Ask about this productRelated genes to: RPS15A Blocking Peptide
- Gene:
- RPS15A NIH gene
- Name:
- ribosomal protein S15a
- Previous symbol:
- -
- Synonyms:
- S15A
- Chromosome:
- 16p12.3
- Locus Type:
- gene with protein product
- Date approved:
- 1998-08-18
- Date modifiied:
- 2014-11-18
Related products to: RPS15A Blocking Peptide
Related articles to: RPS15A Blocking Peptide
- Protein synthesis in Low and High protein deposition (PD) gilts, exploring regulatory pathways within the same genetic background and age were studied. Gilts in Low (157 g/d) and High (219 g/d) PD groups underwent jugular vein cannulation to assess insulin, IGF-I and glucose postprandial responses to the same nutrient intake. L[1-C]valine administration enabled measuring protein synthesis rate and efficiency. Results showed 94% greater (P < 0.05) fractional synthesis rates in the longissimus dorsi and tended (P = 0.10) to a greater (11%) absolute synthesis rate in the liver of High PD gilts. High PD gilts tended (P = 0.10) to be more sensitive to insulin. Transcriptomics analyses in muscle identified 67 up-regulated and 102 down-regulated unique genes. Among the up-regulated genes, four olfactory receptors (OR4L1, OR5D13, OR6B2, OR10R2) and one ribosomal protein (RPS15A) present the highest fold-changes in High vs. Low PD gilts. Functional analyses identified six enriched gene ontology terms relate to muscle development, three to protein metabolism and four to signaling pathways. Rap1 signaling and regulation of actin cytoskeleton were over-represented KEGG pathways. High PD gilts exhibit greater protein synthesis and efficiency of protein synthesis, with transcriptomic evidence suggesting changes in the glucose/insulin metabolism and reduced muscle protein degradation. - Source: PubMed
Publication date: 2026/05/15
Remus AlinePalin Marie-FranceLapierre Hélènevan Milgen JaapPomar Candido - Ochratoxin A (OTA), a group 2B human carcinogen, has been implicated in hepatocellular carcinoma (HCC), yet its precise molecular mechanisms remain elusive. In this study, we investigated the oncogenic role of OTA using both in vitro (Huh7 and Hep-3B cell lines) and in vivo (C57BL/6 mouse models) approaches. Molecular docking, surface plasmon resonance, co-immunoprecipitation coupled with mass spectrometry (Co-IP/MS), and functional rescue experiments were employed to elucidate the underlying pathways. Our results demonstrated that OTA exposure (50 nM) significantly promoted HCC cell proliferation, migration, and invasion. Molecular docking combined with surface plasmon resonance revealed a high-affinity binding interaction between OTA and the gastrin-releasing peptide receptor (GRPR), which was subsequently validated by the observed upregulation of GRPR expression upon OTA treatment. We further demonstrated that OTA activates the canonical GRPR downstream pathway, PLCβ/IP3R/Ca , leading to increased intracellular calcium levels. Furthermore, Co-IP/MS identified ribosomal protein S15A (RPS15A) as a novel GRPR-interacting protein. RPS15A overexpression facilitated HCC progression by recruiting MDM2 to accelerate the degradation of p53, thereby upregulating the SLC7A11/GPX4 axis-a key regulator of ferroptosis. Crucially, GRPR knockdown effectively attenuated OTA-induced tumor growth both in vitro and in vivo. Collectively, our findings reveal a novel mechanism whereby OTA promotes HCC progression by binding to GRPR and activating both the PLCβ/IP3R/Ca signaling cascade and the RPS15A/p53/SLC7A11/GPX4 axis, suggesting that targeting GRPR may represent a promising therapeutic strategy for OTA-associated HCC. - Source: PubMed
Publication date: 2026/02/06
