Ask about this productRelated genes to: RPLP0 antibody
- Gene:
- RPLP0 NIH gene
- Name:
- ribosomal protein lateral stalk subunit P0
- Previous symbol:
- -
- Synonyms:
- PRLP0, P0, L10E, RPP0, LP0
- Chromosome:
- 12q24.23
- Locus Type:
- gene with protein product
- Date approved:
- 1993-12-16
- Date modifiied:
- 2016-10-05
Related products to: RPLP0 antibody
Related articles to: RPLP0 antibody
- Reverse transcription quantitative real-time polymerase chain reaction is the gold standard for gene expression quantification. Yet, this method's accuracy heavily depends on choosing appropriate reference genes for data normalization. Reference genes must display stable expression levels across biological and experimental conditions to ensure accurate and meaningful results. - Source: PubMed
Publication date: 2026/04/24
Mengi Camur NazSeker BusranurKizildag FulyaYanik TulinAdams Michelle M - Neuroinflammation, particularly that involving reactive microglia, the brain's resident immune cells, is implicated in the pathogenesis of major neurodegenerative diseases (NDs). Multiple studies have reported changes in ribosomal protein (RP) expression during neurodegeneration, but the significance of these changes remains unclear. Ribosomes are evolutionarily conserved protein-synthesizing machines, and although commonly viewed as invariant, accumulating evidence suggests functional ribosome specialization through variation in their protein composition. Among RPs, S24, encoded by RPS24 in humans and Rps24 in mice, is unique as its transcripts undergo alternative splicing to produce protein variants with different C-terminal sequences that are differentially expressed across tissues and cell types. Understanding heterogeneous RP expression patterns across brain regions and cell types could reveal mechanisms underlying selective vulnerability in NDs and provide new biomarkers for neuroinflammatory responses. To identify RP expression patterns across brain regions in neurons, astrocytes, and microglia we analyzed cell type-specific translating mRNAs from mice. To investigate Rps24 isoform-specific expression, we performed cell type-resolved transcript analysis and developed antibodies specific for the S24-PKE protein variant encoded by mRNA isoform Rps24c. We examined Rps24c/S24-PKE expression in brains from mouse models of aging and neurodegeneration, as well as in human postmortem tissue from patients with Alzheimer's disease (AD), Parkinson's disease (PD), and Huntington's disease (HD). This work revealed distinct RP expression patterns across brain regions and between neurons, astrocytes, and microglia, including neuron-enriched RPs Rpl13a and Rps10. Analysis of RP paralogs revealed complex expression relationships with their canonical counterparts, suggesting regulated mechanisms for generating heterogeneous ribosomes. Across brain regions and cell types, Rplp0 and Rpl13a, commonly used normalization references, showed heterogeneous expression, raising important methodological considerations for gene expression studies. Rps24 isoforms exhibited striking cell type-specific expression patterns. Rps24c was predominantly expressed in microglia and was increased by neuroinflammation caused by aging, neurodegeneration, or inflammatory chemicals. Using S24-PKE-specific antibodies, we verified increased expression of this protein variant in brains with AD, PD, and HD, and in relevant mouse models. These findings establish heterogeneous RP expression as a feature of brain cell types which may enable cell type-specific translation regulation via specialized ribosomes. This work also identifies Rps24c/S24-PKE as a potential novel marker for neuroinflammation and neurodegeneration and provides new tools for monitoring these responses. - Source: PubMed
Publication date: 2026/05/06
Magadi Srivathsa SJonson MariaLucena Pablo BCaliandro Michele FAlmeida BeatrizBilalli LorinaBudinger DimitriTsoi AnnaNtzouni MariaMaqdissi Joseph AgiKaczmarczyk LechZijlstra Jente JFaketija MatejPerkins MatthewPaul GesineHallbeck MartinIngelsson MartinWatts Joel CReichenbach NicolePetzold Gabor CSchieweck RicoHeneka Michael TJackson Walker S - Phosphorus is an essential element for plant growth, and its deficiency severely limits crop productivity. To explore genetic resources for improving phosphorus use efficiency, this study investigated the differential low-phosphorus tolerance mechanisms of two kudzu (Pueraria lobata) germplasms from Australia (tolerant) and Jiangsu, China (sensitive) using hydroponics, RNA-seq, and WGCNA. The results showed that the Australian germplasm exhibited superior low-phosphorus tolerance through root morphological plasticity, which was characterized by increased root length and tip number under low phosphorus (0.05 mmol L KHPO); enhanced reactive oxygen species scavenging, with higher peroxidase and catalase activities under extremely low phosphorus (0.005 mmol L KHPO), and extensive transcriptome reprogramming, including 8896 upregulated genes in response to phosphorus deficiency. In contrast, the Jiangsu germplasm showed limited adaptive responses, with reduced root hairs and biomass under stress. WGCNA partitioned 21,734 expressed genes into 20 co-expression modules, among which the turquoise and light green modules showed significant correlations with phosphorus treatments and phenotypic traits. Genes in the turquoise module were primarily enriched in oxidative phosphorylation and phenylpropanoid biosynthesis pathways, whereas the light green module was significantly enriched in ribosome-related pathways. Five hub genes, ABCG5, TALDO, VAMP7B, EEF1AS, and RPLP0, were identified as core components of these modules. Collectively, these findings establish the Australian kudzu as a valuable germplasm resource for improving phosphorus use efficiency in crops and provide key molecular targets for precision breeding. - Source: PubMed
Tang YanhuaZhang ShuweiXi YiZhao LiliChen Chao - The potential multidimensional molecular alterations during recovery of severe patients with coronavirus infectious disease (COVID-19) remain to be elucidated. Early assessment of the prognosis of severe COVID-19 may facilitate appropriate medical interventions. - Source: PubMed
Publication date: 2026/04/25
Wang QianWang DelongHu XujuanLong GangyuTang YunRen LehaoFang XiangzhiShang YouZhang DingyuHan YangGong Rui - Some patients with osteoporosis (OP) do not respond to treatment with bisphosphonates; pathways that stimulate osteoclatogenesis may be involved in this failure, such as the myddosome pathway. A total of 40 OP patients and 20 controls were included in the group study. Patients treated with sodium alendronate (SA) for two years were classified according to bone mineral density (BMD) variations of the lumbar spine, femoral neck, and total hip, measured by the method of dual-energy x-ray absorptiometry (DXA) as responsive patients (OP-R) (n = 20) and non-responders (OP-NR) (n = 20), to evaluate the impact of the myddosome pathway gene expression profile in postmenopausal women with OP. The gene expressions were measured through real-time relative quantitative PCR with Taqman® probes; relative quantification was normalized to GAPDH and RPLP0 reference genes. Non-responders showed increased expression levels of MYD88 and IRAK3 compared to responders Fold change (FC) = 2.86±1.54, p=0.0002 e FC= 3.62±0.46, p<0.0001 respectively. Our results demonstrate the influence of the myddosome on OP maintenance and response to sodium alendronate (SA) treatment, highlighting the importance of this pathway as a potential target for new therapeutic approaches in postmenopausal OP. - Source: PubMed
Publication date: 2026/04/17
Oliveira Bianca Maria Ribeiro deMelo Maria Julia Alves deGuaraná Werbson LimaLima Camilla Albertina Dantas deBarbosa Alexandre DominguesSandrin-Garcia Paula