TAPS, sodium salt
- Known as:
- TAPS, sodium salt
- Catalog number:
- TB0920
- Product Quantity:
- 50G
- Category:
- -
- Supplier:
- BioBasic
- Gene target:
- TAPS sodium salt
Related genes to: TAPS, sodium salt
- Gene:
- PSMB8-AS1 NIH gene
- Name:
- PSMB8 antisense RNA 1 (head to head)
- Previous symbol:
- TAPSAR1
- Synonyms:
- XXbac-BPG246D15.8, TAP1-AS1
- Chromosome:
- 6p21.32
- Locus Type:
- RNA, long non-coding
- Date approved:
- 2013-07-25
- Date modifiied:
- 2014-06-09
Related products to: TAPS, sodium salt
((Cys31,Nva34)_Neuropeptide Y (27_36))2 Salt _ Binding (Disulfide_bond) Synonym SumFormula C116H186N36O28S2((Cys31,Nva34)_Neuropeptide Y (27_36))2 Salt _ Binding (Disulfide_bond) Synonym SumFormula C116H186N36O28S2(+)-(2S,5R)-1-Allyl-2,5-dimethylpiperazine, (+)-Camphoric Acid Salt C19H34N2O4 CAS: 186094-00-8(+)-(2S,5R)-1-Allyl-2,5-dimethylpiperazine, (+)-Camphoric Acid Salt CAS: 186094-00-8 Formula: C19H34N2O4(+)-Biotin 4-Amidobenzoic Acid, Sodium Salt C17H20N3NaO4S CAS: 102418-74-6(+)-Biotin 4-Amidobenzoic Acid, Sodium Salt CAS: 102418-74-6 Formula: C17H20N3NaO4S(+)-Tianeptine Monosodium Salt C21H24ClN2NaO4S CAS: 169293-32-7(+)-Tianeptine Monosodium Salt CAS: 169293-32-7 Formula: C21H24ClN2NaO4S(+)_3_Bromocamphor_8_sulfonic acid ammonium Salt(+)_Biotin 4_amidobenzoic acid sodium s N_Biotinyl_p_aminobenz(+)_Dipara tolouyl_d_tartaric acid salt of 4_(+)_Usnic acid sodium salt Usnic acid sodium salt(+__)_3_Methyl_2_oxovaleric acid Sodium salt(+__)_Cloprostenol Cloprostenol sodium(-)-Tianeptine Monosodium Salt C21H24ClN2NaO4S CAS: Related articles to: TAPS, sodium salt
- The human placenta plays a critical role as an immune and mechanical barrier. Notwithstanding, viral pathogens can still cross this barrier. Previously, differential gene expression has been described for protein-coding genes in human-induced-pluripotent-stem-cell-derived (hiPSC-derived) trophoblasts (TBs) from dizygotic twins discordant for congenital Zika syndrome (CZS), in which only one of the twin subjects presented the microcephaly phenotype. However, the involvement of long non-coding RNAs (lncRNAs) in TB development and in the TB response to ZIKV infection remained unexplored. To address this gap, we constructed a trophoblast-specific, lncRNA-enriched transcriptome resource and used it to define co-expression networks linking lncRNAs to trophoblast differentiation and to the antiviral response to ZIKV infection. Here, public RNA-Seq data from hiPSCs and hiPSC-derived TBs from dizygotic twins discordant for CZS were re-mapped to the human reference genome (GRCh38) using an ad hoc compiled hiPSC-TB-specific transcriptome enriched for lncRNAs, followed by differential expression analysis, co-expression network analysis and gene ontology (GO) enrichment. Expression validation by RT-qPCR of a set of novel and known lncRNAs associated with trophoblast differentiation and ZIKV infection was obtained. When comparing hiPSCs and TBs, 218 known and 26 novel lncRNAs were differentially expressed (DE) (FDR < 0.001). Correlated modules were enriched with GO terms related to "epithelial cell differentiation" and "tissue morphogenesis". Upon comparing TBs derived from the dizygotic twins, before and after ZIKV infection, 96 known and 6 novel lncRNAs were DE (FDR < 0.05). Correlated modules were enriched with interferon-related GO terms, including "regulation of defense response to virus" and "response to interferon". ZIKV-infected TBs from microcephaly-affected twins showed a 2.5-fold lower number of DE protein-coding genes and a 2-fold lower number of DE lncRNAs, compared with ZIKV-infected TBs from non-affected twins. These results indicate lncRNAs associated with TB development and response to ZIKV infection, highlighting candidates to be prioritized in future functional studies, such as , , , and imprinted and lncRNAs. - Source: PubMed
Publication date: 2026/08/15
Souza-Lopes ThallesFischer-Carvalho AgathaFreire Caio FPoli Pedro JFerreira Raiane OAmarante Maria F CZatz MayanaTahira Ana CAmaral Murilo SVerjovski-Almeida Sergio - Preterm birth (PTB, < 37 weeks of gestation) is a major public health concern in the United States, with Black women experiencing a higher incidence compared to White women. Although some studies have identified social, medical, and obstetric risk factors for PTB, the biological mechanisms underlying spontaneous PTB (sPTB) risk remain unclear. We conducted a secondary analysis using data from Black participants enrolled in the Nulliparous Pregnancy Outcomes Study: Monitoring Mothers-to-be (nuMoM2b), (n = 1073) from 2010 to 2013. Peripheral whole blood samples were collected from all participants between 6 + 0/7 and 13 + 6/7 weeks of gestation. Demographic, behavioral and clinical data were gathered through surveys, and pregnancy outcomes were obtained through chart abstraction. We used the Infinium Methylation EPIC v2.0 BeadChip for epigenome-wide association (EWAS) of DNA methylation and sPTB. - Source: PubMed
