The reference OMIM entry for this protein is 604180

Ribosomal protein l24; rpl24

The mammalian ribosome is composed of 4 RNA species (see 180450) and approximately 80 different proteins (see 180466).

CLONING

During hybridization screening of a human choriocarcinoma cDNA library, Johnson (1993) identified, by chance, a cDNA encoding RPL24, which he called L30. He isolated additional RPL24 cDNAs by screening a normal human diploid fibroblast cell line cDNA library. The deduced sequence of the RPL24 protein is similar to those of the Saccharomyces cerevisiae ribosomal proteins L30A and L30B. RPL24 contains 157 amino acids and has a calculated pI of 9.6. The 5-prime untranslated region of the RPL24 cDNA contains a pyrimidine-rich sequence, a feature typical of mammalian ribosomal protein mRNAs. Northern blot analysis detected an approximately 700-bp RPL24 transcript in several human cell lines.

GENE FUNCTION

Barna et al. (2008) intercrossed Myc (190080) transgenic mice, in which Myc is overexpressed in the B-cell compartment (termed E(mu)-Myc/+) with L24 (Rpl24) heterozygous mice, which have overall decreased protein synthesis. By lowering the threshold of protein production in L24 heterozygote mice, the increased protein synthesis rates and cell size in the E(mu)-Myc heterozygote cells were restored to normal levels in the compound heterozygote mice. This effect suppressed the oncogenic potential of Myc in this context. Barna et al. (2008) concluded that the ability of Myc to increase protein synthesis directly augments cell size and is sufficient to accelerate cell cycle progression independently of known cell cycle targets transcriptionally regulated by Myc. In addition, when protein synthesis is restored to normal levels, Myc-overexpressing precancerous cells are more efficiently eliminated by programmed cell death. Barna et al. (2008) suggested that their findings revealed a mechanism that links increases in general protein synthesis rates downstream of an oncogenic signal to a specific molecular impairment in the modality of translation initiation used to regulate the expression of selective mRNAs. Barna et al. (2008) showed that an aberrant increase in cap-dependent translation downstream of Myc hyperactivation specifically impairs the translational switch to internal ribosomal entry site (IRES)-dependent translation that is required for accurate mitotic progression. Failure of this translational switch results in reduced mitotic-specific expression of the endogenous IRES-dependent form of Cdk11 (176873), which leads to cytokinesis defects and is associated with increased centrosome numbers and genome instability in E(mu)-Myc/+ mice. When accurate translational control is reestablished in E(mu)-Myc/+ mice, genome instability is suppressed. Barkic et al. (2009) found that RPL24 deficiency in human A549 cells triggered the p53 (TP53; 191170)-dependent checkpoint response. Signer et al. (2014) compared protein synthesis in hematopoietic stem cells (HSCs) and restricted hematopoietic progenitors. Signer et al. (2014) found that the amount of protein synthesized per hour in HSCs in vivo was lower than in most other hematopoietic cells, even if differences in cell cycle status were controlled for or HSCs were forced to undergo self-renewing divisions. Reduced ribosome function in Rpl24(Bst/+) mice (see

ANIMAL MODEL

) further reduced protein synthesis in HSCs and impaired HSC function. Pten (601728) deletion increased protein synthesis in HSCs but also reduced HSC function. Rpl24(Bst/+) c ... More on the omim web site

Subscribe to this protein entry history

June 29, 2020: Protein entry updated
Automatic update: OMIM entry 604180 was added.

Feb. 22, 2019: Protein entry updated
Automatic update: model status changed

Oct. 19, 2018: Additional information
Initial protein addition to the database. This entry was referenced in Bryk and co-workers. (2017).