ribosomal protein L26
[Molecular mechanisms underlying the pathology of Diamond-Blackfan anemia].
Hirosaki, Japan. In Rinsho Ketsueki, Jul 2015
In DBA, mutations or large deletions in RP genes include RPS7, RPS10, RPS17, RPS19, RPS24, RPS26, RPL5, RPL11, RPL26 and RPL35A.
Loss of function mutations in RPL27 and RPS27 identified by whole-exome sequencing in Diamond-Blackfan anaemia.
Hirosaki, Japan. In Br J Haematol, Mar 2015
The disease has been associated with mutations or large deletions in 11 ribosomal protein genes including RPS7, RPS10, RPS17, RPS19, RPS24, RPS26, RPS29, RPL5, RPL11, RPL26 and RPL35A as well as GATA1 in more than 50% of patients.
Novel deletion of RPL15 identified by array-comparative genomic hybridization in Diamond-Blackfan anemia.
Boston, United States. In Hum Genet, 2013
The disease has been associated with point mutations and large deletions in ten ribosomal protein (RP) genes RPS19, RPS24, RPS17, RPL35A, RPL5, RPL11, RPS7, RPS10, RPS26, and RPL26 and GATA1 in about 60-65 % of patients.
Cellular adaptation to hypoxia and p53 transcription regulation.
Hangzhou, China. In J Zhejiang Univ Sci B, 2009
One, involving ataxia telangiectasia-mutated protein (ATM), is that the interaction between p53 and its down-regulation factor murine double minute 2 (MDM2) decreases, leading to p53 phosphorylation on Ser15, as determined by the post-translational mechanism; the other holds that p53 increases and is activated through the binding of ribosomal protein L26 (RPL26) or nucleolin to p53 mRNA 5( untranslated region (UTR), regulating p53 translation.