RPS27L Lysate
- Known as:
- RPS27L Lysate
- Catalog number:
- NBL1-15569
- Product Quantity:
- 0.1 mg
- Category:
- -
- Supplier:
- ACR
- Gene target:
- RPS27L Lysate
Related genes to: RPS27L Lysate
- Gene:
- RPS27L NIH gene
- Name:
- ribosomal protein S27 like
- Previous symbol:
- -
- Synonyms:
- -
- Chromosome:
- 15q22.2
- Locus Type:
- gene with protein product
- Date approved:
- 2002-05-03
- Date modifiied:
- 2016-10-05
Related products to: RPS27L Lysate
Related articles to: RPS27L Lysate
- Rapid molecular biodosimetry may support radiation exposure assessment during mass casualty or mixed-field radiological incidents, but how gene expression responses vary across radiation qualities and dose rates remains incompletely characterized. Gene expression biodosimetry, including transcript-variant-aware measurements resulting from alternative splicing, may improve sensitivity for determining radiation quality and dose rate. We profiled nine radiation-responsive genes (AEN, APOBEC3H, DDB2, EDA2R, FDXR, PCNA, RPS27L, TRIAP1, ZMAT3) and six FDXR transcript variants using custom 384-well microfluidic RT-qPCR array cards (TaqMan Low Density Array, TLDA) of ex vivo leukopak-derived samples (leukocyte-enriched blood products) from three healthy donors, harvested 24 h after irradiation. Samples received an acute exposure of X rays (0.1-4 Gy), a protracted exposure of X rays (2 Gy at 0.1, 0.01, 0.004 Gy·min-1), and a mixed neutron field exposure with approximately 81% neutrons and 19% concomitant γ-rays (0.1-2 Gy at 0.6-1 Gy·h-1). In a separate experiment, gene expression of leukopaks was concordant with whole blood responses for FDXR and CDKN1A, with FDXR exceeding a 30-fold induction after exposure to 4 Gy of X rays. In the TLDA dataset, all targets were upregulated in a dose-dependent manner. Over the range of 0.1-1 Gy, neutrons elicited higher induction than X rays for APOBEC3H, DDB2, and FDXR, with convergence at 2 Gy as X-ray responses plateaued. Variant-level analysis showed isoform-specific behavior: FDXR-203 and FDXR-206 mRNA isoforms were induced by neutrons (especially at higher doses), while FDXR-202, FDXR-205, and FDXR-217 responded preferentially to X rays and FDXR-204 was moderately upregulated after X-ray irradiation. After protracted X-ray exposure, most genes were up-regulated with minimal dose-rate effects; AEN was the only target that differed significantly between 0.004 and 0.01 Gy·min-1, and FDXR-202/-204/-205 showed a higher fold change at the lowest dose rate. Analysis of dose-response behavior and derived relative biological effectiveness (RBE) values revealed three patterns when comparing neutrons with X rays. First, FDXR, DDB2 and EDA2R were more responsive to neutrons than to X rays at low doses (0.1-1 Gy), with fold changes increasing faster for neutrons. Depending on the gene, neutrons were equivalent to X-ray doses that were approximately 2-4 times higher, consistent with results reported previously for cytogenetic endpoints. Second, APOBEC3H, FDXR-217, RPS27L, PCNA and FDXR-203 showed similar dose-response behavior after exposure to neutrons and X rays, with occasional plateau differences. Third, AEN, TRIAP1 and the remaining assayed FDXR variants showed high variability and were not studied further here. Overall, several genes showed little discrimination across low dose rates, supporting their use for estimating total dose, while others showed clear differences between radiations of different qualities. Taken together, our results support the further development of multi-gene, variant-resolved approaches for radiation exposure assessment in mixed-field scenarios. - Source: PubMed
Publication date: 2026/06/11
