DUSP14 Antibody
- Known as:
- DUSP14 Antibody
- Catalog number:
- XW-7971
- Product Quantity:
- 0.05 mg
- Category:
- -
- Supplier:
- Prosci
- Gene target:
- DUSP14 Antibody
Related genes to: DUSP14 Antibody
- Gene:
- DUSP14 NIH gene
- Name:
- dual specificity phosphatase 14
- Previous symbol:
- -
- Synonyms:
- MKP-L, MKP6
- Chromosome:
- 17q12
- Locus Type:
- gene with protein product
- Date approved:
- 2002-01-09
- Date modifiied:
- 2015-02-02
Related products to: DUSP14 Antibody
Related articles to: DUSP14 Antibody
- Colorectal cancer (CRC) is a leading cause of cancer-related deaths worldwide, underscoring the urgent need for precise and personalized therapeutic strategies. Globo-H has emerged as a clinically relevant glycan target with promising diagnostic and therapeutic utility across multiple cancer types. In this study, we stratified colorectal cancer patients into Globo-H-high and Globo-H-low groups using a histology-based classification, followed by RNA-sequencing analyses to elucidate the key signaling pathways associated with Globo-H overactivation. Among the 31 genes that were identified to meet the Globo-H histology criterion, DUSP14 (dual specificity phosphatase 14) emerged as a promising pharmacological target associated with Globo-H abundance. DUSP14 is an underexplored but pharmacologically actionable therapeutic target. DUSP14 protein in colon cancer cells is inversely correlated with total Transforming growth factor-β-activated kinase 1 (TAK1) protein. The druggability of DUSP14 was demonstrated through in vitro using cell lines and patient-derived organoids (PDO). These results enhance current diagnostic frameworks and provide a foundation for developing novel targeted therapies. Further, in vivo studies are warranted to evaluate the potential of Globo-H targeting in combination with standard treatment regimens. Overall, our work highlights the value of integrating PDO-based functional assays with molecular profiling to uncover and validate actionable targets for CRC theranostics. - Source: PubMed
Publication date: 2026/04/01
Zohar KerenStrecker MarcoWartmann ThomasShi WenjieStelter FrederikeDoelling MaximilianAndric MihailoKakhlon OrTäger ChristianSchanze DennyLinnebacher MichaelNaumann MichaelStange Daniel EJechorek DörtheCroner Roland SLinial MichalKahlert Ulf D - Triple-negative breast cancer (TNBC) treatment remains challenging. Here, we found that dual-specificity phosphatase 14 (DUSP14) is highly expressed in TNBC and is associated with shorter relapse-free survival in patients. DUSP14 knockdown effectively inhibited the proliferation, migration, and invasion of TNBC cells in vitro and significantly suppressed tumor growth in vivo. Mechanistically, DUSP14 knockdown increased phosphorylation of protein tyrosine phosphatase non-receptor type 12 (PTPN12), thereby inhibiting the transcriptional activity of peroxisome proliferator-activated receptor alpha (PPARα) and ultimately downregulating the expression of stearoyl-coenzyme A (CoA) desaturase (SCD), a target gene involved in tumor progression and chemoresistance. This mechanism promoted lipid peroxidation in breast cancer cells, triggering ferroptotic cell death. In clinical analyses, DUSP14 and SCD protein levels in TNBC were strongly correlated. Targeting the DUSP14-PTPN12-PPARα/SCD axis with a small-molecule drug effectively restricted the malignant phenotype of TNBC cells. These findings reveal the role of DUSP14 in regulating ferroptosis. Targeting DUSP14 represents a promising strategy for TNBC treatment. - Source: PubMed
Publication date: 2025/09/30
Cao YueyueZheng YitianNiu RuiqiWang TingtingYu HaiyangTong YichengTang Yi-DaPan Yueyin - Allergic asthma is characterized by persistent chronic airway inflammation, leading to mucus hypersecretion and airway hyperresponsiveness. Dual-specificity phosphatase 14 (DUSP14), a member of the DUSP family, is a key regulator in various biological processes. However, the function of DUSP14 in allergic asthma remains to be elucidated. In this study, we aim to explore the function and mechanism of DUSP14 in asthma-related airway inflammation. In an ovalbumin (OVA) asthma mouse model, DUSP14 was found to be significantly diminished. DUSP14 overexpression relieved airway inflammation and attenuated airway mucus production. In vitro, overexpression of DUSP14 attenuated IL-13-induced cellular inflammation and mucus hypersecretion in bronchial epithelial cells (BEAS-2B). Afterwards, we used the co-immunoprecipitation assay to confirm that DUSP14 interacted with TAK1. DUSP14 overexpression restrained the activation of TAK1 and NF-κB signaling pathway in vitro and in vivo. Taken together, our findings clearly showed that DUSP14 could alleviate airway inflammation by inhibiting TAK1 activity and NF-κB signaling pathway, positioning the DUSP14-TAK1-NF-κB regulatory axis as a potential therapeutic target for allergic asthma. - Source: PubMed
Publication date: 2025/05/29
Kong RuiBai JunYao QingXu Xiaoqing - Gastric cancer (GC), a common and deadly malignancy worldwide, is a serious burden on society and individuals. However, available diagnostic biomarkers for GC are very limited. The current study aimed to identify potential diagnostic biomarkers for GC and analyze the activity of infiltrating immune cells in this pathology. - Source: PubMed
Publication date: 2025/05/23
Xia ChengweiLiu YiniQing Xin - Hypothyroidism leads to multiple organ dysfunction, with the heart the most affected. However, the pathologic mechanism of hypothyroidism-induced heart failure remains to be completely elucidated. Thyroid hormone replacement therapy enhances myocardium systolic function but increases the occurrence of arrythmias. There is an urgent need to explore these mechanisms in detail and to discover and develop drugs that can target and manage heart failure in patients with hypothyroidism. - Source: PubMed
Publication date: 2025/05/13
Zheng YitianCao YueyueWang WenyaoTong YichengWang ShuaixingLi ChenZhao MingmingSong YaoWang Yuan-Geng-ShuoQi JiatingWu ChaoYang JieZheng JilinGao JunWang JingjiaYang QingLiu GangZhao JiajunZhang YanXiao HanZhang You-YiTang Yi-Da