Publication date: 2026/05/24
Zhao TingtingZhao YihongReho PaoloSamari GoleenWapner RonaldHazi ArielleWu HaotianBarcelona Veronica - Long non-coding RNA PSMB8-AS1 involvement in heart failure (HF) following acute myocardial infarction (AMI) remains unclear. - Source: PubMed
Publication date: 2026/04/15
Wu WenwuChai Miaomiao - Long non-coding RNAs (lncRNAs) are important regulators of oncogenesis. In this study, we investigated the tumor-promoting role and prognostic value of the lncRNA PSMB8-AS1 in renal cell carcinoma (RCC). Using lncRNA microarray analysis, we identified PSMB8-AS1 as a candidate gene associated with disease progression and immune checkpoint inhibitor resistance. We examined PSMB8-AS1 expression in tumors and adjacent normal renal tissues from 192 patients with RCC. In vitro functional assays were performed to assess their role in cell proliferation and invasion. We also conducted bioinformatics and luciferase reporter assays to clarify the interaction between miR-204-5p/miR-211 and the transcription factor TFAP2A. PSMB8-AS1 was significantly overexpressed in clear cell RCC (ccRCC) tissues and correlated with poor prognosis. Knockdown experiments revealed that PSMB8-AS1 promoted proliferation and invasion. Mechanistically, PSMB8-AS1 functions as a competing endogenous RNA, sponging miR-204-5p/miR-211 and enhancing TFAP2A expression. These findings suggest that PSMB8-AS1 represents a promising biomarker for postoperative ccRCC recurrence. - Source: PubMed
Publication date: 2026/03/11
Baba ChiekoHirata HiroshiHiyoshi KoichiroTokunaga TakanoriFujii NakanoriShimizu KosukeKobayashi KeitaHayano TakahideAsai YoshiyukiShiraishi Koji - Sulforaphane (SFN) plays a vital role in many types of cancer as a natural extract from plants. However, whether SFN can inhibit gastric carcinogenesis by regulating the lncRNA-miRNA-mRNA axis is unclear. In the current work, the significantly differentially expressed lncRNA PSMB8AS1 was obtained by performing high-throughput sequencing of gastric cancer cells treated with SFN. The qRT-PCR assay results confirmed the inhibitory effect of SFN on PSM8AS1. Subsequently, using gastric cancer data from TCGA and 11 pairs of clinical samples from gastric and paracancerous tissues, we found that PSMB8-AS1 was upregulated in gastric cancer, and high expression of PSMB8-AS1 was associated with low survival of patients with gastric cancer. MTT, cell colony formation, scratch healing, flow cytometry, and qRT-PCR assays showed that the knockdown of PSMB8-AS1 significantly reduced the proliferation and migration of gastric cancer cells as well as promoted apoptosis. Dual luciferase reporter gene and RNA immunoprecipitation (RIP) assay confirmed that PSMB8-AS1 can function as the molecular sponge for miR-888-5p. Meanwhile, bioinformatics analysis and dual-luciferase reporter gene assay showed that miR-888-5p regulates SLC4A7. Overexpression of miR-888-5p or knockdown of SLC4A7 reduced the proliferation and migration of gastric cancer cells. In addition, rescue experiments confirmed that the inhibitory effects of the knockdown of PSMB8-AS1 or the knockdown of SLC4A7 on the proliferation and migration of gastric cancer cells could be reversed by miR-888-5p inhibitor treatment. Subcutaneous tumor formation experiments in nude mice demonstrated that the tumor volume of nude mice transplanted with PSMB8-AS1-knockdown gastric cancer cells was significantly reduced compared with that of the control group. Transcription factors can usually bind to the promoter regions of lncRNAs and regulate the transcription of lncRNAs. We demonstrated through website prediction and experiments that SFN can inhibit the level of PSMB8-AS1 by regulating the transcription factor YY1. These results suggest that SFN inhibits gastric cancer growth through the YY1/PSMB8-AS1/miR-888-5p/SLC4A7 axis. Therefore, SFN might be a promising therapeutical agent for GC prevention and therapy. - Source: PubMed
Publication date: 2025/10/04
Guo FanLi BoyuRen YitaoWang Yan-DongChen Wei-Dong