Polozova MariaCruz-Garcia LourdesGhandhi Shanaz AKaur Salan PreetGarty GuyDeoli NareshHarken AndrewTurner Helen CGoriacha VeronikaBadie Christophe - Tetralogy of Fallot (TOF) is the most common cyanotic congenital heart disease, among which non-syndromic TOF (nsTOF) represents the most common subtype; however, the molecular mechanisms underlying right ventricular outflow tract (RVOT) remodeling in nsTOF remain incompletely understood. Bulk transcriptomic and single-nucleus RNA sequencing (snRNA-seq) datasets derived from fetal and infant RVOT tissues were integrated for analysis. Differential expression, miRNA-mRNA regulatory network construction, protein-protein interaction analysis, functional enrichment, and pseudotime trajectory analyses were performed to identify candidate hub genes and dynamic transcriptional alterations associated with nsTOF. A total of 842 differentially expressed mRNAs and 66 differentially expressed miRNAs were identified. Integration analyses yielded a regulatory network containing 54 DE-miRNAs and 538 DE-mRNAs. Fourteen hub genes, including PSMD14, NDUFA5, RPS27L, MRPS16, FOS, and SNRNP70, were identified through consensus topological filtering. Functional analyses suggested potential involvement of pathways related to protein homeostasis, ribosome-associated quality control, RNA splicing, mitochondrial metabolism, and stress-response signaling. snRNA-seq analysis demonstrated cell type-specific expression patterns of hub genes. Pseudotime analysis further suggested stage-dependent transcriptional alterations during RVOT remodeling. Integrated multi-omics analysis identified 14 candidate hub genes potentially involved in RVOT remodeling in nsTOF. These findings suggest that dysregulation of protein homeostasis, RNA-processing pathways, and mitochondrial metabolic processes may contribute to nsTOF pathology. Further experimental validation is required to confirm these observations. - Source: PubMed
Publication date: 2026/06/03
Wang HongpanYong XinGao YuyangLi WenyanChen ZhiyuLiu ZhenXu Wenli - Rheumatoid arthritis (RA) is a chronic autoimmune disease that can lead to multiple complications. Sjögren's syndrome (SS) is another autoimmune condition that may occur as a primary disorder or in conjunction with other autoimmune diseases, including RA. This study aimed to investigate the shared gene signatures between RA and SS. Gene expression datasets for RA (GSE15573, GSE93776) and SS (GSE48378, GSE94510, GSE93683) were obtained and analyzed to identify differentially expressed genes (DEGs) in peripheral blood mononuclear cells (PBMCs) and T cells. Gene ontology (GO) analysis and Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway enrichment analysis were performed on the DEGs identified. Quantitative real-time PCR (qRT-PCR) was used to validate the expression levels of DEGs in PBMCs from patients with RA and SS. A total of 244 DEGs were identified from the RA PBMC dataset, comprising 142 upregulated genes and 102 downregulated genes. These DEGs were significantly enriched in biological processes related to immune responses, including cellular response to lipopolysaccharide, defense response against fungi, inflammatory responses, and antibacterial humoral responses. In contrast, 335 DEGs were identified from the SS PBMC dataset; among these, 320 genes were upregulated, while 15 were downregulated. The DEGs associated with SS showed strong involvement in defense responses against viruses, innate immune responses, viral responses, as well as cellular reactions to lipopolysaccharide. Moreover, we identified 12 shared DEGs between RA and SS PBMCs: RNASE2, NDUFB3, LY96, ANKRD22, EIF2AK2, RNASE3, CLEC4D, TNFAIP6, DYNLT1, RPS27L, LILRA5, and F5. Validation through qRT-PCR confirmed increased expression levels of RNASE2, RNASE3, NDUFB3, and EIF2AK2 in PBMCs. This study successfully delineated key DEGs along with their associated biological processes within the context of RA and SS PBMCs. Through bioinformatics analyses combined with qRT-PCR validation, we have identified four critical genes that may serve as potential biomarkers or therapeutic targets for further investigation. - Source: PubMed
Publication date: 2026/04/25
