C1orf144 Blocking Peptide
- Known as:
- C1orf144 Blocking Peptide
- Catalog number:
- 33r-6383
- Product Quantity:
- USD
- Category:
- -
- Supplier:
- Fitzgerald industries international
- Gene target:
- C1orf144 Blocking Peptide
Related genes to: C1orf144 Blocking Peptide
- Gene:
- SZRD1 NIH gene
- Name:
- SUZ RNA binding domain containing 1
- Previous symbol:
- C1orf144
- Synonyms:
- DKFZp566C0424
- Chromosome:
- 1p36.13
- Locus Type:
- gene with protein product
- Date approved:
- 2005-07-08
- Date modifiied:
- 2014-11-19
Related products to: C1orf144 Blocking Peptide
Related articles to: C1orf144 Blocking Peptide
- Tinnitus, the perception of sound without any external sound source, is a prevalent hearing health concern. Mounting evidence suggests that a confluence of genetic, environmental, and lifestyle factors can influence the pathogenesis of tinnitus. We hypothesized that alteration in DNA methylation, an epigenetic modification that occurs at cytosines of cytosine-phosphate-guanine (CpG) dinucleotide sites, where a methyl group from S-adenyl methionine gets transferred to the fifth carbon of the cytosine, could contribute to tinnitus. DNA methylation patterns are tissue-specific, but the tissues involved in tinnitus are not easily accessible in humans. This pilot study used saliva as a surrogate tissue to identify differentially methylated CpG regions (DMRs) associated with tinnitus. The study was conducted on healthy young adults reporting bilateral continuous chronic tinnitus to limit the influence of age-related confounding factors and health-related comorbidities. - Source: PubMed
Publication date: 2024/08/15
Bhatt Ishan SunilkumarGaray Juan Antonio RaygozaTorkamani AliDias Raquel - Cancer is one of the major causes of death worldwide and the development of multidrug resistance (MDR) in cancer cells is the principal cause of chemotherapy failure. To gain insights into the specific mechanisms of MDR in cancer cell lines, we developed a novel method for the combined analysis of recently published datasets on drug sensitivity and CRISPR loss-of-function screens for the same set of cancer cell lines. For our analysis, we first selected cell lines that consistently exhibit drug resistance across several classes of compounds. We then identified putative resistance genes for each class of compound and used inferred gene regulatory networks (GRNs) to study possible mechanisms underlying the development of MDR in the identified cancer cell lines. We show that the same method of analysis can also be used to identify cell lines that consistently exhibit resistance to the gene knockout effect of the CRISPR-Cas9 technique and to study the possible underlying mechanisms. In the GRN associated to the drug resistant cell lines, we identify genes previously associated with resistance (UHMK1, RALYL, MGST3, USP9X, and ESRG), genes for which an indirect association can be identified (SPINK13, LINC00664, MRPL38, and EMILIN3), and genes that are found to be overexpressed in non-resistant cancer cell lines (MRPL38, EMILIN3 and RALYL). In the GRNs associated to the CRISPR-Cas9 resistance mechanism, none of the identified genes has been previously reported in the admittedly sparse literature on the subject. However, some of these genes have a common role: APBB2, RUNX1T1, ZBTB7C, and ISX regulate transcription, while APBB2, BTG3, ZBTB7C, SZRD1 and LEF1 have a function in regulating proliferation, suggesting a role for these two pathways. While our results are specific for the lung cancer cell lines we selected for this work, our method of analysis can be applied to cell lines from other tissues and for which the required data is available. - Source: PubMed
Publication date: 2024/03/05
Tomasi FrancescaPozzi MatteoLauria Mario - Many transcripts are targeted by nonsense-mediated decay (NMD), leading to their degradation and the inhibition of their translation. We found that the protein SUZ domain-containing protein 1 (SZRD1) interacts with the key NMD factor up-frameshift 1. When recruited to NMD-sensitive reporter gene transcripts, SZRD1 increased protein production, at least in part, by relieving translational inhibition. The conserved SUZ domain in SZRD1 was required for this effect. The SUZ domain is present in only three other human proteins besides SZRD1: R3H domain-containing protein 1 and 2 (R3HDM1, R3HDM2) and cAMP-regulated phosphoprotein 21 (ARPP21). We found that ARPP21, similarly to SZRD1, can increase protein production from NMD-sensitive reporter transcripts in an SUZ domain-dependent manner. This indicated that the SUZ domain-containing proteins could prevent translational inhibition of transcripts targeted by NMD. Consistent with the idea that SZRD1 mainly prevents translational inhibition, we did not observe a systematic decrease in the abundance of NMD targets when we knocked down SZRD1. Surprisingly, knockdown of SZRD1 in two different cell lines led to reduced levels of the NMD component UPF3B, which was accompanied by increased levels in a subset of NMD targets. This suggests that SZRD1 is required to maintain normal UPF3B levels and indicates that the effect of SZRD1 on NMD targets is not limited to a relief from translational inhibition. Overall, our study reveals that human SUZ domain-containing proteins play a complex role in regulating protein output from transcripts targeted by NMD. - Source: PubMed
Publication date: 2023/07/26
Halbout MathiasBury MarinaHanet AoifeGerin IsabelleGraff JulieKillian TheodoreGatto LaurentVertommen DidierBommer Guido T - Hsa_circRNA_0008344 (circ_0008344) is a new glioma-related circular RNA. Our study aims to explore its functions in glioma tumor progression. Real-time quantitative PCR and western blotting were used to detect RNA and protein abundances. RNase R assay, actinomycin D assay, and subcellular fractionation method were performed to identify the features of circ_0008344. Cell-counting kit-8, 5-ethynyl-2'-deoxyuridine assays, transwell assays, tube formation assay, flow cytometry, and nude mice xenograft tumor model were performed. Target relationship was predicted by bioinformatics algorithms and confirmed by dual-luciferase reporter assay. Abundances of circ_0008344 and SUZ RNA binding domain containing 1 (SZRD1) were highly elevated, while miR-638 was downregulated in glioma tumors and cells. Circ_0008344 was identified as a stable circRNA with a circular structure. Silencing circ_0008344 could restrain glioma proliferation, migration, invasion, and angiogenesis. Circ_0008344 functioned as a sponge for miR-638. The negative regulation of circ_0008344 knockdown on glioma progression and angiogenesis could be reversed by miR-638 inhibitor. SZRD1 was a target of miR-318, and its overexpression overturned the inhibition effect of miR-638 mimic on glioma progression and angiogenesis. Meanwhile, we confirmed that circ_0008344 knockdown inhibited SZRD1 expression, and its effect was reversed by miR-638 inhibitor. Also, circ_00008344 knockdown suppressed glioma tumor growth. Circ_0008344 might contribute to glioma progression through miR-638/SZRD1 axis, which might be a novel pathology and treatment target in glioma. - Source: PubMed
Publication date: 2022/04/08
Deng LiyongGong KuiyuWang Guihua - [This retracts the article DOI: 10.2147/CMAR.S324920.]. - Source: PubMed
Publication date: 2022/01/20