Yang Yan-QiLi Wen-XingZhao Xin-LiangYang YangLiu Zhi-GangCheng Shao-LiZhou KaiDiao Dong-MeiGe PanLv Mo-QiSun YingKang Jia-YingSun Rui-FangZhou Dang-XiaGao Jun-Hong - The aim of this study is to find potential biomarkers and drugs in intrahepatic cholestasis of pregnancy (ICP) by combining bioinformatics and experimental validation strategies. - Source: PubMed
Publication date: 2025/11/24
Zheng WenfeiZhan JingqiongCao HuarongWen MinYu MengmengPoochali Chandana Vayakkali - Hypoplastic left heart syndrome (HLHS) is the most lethal congenital heart disease (CHD) whose genetic basis remains elusive, likely due to oligogenic complexity. To identify regulators of cardiomyocyte (CM) proliferation relevant to HLHS, we performed a genome-wide siRNA screen in human iPSC-derived CMs, revealing ribosomal protein (RP) genes as the most prominent effectors of CM proliferation. Whole-genome sequencing of 25 HLHS proband-parent trios similarly showed enrichment of rare RP gene variants, including a damaging RPS15A promoter variant shared in a familial CHD case. Cross-species functional analyses demonstrated that perturbation of RP genes impairs cardiac growth: knockdown of RPS15A, RPS17, RPL26L1, RPL39, or RPS15 reduced CM proliferation, caused cardiac malformations in , and produced hypoplastic or dysfunctional hearts in zebrafish. Genetic interactions between RP genes and key cardiac transcription factors (TBX5 and NKX2-7) further support their developmental role. Importantly, p53 suppression or Hippo activation partially rescued RP deficiency phenotypes. Together, these findings implicate RP genes as critical regulators of cardiogenesis and candidate contributors to HLHS. - Source: PubMed
Publication date: 2025/12/11
Nielsen TanjaKervadec AnaïsTheis Jeanne LMissinato Maria AMarchant JamesRomero MichaelaMarchetti KatyaLamba AashnaZeng Xin-Xin IBerenguer MarieWalls Stanley MSchroeder AnalyneBirker KatjaDuester GregGrossfeld PaulNelson Timothy JOlson Timothy MOcorr KarenBodmer RolfVogler GeorgColas Alexandre R - Hypoxic microenvironment is a hallmark feature of hepatocellular carcinoma (HCC) and contributes to cancer progression. RHPN1-AS1, a long noncoding RNA (lncRNA), plays an important role in multiple cancers. However, its expression and oncogenic function under hypoxic conditions have not yet been determined. In this study, we investigated the expression changes of RHPN1-AS1 in HCC cells upon hypoxia. The effects of RHPN1-AS1 knockdown and overexpression on hypoxic HCC cells were explored. The protein partner involved in RHPN1-AS1 action in hypoxic HCC cells was characterized. We found that exposure to hypoxia led to an increase in the RHPN1-AS1 level in HCC cells, which was blocked by depletion of HIF-1α. Chromatin immunoprecipitation assay revealed the enrichment of HIF-1α at the promoter of RHPN1-AS1 in hypoxic HCC cells. Knockdown of RHPN1-AS1 suppressed HCC cell proliferation, colony formation, and invasion under hypoxia, whereas overexpression of RHPN1-AS1 promoted the proliferation and invasion of hypoxic HCC cells. Mechanistically, RHPN1-AS1 interacted with and stabilized RPS15A protein in hypoxic HCC cells. Elevated expression of RPS15A protein enhanced the proliferation and invasion of hypoxic HCC cells through activation of β-catenin signaling. Silencing of RPS15A attenuated RHPN1-AS1-induced aggressiveness and β-catenin activation in hypoxic HCC cells. In vivo tumorigenic studies confirmed that RPS15A depletion significantly reduced the growth of RHPN1-AS1-overexpressing HCC xenograft tumors. RHPN1-AS1 serves as a hypoxia-responsive lncRNA and interacts with the RPS15A protein partner to activate the β-catenin pathway, consequently enhancing HCC progression under hypoxia. - Source: PubMed
Publication date: 2025/09/30
Peng QinCai Yu-TingDing QiQian Xiang-YunXu CongZhou Hang-ChengChen HaoLi HengWang Wei