ENAapplication/xmlftp://ftp.sra.ebi.ac.uk/vol1/fastq/SRR626/000/SRR6263270/SRR6263270.fastq.gzftp://ftp.sra.ebi.ac.uk/vol1/fastq/SRR626/007/SRR6263267/SRR6263267.fastq.gzftp://ftp.sra.ebi.ac.uk/vol1/fastq/SRR626/001/SRR6263271/SRR6263271.fastq.gzftp://ftp.sra.ebi.ac.uk/vol1/fastq/SRR626/006/SRR6263266/SRR6263266.fastq.gzftp://ftp.sra.ebi.ac.uk/vol1/fastq/SRR626/003/SRR6263273/SRR6263273.fastq.gzftp://ftp.sra.ebi.ac.uk/vol1/fastq/SRR626/008/SRR6263268/SRR6263268.fastq.gzftp://ftp.sra.ebi.ac.uk/vol1/fastq/SRR626/002/SRR6263272/SRR6263272.fastq.gzftp://ftp.sra.ebi.ac.uk/vol1/fastq/SRR626/009/SRR6263269/SRR6263269.fastq.gzprimaryOK200GenomicsThe Ohio State Universityhttps://www.ebi.ac.uk/ena/browser/view/PRJNA390535Homo sapiensFhit is a tumor suppressor/genomic protective protein that is lost in more than 50% of cancers but the mechanism by which it works is unknown. Unlike most tumor suppressors Fhit is a cytoplasmic protein with no known interacting partners. A previous study found that Fhit regulates the translation of thymidine kinase 1 (TK1) mRNA into protein, with greater TK1 translation in Fhit-positive versus Fhit-negative cells. Increased TK1 translation was dependent on the ability of Fhit to degrade small RNA fragments termed nucleoside 5’,5’-triphosphates. The goal of this study was to identify mRNAs whose translation is regulated by Fhit, and use this information to identify the proteins that are responsible for its tumor suppressor/genome protective effects.xref:EuropePMC:PMC5745650ENApreventive measures, Fra14A2, Controlling, FRA3B, preventive therapy, reference sample, control, prophylaxis, AP3Aase, prevention and control, Controlled, prevention, AW045638.Human, strain, H1299, human being, Man (Taxonomy), Homo sapiens, CRL-5803., Modern Man, Modern, cultivar, NCI-H1299, man, Man, ecotype, humanfalseHomo sapiens cultivar:NCI-H1299Identification of mRNAs under translational control by Fhit2025-09-242018-06-14PRJNA3905359606