DDX49 antibody - N-terminal region (ARP36465_T100)
- Known as:
- DDX49 (anti-) - N-terminal region (ARP36465_T100)
- Catalog number:
- arp36465_t100
- Product Quantity:
- USD
- Category:
- -
- Supplier:
- Aviva Systems Biology
- Gene target:
- DDX49 antibody - N-terminal region (ARP36465_T100)
Related genes to: DDX49 antibody - N-terminal region (ARP36465_T100)
- Gene:
- DDX49 NIH gene
- Name:
- DEAD-box helicase 49
- Previous symbol:
- -
- Synonyms:
- FLJ10432, Dbp8
- Chromosome:
- 19p13.11
- Locus Type:
- gene with protein product
- Date approved:
- 2003-06-13
- Date modifiied:
- 2017-05-26
Related products to: DDX49 antibody - N-terminal region (ARP36465_T100)
Related articles to: DDX49 antibody - N-terminal region (ARP36465_T100)
- Liver hepatocellular carcinoma (LIHC) is a common malignancy, yet the core genes driving its progression and potential therapeutic targets remain insufficiently explored. Ribosome biogenesis (RB) is a critical biological process linked to various cancers; however, its systematic role in LIHC remains unclear. - Source: PubMed
Publication date: 2026/05/14
Qi YajieLi KunLi PinchengYan JianyuFeng ShuyueWan DanDu KeLiang XiaoYang FanZhou ErzhengHuang NaWang QianLiu Nanbin - Intracellular membraneless organelles, including granules, bodies, speckles, etc., play critical roles in physiological and pathological processes. The discovery of new membraneless organelles has generated significant attention. DEAD-box helicase (DDX) family members possess the potential to undergo liquid-liquid phase separation (LLPS), the foundation for the assembly of membraneless organelles. Here, to identify new granules assembled in steatotic hepatocytes, we screened DDX family members and found that lipids, especially arachidonic acid (AA) metabolites, induced LLPS of DDX49 in hepatocytes, forming an assembled granule named as lipid-induced granule (LIG). The assembled LIGs by DDX49 feedback restrained metabolic dysfunction-associated steatotic liver disease (MASLD)-associated fibrosis. Mechanistically, C5-methylcytosine (mC)-modified mRNA of pro-fibrotic hepatokine tissue inhibitor of metalloproteinase 2 (Timp2) and its reader Y-box binding protein 1 (YBX1) were recruited into LIGs, thereby inhibiting Timp2 mRNA translation and consequently feedback suppressing liver fibrosis. Moreover, LIGs were identified in human MASLD livers and exhibited reverse correlation with fibrosis progression. Therefore, we identified a new granule in steatotic hepatocytes and elucidated its role in restraining liver fibrosis. - Source: PubMed
Publication date: 2026/01/09
Li YunhuiLei TingNie WenMa MingruiZhao WeiZhou YeLiu YanfangWang MinjunJia KaiweiLiu ShanrongWang YuanyuanFan YiwenChen LongHe XingYuan JihangCao XuetaoHou Jin - Colorectal cancer (CRC) ranks as the third most common global cancer. This study aims to explore the expression, function, and mechanism of DEAD-box helicase 49 (DDX49) in CRC. - Source: PubMed
Publication date: 2025/12/08
Huang BaoyuYin ZhipengGao GangLi LonghaiYang Miao - The incidence of thyroid cancer is rising worldwide, underscoring the urgent need for novel molecular targets in the management of aggressive disease. This study identifies bystin-like protein (BYSL) as a previously unrecognized oncogenic driver in thyroid carcinoma. Comprehensive analyses of clinical specimens, established cell lines, and patient-derived tumor-like clusters revealed that BYSL is significantly upregulated in thyroid malignancies and is strongly correlated with adverse patient outcomes. Functional assays demonstrated that BYSL promotes tumor cell proliferation, migration, and invasion while suppressing apoptosis. Mechanistically, BYSL interacts directly with DEAD-box helicase 49 (DDX49) to form a functional protein complex that impairs the biogenesis of the tumor suppressor miR-145-5p by inhibiting its DICER-mediated processing. Dual knockdown of BYSL and DDX49 synergistically suppressed tumor growth and induced apoptosis in patient-derived tumor-like cell clusters, with these effects reversed by inhibition of miR-145-5p. Collectively, these findings demonstrate the BYSL-DDX49 complex as a pivotal modulator of thyroid cancer progression and underscore its promise as a therapeutic intervention for restoring tumor-suppressive pathways. - Source: PubMed
Publication date: 2025/12/19
Wang YueXing XiaoxiaoZhang DongpoSun TaoZhang YurenLi JunLiao DaixiangLi Junyi - Reperfusion injury following myocardial infarction (MI) poses a significant challenge, as it can exacerbate heart failure despite being the primary treatment. Adenosine is a promising cardioprotective drug, but its rapid degradation in circulation limits its therapeutic potential. Here, we report the design of self-assembled squalene adenosine nanoparticles (SQAdNPs) as a novel strategy to enhance adenosine's therapeutic potential in MI. In a rat ischemia/reperfusion MI model, it was observed that fluorescent SQAd NPs accumulated in the ischemic myocardium for at least 24 h post-intravenous administration. We evaluated the cardioprotective efficacy of SQAd NPs alone and in combination with antioxidant vitamin E (SQAd/VitE NPs), while assessing the impact of pre- vs post-reperfusion administration. Both nanoparticles' formulations improved cardiac function after 3 months, but only SQAd NPs prevented infarct expansion and adverse left ventricle remodelling with no differences between pre- or post-reperfusion treatment administration. Transcriptome analysis revealed that SQAd NPs upregulated genes linked to calcium signalling (Stac), mitochondrial function, as well as angiogenesis (Uqcrb), and DNA regulation (Ddx49), supporting enhanced cardiomyocyte survival. Functional analysis further indicated activation of pathways involved in cardiac repair, including SCF-KIT and EPH-Ephrin signalling, both associated with myocardial protection. Self-assembled SQAd NPs thus offer a unique therapeutic approach for reperfusion injuries, with enhanced efficacy and reduced side effects. - Source: PubMed
Publication date: 2025/10/30
Saludas LauraGarbayo ElisaAbizanda GloriaDormont FlavioSantamaría EnriquePrósper FelipeCouvreur PatrickBlanco-Prieto María J