Meter kit for conductivity: C5010 + conductivity_ATC electrode SK10T + 50 ml conductivity standard (0.01 M KCI) carrying case
- Known as:
- Meter reagent conductivity: C5010 + conductivity_ATC electrode SK10T + 50 milliliter conductivity control (0.01 M KCI) carrying case
- Catalog number:
- C5010K
- Category:
- -
- Supplier:
- Cleaver
- Gene target:
- Meter kit for conductivity: C5010 + conductivity_ATC electrode SK10T 50 conductivity standard (0.01 KCI) carrying case
Related genes to: Meter kit for conductivity: C5010 + conductivity_ATC electrode SK10T + 50 ml conductivity standard (0.01 M KCI) carrying case
- Gene:
- A1BG-AS1 NIH gene
- Name:
- A1BG antisense RNA 1
- Previous symbol:
- NCRNA00181, A1BGAS, A1BG-AS
- Synonyms:
- FLJ23569
- Chromosome:
- 19q13.43
- Locus Type:
- RNA, long non-coding
- Date approved:
- 2009-07-20
- Date modifiied:
- 2013-06-27
- Gene:
- AADACL2 NIH gene
- Name:
- arylacetamide deacetylase like 2
- Previous symbol:
- -
- Synonyms:
- MGC72001
- Chromosome:
- 3q25.1
- Locus Type:
- gene with protein product
- Date approved:
- 2005-03-18
- Date modifiied:
- 2018-05-03
- Gene:
- AADACL3 NIH gene
- Name:
- arylacetamide deacetylase like 3
- Previous symbol:
- -
- Synonyms:
- OTTHUMG00000001887
- Chromosome:
- 1p36.21
- Locus Type:
- gene with protein product
- Date approved:
- 2006-06-30
- Date modifiied:
- 2018-05-03
- Gene:
- AADACL4 NIH gene
- Name:
- arylacetamide deacetylase like 4
- Previous symbol:
- -
- Synonyms:
- OTTHUMG00000001889
- Chromosome:
- 1p36.21
- Locus Type:
- gene with protein product
- Date approved:
- 2006-06-30
- Date modifiied:
- 2018-04-17
- Gene:
- ACTA2-AS1 NIH gene
- Name:
- ACTA2 antisense RNA 1
- Previous symbol:
- -
- Synonyms:
- uc001kfo.1, ZXF1, UC001kfo
- Chromosome:
- 10q23.31
- Locus Type:
- RNA, long non-coding
- Date approved:
- 2013-03-01
- Date modifiied:
- 2018-08-15
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- The messenger RNA (mRNA) 3' untranslated region (3'UTR) contains important regulatory sequences, including upstream sequence elements (USEs), which regulate gene expression. One well-characterised USE in the 3'UTR of the Drosophila polo gene affects adult fly phenotypes when disrupted. We have now identified a highly conserved sequence within this USE (DplUSE) in the 3'UTR of several vertebrate genes, including in zebrafish, mouse, and human genomes and show that DplUSE enhances gene expression in human cells and zebrafish embryos. We show that, in humans, DplUSE-containing genes are associated with congenital disease processes, and that disruption of DplUSE function impairs zebrafish development. We also found that HuR/ELAVL1, hnRNPC, and PTBP1/hnRNPI bind to DplUSE RNA and are required for its activity in a human cell line, suggesting a highly conserved mechanism across distantly related species. Our results indicate that PTBP1 has a global function in alternative polyadenylation, activating the selection of distal polyA sites and repressing intronic polyadenylation in DplUSE-containing genes while hnRNPC and HuR modulate their expression. Additionally, we found that a colon cancer-associated SNP in the POU2AF2/C11orf53 3'UTR creates an ectopic DplUSE site, increasing gene expression in zebrafish gut cells and in a human cell line. We have therefore identified a short 3'UTR motif present in diverse vertebrate genes that controls their expression through conserved RBPs interactions and is implicated in human disease. - Source: PubMed
