DUSP19 antibody Polyclonal Antibodies Primary antibodies
- Known as:
- DUSP19 (anti-) Polyclonal Antibodies Primary antibodies
- Catalog number:
- orb117392
- Product Quantity:
- 100
- Category:
- -
- Supplier:
- Biorb
- Gene target:
- DUSP19 antibody Polyclonal Antibodies Primary antibodies
Related genes to: DUSP19 antibody Polyclonal Antibodies Primary antibodies
- Gene:
- DUSP19 NIH gene
- Name:
- dual specificity phosphatase 19
- Previous symbol:
- -
- Synonyms:
- SKRP1, DUSP17
- Chromosome:
- 2q32.1
- Locus Type:
- gene with protein product
- Date approved:
- 2002-11-11
- Date modifiied:
- 2014-11-18
Related products to: DUSP19 antibody Polyclonal Antibodies Primary antibodies
Related articles to: DUSP19 antibody Polyclonal Antibodies Primary antibodies
- Newly synthesized derivatives based on ligustrazine (TMP) demonstrate superior anticancer effects and reduced adverse effects. However, the efficacy and mechanism of the most potent TMP derivatives against thyroid cancer (TC) remain unclear. Through a mini screening, we identify that the TMP-based dimeric compound 8e has the strongest anti-tumor effect against TC. We further demonstrate that 8e impedes TC progression primarily by inhibiting proliferation and inducing apoptosis, while showing minimal cytotoxicity in normal human thyroid epithelial cells and negligible impact on visceral organs in nude mice, confirming its safety. Mechanistically, 8e regulates H3K27 and H3K18 acetylation of the promoter in a p300-independent manner, thereby activating the DUSP19-pJNK axis to slow TC progression. Furthermore, combination treatment with 8e and the histone acetyltransferase P300 inhibitor C646 synergistically suppresses TC development both and with minimal toxicity. Our data identify 8e as a highly promising and hypotoxic epigenetic inhibitor and apoptotic agent, and suggest that 8e/C646 combination therapy holds significant potential as a novel therapeutic strategy for advanced TC patients. - Source: PubMed
Publication date: 2026/05/08
Gu PengfeiZeng YuMeng ShuaiHao WeijingZhang WeiWan XingLiu YuChi JiadongHu LinfeiLi DapengZhao JingzhuWei SongfengZhang JieLiu TianjunRuan XianhuiZheng XiangqianGao Ming - Prostate cancer (PC) is a common urinary system malignancy, and advanced PC patients had a poor prognosis due to recurrence or distant metastasis. Therefore, it's imperative to reveal more details in tumorigenesis and prognosis of PC patients. - Source: PubMed
Publication date: 2023/11/16
Hu PingWang TaoYan HuiHuang YingZhao YanjiaoGao Yuanyuan - Phosphatase and tensin homolog (PTEN) is a tumor suppressor. Low PTEN expression has been observed in pancreatic neuroendocrine tumors (pNETs) and is associated with increased liver metastasis and poor survival. Vascular endothelial growth factor receptor 3 (VEGFR3) is a receptor tyrosine kinase and is usually activated by binding with vascular endothelial growth factor C (VEGFC). VEGFR3 has been demonstrated with lymphangiogenesis and cancer invasiveness. PTEN is also a phosphatase to dephosphorylate both lipid and protein substrates and VEGFR3 is hypothesized to be a substrate of PTEN. Dual-specificity phosphatase 19 (DUSP19) is an atypical DUSP and can interact with VEGFR3. In this study, we investigated the function of PTEN on regulation of pNET invasiveness and its association with VEGFR3 and DUSP19. - Source: PubMed
Publication date: 2022/11/06
Chang Tsung-MingChu Pei-YiLin Hui-YouHuang Kuo-WeiHung Wen-ChunShan Yan-ShenChen Li-TzongTsai Hui-Jen - Circular RNA (circRNA) homeodomain-interacting protein kinase 3 (circ_HIPK3) has recently reported as regulator in spinal cord injury (SCI). The regulatory mechanism of circ_HIPK3 in SCI was further researched in this study. Circ_HIPK3 expression was inhibited by CoCl in AGE1.HN cells. The CoCl-induced cell cycle arrest, cell proliferation inhibition and apoptosis promotion were mitigated by overexpression of circ_HIPK3. Circ_HIPK3 could target miR-222-3p and circ_HIPK3 repressed the CoCl-induced neuronal cell injury by sponging miR-222-3p. DUSP19 was a target gene of miR-222-3p and circ_HIPK3 affected the expression of DUSP19 via binding to miR-222-3p. The regulation of circ_HIPK3 in CoCl-induced injury of AGE1.HN cells was associated with the upregulation of DUSP19. Circ_HIPK3 acted as a pathogenic inhibitor in the progression of SCI via the miR-222-3p-mediated DUSP19 upregulation. - Source: PubMed
Publication date: 2021/03/23
Liu YuAo ShuangZhang HaoZhang YapengWang YuYang XiaotianLeng Hui - : Spinal cord injury (SCI) is a common injury that seriously threatens human health. NF-κB may be involved in the secondary injury of SCI that is mediated by inflammation and aggravates damage. Our study was aimed to investigate the role of NF-κB signaling in DUSP19-mediated cleaved Caspase-3 expression and the release of inflammatory factors and .: DUSP19 mRNA expression and the content of IL-6 and IL-8 in patients with traumatic SCI (TSCI) were measured by real-time PCR and ELISA, respectively. The levels of p-NF-κBp65, NF-κBp65 and cleaved Caspase-3 expression and the concentrations of IL-6 and IL-8 were measured by western blotting and ELISA, respectively.: Patients with TSCI showed lower DUSP19 expression and higher concentration of IL-6 and IL-8 compared with healthy controls. DUSP19 overexpression inhibited p-NF-κBp65 level, cleaved Caspase-3 expression, and production of IL-8 and IL-6 in the mice induced by TSCI. DUSP19 silencing increased p-NF-κBp65 level, cleaved Caspase-3 expression, and concentration of IL-6 and IL-8 in mouse primary microglia cells. DUSP19 overexpression had an inverse effect. Importantly, DUSP19 silencing and overexpression mediated p-NF-κBp65 level, cleaved Caspase-3 expression, and concentration of IL-6 and IL-8 in mouse primary microglia cells were reversed by NF-κB inhibitor pyrrolidine dithiocarbamate (PDTC) and NF-κB activator 12-myristate 13-acetate (PMA), respectively.: These results suggested that DUSP19-mediated SCI-induced apoptosis and inflammation via NF-κB signaling and might therefore serve as a potential therapeutic target for SCI. - Source: PubMed
Publication date: 2019/12/08
Xie Xian-KuanXu Zheng-KuanXu KanXiao Yu-Xiang