Li Yi-FanGao Zhao-WeiLiu LiWang XiFan KunLin FangHei Ruo-Xuan - Radiotherapy resistance remains a major obstacle in nasopharyngeal carcinoma (NPC). This study delineates the role of protein phosphatase 2 regulatory subunit B gamma (PPP2R2C) in NPC radioresistance and its underlying mechanism to identify therapeutic targets. Through integrated bioinformatic analysis, PPP2R2C was identified as a candidate radioresistance driver. In vitro and in vivo functional assays demonstrated that PPP2R2C depletion significantly impaired NPC cell proliferation, migration, and radioresistance, while its overexpression enhanced these phenotypes. Mechanistic investigations revealed PPP2R2C inhibits radiation-induced ferroptosis, evidenced by transmission electron microscopy (TEM), lipid reactive oxygen species (ROS) quantification, malondialdehyde (MDA) assays, and immunoblotting of glutathione peroxidase 4 (GPX4) and solute carrier family 7 member 11 (SLC7A11). Crucially, immunoprecipitation-mass spectrometry (IP-MS), co-immunoprecipitation (Co-IP), and immunofluorescence (IF) confirmed PPP2R2C physically interacts with RPS27L. Further analysis via qPCR, Western blotting, cycloheximide chase, and proteasome inhibition showed PPP2R2C stabilizes RPS27L protein by blocking proteasomal degradation. RPS27L knockdown reversed PPP2R2C-mediated radioresistance and ferroptosis suppression. Clinically, high PPP2R2C expression correlated with poor patient survival. These findings establish that PPP2R2C promotes NPC radioresistance by stabilizing RPS27L to inhibit ferroptosis, positioning the PPP2R2C-RPS27L axis as a novel prognostic biomarker and therapeutic target for overcoming radioresistance. - Source: PubMed
Publication date: 2026/05/11
Fang JianboYang QiYang LuxiLiu HuiyingHu ShuluShen WeitaoZhang YuemingShen JieWei TingLyu QiongLuo PengWu XiaowenZhang JianMeng Hui - Carbon dots offer excellent physico-chemical properties and biocompatibility for cancer theranostics systems, either as therapeutic agents themselves, or as potential drug carriers. It is, however, postulated that the drug carrier affects the mechanism of action and intracellular target molecules of a drug. Therefore, in the present study, we systematically evaluated protein alterations in HeLa cervical cancer cells after treatment with sulfur-doped carbon dots (S-CDs). Synchrotron Radiation μFTIR spectroscopy and label-free LC-MS/MS proteomics integrated with bioinformatics were used to assess molecular changes. μFTIR revealed a shift and increased intensity of α-helices, indicating structural changes in proteins as a result of the interaction between S-CDs and cells. Proteomic analysis identified 122 statistically significant ( ≤ 0.05) proteins with increased abundance and 61 with decreased abundance following S-CD exposure, many of which possess high α-helix content, consistent with μFTIR findings. Functional analyses showed that up-regulated proteins were enriched in molecular adaptor, transporter, and transcription regulator activities, particularly those involved in RNA metabolism and translation. Down-regulated proteins were dominated by protein-modifying enzymes and cytoskeletal components. Pathway enrichment analysis indicated alterations in mRNA processing, ribosomal pathways, translation factors, aminoacyl-tRNA biosynthesis, and proteasome degradation. Key hub proteins included ribosomal proteins and translation initiation factors. S-CD treatment led to opposite regulation of many proteins compared to their regulation in untreated HeLa cells including down-regulation of ribosomal proteins (RPS27L, RPS19, and RPS5), aminoacyl-tRNA biosynthesis proteins (IARS1, LARS1, and MARS1), and proteasome degradation proteins (PSMD2, PSMD3, and PSMD11), which aligns with the observed cytotoxic effect of S-CDs on cervical cancer cells. Overall, these results highlight significant proteomic and structural protein changes induced by S-CDs and support their potential for cervical cancer treatment, warranting further investigation of this nanomaterial's biological applications. - Source: PubMed
Publication date: 2026/03/26
Davalieva KatarinaRalić VanjaBozhinovski GjorgjiGemović BranislavaNešić Maja DKorićanac LelaDučić TanjaAlgarra ManuelPopović Iva AStepić MilutinPetković Marijana