DBP5 _ DDX19
- Known as:
- DBP5 _ DDX19
- Catalog number:
- Y213664
- Product Quantity:
- 200ul
- Category:
- -
- Supplier:
- ABM
- Gene target:
- DBP5 _ DDX19
Related genes to: DBP5 _ DDX19
- Gene:
- DDX19A NIH gene
- Name:
- DEAD-box helicase 19A
- Previous symbol:
- DDX19L
- Synonyms:
- FLJ11126
- Chromosome:
- 16q22.1
- Locus Type:
- gene with protein product
- Date approved:
- 2004-11-03
- Date modifiied:
- 2019-02-19
- Gene:
- DDX19B NIH gene
- Name:
- DEAD-box helicase 19B
- Previous symbol:
- DDX19
- Synonyms:
- DBP5
- Chromosome:
- 16q22.1
- Locus Type:
- gene with protein product
- Date approved:
- 1999-12-07
- Date modifiied:
- 2016-10-05
Related products to: DBP5 _ DDX19
Anti- DBP5 DDX19 AntibodyAntibodies: DBP5 _ DDX19 HOST: Goat Clonality: pAbATP-dependent RNA helicase DDX19A - EC 3.6.1.-; DEAD box protein 19A; DDX19-like protein PolyclonalATP-dependent RNA helicase DDX19A,Ddx19,Ddx19a,DEAD box protein 19A,DEAD box RNA helicase DEAD5,Eif4a-rs1,Eukaryotic translation initiation factor 4A-related sequence 1,mDEAD5,Mouse,Mus musculusATP-dependent RNA helicase DDX19A,DDX19A,DDX19L,DDX19-like protein,DEAD box protein 19A,Homo sapiens,HumanATP-dependent RNA helicase DDX19B,DBP5,DDX19,DDX19B,DEAD box protein 19B,DEAD box RNA helicase DEAD5,Homo sapiens,Human,TDBPBASS1,Bax antagonist selected in saccharomyces 1,C21orf50,DBP5,Homo sapiens,HSPC310,HSPC312,Human,KIAA1019,Negative regulatory element-binding protein,NRE-binding protein,NREBP,Protein DBP-5,Protein SDBP5 AntibodyDBP5 antibodyDBP5 antibody Polyclonal Antibodies Primary antibodiesDBP5 antibody Polyclonal Antibody Host: GoatDBP5 Antibody. This antibody is expected to recognize DDX19A (NP_060802.1) and all reported isoforms of DDX19B (NP_009173.1, NP_001014451.1 and NP_001014449.1).DBP5 PeptideDBP5 PeptideDBP5 Peptide Please note that this peptide has a delivery time of approximately 3 weeks. If the peptide is out of stock, the delivery time may take up to 1-3 months. Related articles to: DBP5 _ DDX19
- Selinexor, a first-in-class exportin1 (XPO1) inhibitor, is an attractive anti-tumor agent because of its unique mechanisms of action; however, its dose-dependent toxicity and lack of biomarkers preclude its wide use in clinical applications. To identify key molecules/pathways regulating selinexor sensitivity, we performed genome-wide CRISPR/Cas9 dropout screens using two B-ALL lines. We identified, for the first time, that paralogous DDX19A and DDX19B RNA helicases modulate selinexor sensitivity by regulating MCL1 mRNA nuclear export. While single depletion of either DDX19A or DDX19B barely altered MCL1 protein levels, depletion of both significantly attenuated MCL1 mRNA nuclear export, reducing MCL1 protein levels. Importantly, combining selinexor treatment with depletion of either DDX19A or DDX19B markedly induced intrinsic apoptosis of leukemia cells, an effect rescued by MCL1 overexpression. Analysis of Depmap datasets indicated that a subset of T-ALL lines expresses minimal DDX19B mRNA levels. Moreover, we found that either selinexor treatment or DDX19A depletion effectively induced apoptosis of T-ALL lines expressing low DDX19B levels. We conclude that XPO1 and DDX19A/B coordinately regulate cellular MCL1 levels and propose that DDX19A/B could serve as biomarkers for selinexor treatment. Moreover, pharmacological targeting of DDX19 paralogs may represent a potential strategy to induce intrinsic apoptosis in leukemia cells. - Source: PubMed
Publication date: 2024/07/11
Terasaki TatsuyaSemba YuichiroSasaki KensukeImanaga HiroshiSetoguchi KiyokoYamauchi TakujiHirabayashi ShigekiNakao FumihikoAkahane KoshiInukai TakeshiSanda TakaomiAkashi KoichiMaeda Takahiro - Nuclear export of mRNAs is a critical regulatory step in eukaryotic gene expression. The mRNA transcript undergoes extensive processing, and is loaded with a set of RNA-binding proteins (RBPs) to form export-competent messenger ribonucleoprotein particles (mRNPs) in the nucleus. During the transit of mRNPs through the nuclear pore complex (NPC), the DEAD-box ATPase - DDX19 (herein referring to DDX19A and DDX19B) - remodels mRNPs at the cytoplasmic side of the NPC, by removing a subset of RNA-binding proteins to terminate mRNP export. This requires the RNA-dependent ATPase activity of DDX19 and its dynamic interactions with Gle1 and Nup214. However, the regulatory mechanisms underlying these interactions are unclear. We find that DDX19 gets covalently attached with a small ubiquitin-like modifier (SUMO) at lysine 26, which enhances its interaction with Gle1. Furthermore, a SUMOylation-defective mutant of human DDX19B, K26R, failed to provide a complete rescue of the mRNA export defect caused by DDX19 depletion. Collectively, our results suggest that SUMOylation fine-tunes the function of DDX19 in mRNA export by regulating its interaction with Gle1. This study identifies SUMOylation of DDX19 as a modulatory mechanism during the mRNA export process. This article has an associated First Person interview with the first author of the paper. - Source: PubMed
Publication date: 2022/02/18
Banerjee PoulomiMarkande ShubhaKalarikkal MishaJoseph Jomon - The emergence and recurrence of ovarian cancer are associated with ovarian cancer stem cells. For cancer treatment, gene delivery of microbubbles (MB)-mediated microRNA (miRNA) is considered as a promising approach. In this study, our aim is to investigate the effects of MB-mediated let-7b-5p inhibitor on the proliferation and stemness characteristics of ovarian cancer (OVCA) cells. Let-7b-5p inhibitor mediated by MB was prepared (termed MB-let-7b-5p inhibitor), and the effects of MB-let-7b-5p inhibitor and let-7b-5p inhibitor on OVCA cell viability, proliferation and stemness characteristics were investigated. We found that MB-let-7b-5p inhibitor presented a higher transfection efficiency than let-7b-5p inhibitor alone. The inhibitory effect of MB-let-7b-5p inhibitor on OVCA cells was more significant than let-7b-5p inhibitor. Let-7b-5p targeted DEAD (Asp-Glu-Ala-Asp)-box helicase 19A (DDX19A), which was downregulated in OVCA cells. The downregulation of DDX19A reversed the inhibitory effects of MB-let-7b-5p inhibitor on OVCA cells. To sum up, we found that MB-let-7b-5p suppressed OVCA cell malignant behaviors by targeting DDX19A. - Source: PubMed
Huang XiujuanDong HongxiaLiu YangYu FenYang ShunshiChen ZhenLi Jueying - To screen the regulatory proteins involved in Nox1 promoter activation in a cell model of inflammation and oxidative stress. - Source: PubMed
Qiu XianHu ShuiwangXu JunLi LiHuang Wenjie