Protein)
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NRAS mutation