Eufrásio AnaMachado JoanaAzevedo JoanaPereira-Castro IsabelFerreira AlexandreMoutinho AnaHenriques FilipeJesus AnaAraújo MafaldaTavares JoanaSousa BrunoCavadas BrunoKessler Iris GeorgiaTeixeira JoanaPinto Pedro BorgesBessa JoséMoreira Alexandra - Small cell lung cancer (SCLC), the most malignant subtype of lung cancer, is a major cause of death among lung cancer patients. Drug resistance, high recurrence, and limitations of surgery are all obstacles to SCLC treatment. Consequently, clarifying the underlying mechanism of SCLC progression and identifying potential targets for therapeutic intervention are of paramount significance for improving the clinical outcomes of SCLC patients. C11orf53 has been demonstrated to play a crucial role in the NCI-H526 cell activity. However, few studies have focused on how C11orf53 affects the activity of NCI-H526 cells and the corresponding regulatory pathways. Herein, our study shows that C11orf53 affects the viability and proliferation of SCLC NCI-H526 cells by influencing the glycolytic pathway. We established the C11orf53 overexpression and knockdown systems in the NCI-H526 cell line with C11orf53-specific small-interfering RNA and lentivirus to assess the effects of C11orf53 on the activity and proliferation of NCI-H526 cells. Furthermore, the NCI-H526 cells with C11orf53 knockdown and overexpression were utilized to elucidate the molecular mechanism of C11orf53. Our study shows that C11orf53 knockdown significantly reduced the viability and proliferation of NCI-H526 cells. Additionally, adenosine triphosphate levels, glucose consumption, lactate secretion, and the expression of key enzymes involved in the glycolytic pathway were markedly decreased in NCI-H526 cells. These findings confirmed that the effect of C11orf53 on the activity and proliferation of NCI-H526 cells is mediated by its role in regulating cellular glycolysis. - Source: PubMed
Publication date: 2025/10/10
Liao ShuxianZhang MengxiaLi ShengfenGao YuanHuang RuileiZhao XuhongNing QianTang Shengsong - Epigenetic changes contribute to colorectal cancer (CRC) pathogenesis. We investigated whether methylation quantitative trait loci (mQTLs) are associated with CRC risk, survival and recurrence. - Source: PubMed
Publication date: 2025/06/12
Mesa-Eguiagaray InesIakovliev AndriiLi XueTimofeeva MariaHe YazhouZhang XiaomengDin Farhat V NFarrington Susan MSpiliopoulou AthinaDunlop Malcolm GTheodoratou Evropi - Recent studies have identified a previously uncharacterized protein C11orf53 (now named POU2AF2/OCA-T1), which functions as a robust co-activator of POU2F3, the master transcription factor which is critical for both normal and neoplastic tuft cell identity and viability. Here, we demonstrate that POU2AF2 dictates opposing transcriptional regulation at distal enhance elements. Loss of POU2AF2 leads to an inhibition of active enhancer nearby genes, such as tuft cell identity genes, and a derepression of Polycomb-dependent poised enhancer nearby genes, which are critical for cell viability and differentiation. Mechanistically, depletion of POU2AF2 results in a global redistribution of the chromatin occupancy of the SWI/SNF complex, leading to a significant 3D genome structure change and a subsequent transcriptional reprogramming. Our genome-wide CRISPR screen further demonstrates that POU2AF2 depletion or SWI/SNF inhibition leads to a PTEN-dependent cell growth defect, highlighting a potential role of POU2AF2-SWI/SNF axis in small cell lung cancer (SCLC) pathogenesis. Additionally, pharmacological inhibition of SWI/SNF phenocopies POU2AF2 depletion in terms of gene expression alteration and cell viability decrease in SCLC-P subtype cells. Therefore, impeding POU2AF2-mediated transcriptional regulation represents a potential therapeutic approach for human SCLC therapy. - Source: PubMed
Publication date: 2024/03/07
Szczepanski AileenTsuboyama NatsumiLyu HuijueWang PingBeytullahoglu OguzhanZhang TeSinger Benjamin DavidYue FengZhao ZiboWang Lu - - Source: PubMed
Publication date: 2022/10/18
Zhou ChenHuang HuiWang YunyiSendinc ErdemShi Yang