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Partial silencing of RPS14 inhibits the proliferation of SKM-1, an acute myeloid leukemia cell line, and RPS14 negatively regulates p53 activation in SKM-1 cells.
RPS14 stabilized and activated p53 by inhibiting HDM2-mediated p53 polyubiquitination and degradation
Patients with nonclassical Diamond Blackfan anemia and other hypoproliferative anemias may have somatically acquired 5q deletions with RPS14 haploinsufficiency
Data indicate that RPS14 negates c-Myc functions by directly inhibiting its transcriptional activity and mediating its mRNA degradation via miRNA.
lower RPS14 predicts prolonged survival and possible response to lenalidomide in lower risk MDS patients.
RPS14 and RPS19 have distinct roles in regulating the MDM2-p53 feedback loop in response to ribosomal stress
Loss of RPS14 is associated with 5q-syndrome.
Combined loss of miR-145 and RPS14 cooperates to alter erythroid-megakaryocytic differentiation in a manner similar to the 5q- syndrome.
Myelodysplactic syndrome patients with an intermediate-1 risk score and low RPS14 expression have a superior median overall survival compared to patients with high RPS14 expression.
p53 accumulates selectively in the erythroid lineage in primary human hematopoietic progenitor cells after expression of shRNAs targeting RPS14, the ribosomal protein gene deleted in the 5q-syndrome, or RPS19.
observations in the patient setting support the importance of RPS14 in the pathogenesis of MDS with del(5q)
Studied the methylation status of the RPS14 gene in 5q deletion (5q21.3q33.1) in 24 patients. In all, 21 of the 37 patients (57%) had copy number alterations. No homozygous losses or amplifications were observed.
results indicate that the 5q- syndrome is caused by a defect in RPS14 ribosomal protein function
low expression of RPS14 is not due to promoter hypermethylation, further supporting the haploinsufficiency model suggested by Ebert et al4 for the 5q- syndrome
Rps14 haploinsufficiency in del(5q) myelodysplastic syndrome is linked to activation of the innate immune system and induction of S100A8-S100A9 expression, leading to a p53-dependent erythroid differentiation defect.
ribosomal protein RPS-14 is able to modulate let-7 function in C. elegans
p53 synthesis is affected in zebrafish tumors with ribosomal protein gene mutations
Ribosomes, the organelles that catalyze protein synthesis, consist of a small 40S subunit and a large 60S subunit. Together these subunits are composed of 4 RNA species and approximately 80 structurally distinct proteins. This gene encodes a ribosomal protein that is a component of the 40S subunit. The protein belongs to the S11P family of ribosomal proteins. It is located in the cytoplasm. Transcript variants utilizing alternative transcription initiation sites have been described in the literature. As is typical for genes encoding ribosomal proteins, there are multiple processed pseudogenes of this gene dispersed through the genome. In Chinese hamster ovary cells, mutations in this gene can lead to resistance to emetine, a protein synthesis inhibitor. Multiple alternatively spliced transcript variants encoding the same protein have been found for this gene.
40S ribosomal protein S14
, emetine resistance
, ribosomal protein S14
, ribosomal protein S14b