DAPK3 (Phospho-Thr265) Polyclonal Antibody
- Known as:
- DAPK3 (Phospho-Thr265) Polyclonal Antibody
- Catalog number:
- 12271
- Product Quantity:
- USD
- Category:
- -
- Supplier:
- Signalway
- Gene target:
- DAPK3 (Phospho-Thr265) Polyclonal Antibody
Related genes to: DAPK3 (Phospho-Thr265) Polyclonal Antibody
- Gene:
- DAPK3 NIH gene
- Name:
- death associated protein kinase 3
- Previous symbol:
- -
- Synonyms:
- ZIP, ZIPK
- Chromosome:
- 19p13.3
- Locus Type:
- gene with protein product
- Date approved:
- 1998-05-05
- Date modifiied:
- 2016-05-31
Related products to: DAPK3 (Phospho-Thr265) Polyclonal Antibody
Related articles to: DAPK3 (Phospho-Thr265) Polyclonal Antibody
- Acute kidney injury (AKI) is characterized by a rapid decline in renal function, often associated with tubular cell death. Insulin-induced gene 1 (Insig1), a key regulator of cholesterol metabolism, has not been previously implicated in AKI pathogenesis. - Source: PubMed
Publication date: 2026/05/16
Cao ShihanWang QianZhou MengyuSun ZhenzhenSun LeZhu WenpingWang XuHuang SongmingZhang AihuaHua HuDing GuixiaZhang YueJia Zhanjun - Quiescent cancer cells (QCCs) evade conventional therapies and contribute to minimal residual disease (MRD) and relapse, yet the signaling pathways governing their survival remain poorly understood. - Source: PubMed
Publication date: 2026/04/30
Csergeová LuciaJanoštiak Radoslav - Colorectal cancer liver metastasis (CRLM) and chemotherapy resistance remain major clinical challenges, with the underlying molecular mechanisms yet to be fully elucidated. In this study, based on analyses of five initial clinical cohorts from FUSCC, the E3 ubiquitin ligase COP1 was identified as a critical driver of CRLM and resistance to oxaliplatin-based chemotherapy. Using an organoid biobank derived from paired primary colorectal tumors and liver metastases, integrated multi-omics analyses (WES, bulk RNA-seq, scRNA-seq) of patient-derived organoids (PDOs) from CRLM revealed significantly elevated COP1 expression in liver metastases compared to primary tumors. High COP1 levels were associated with poor prognosis, increased liver metastatic burden, and resistance to oxaliplatin-based chemotherapy. In vitro and in vivo functional experiments demonstrated that COP1 facilitates CRLM progression by ubiquitinating and degrading LUZP1, thereby releasing DAPK3 from LUZP1-mediated suppression. This process leads to enhanced MYL9 phosphorylation and activation of epithelial-mesenchymal transition (EMT) as well as the JAK2-STAT3-CCND2 signaling axis-pathways crucial for liver metastasis and resistance to oxaliplatin-based chemotherapy. These findings establish the COP1-LUZP1-MYL9 axis as a therapeutic target for CRLM and oxaliplatin-based chemoresistance. Clinically, COP1 expression profiling in PDOs from postoperative specimens enables a precision strategy for managing oxaliplatin-based chemoresistance, especially in the context of FOLFOX. - Source: PubMed
Publication date: 2026/04/05
Zhang RuijiaLuo WenqinZhou QikaiLiang DongguoHao YuankaiChen FanQiu YulinCao YixianShan ZezhiZhang YuLi QingguoCai SanjunLuo DakuiMo ShaoboMa BinLi Xinxiang - Osteoporosis (OP) is a metabolic bone disease characterized by low bone mineral density (BMD), and its pathogenesis involves endoplasmic reticulum (ER) stress-related cell death. This study aimed to identify diagnostic biomarkers associated with ER stress-related cell death in OP and explore their underlying mechanisms. The training dataset (GSE56815), validation dataset (GSE56814), and single-cell RNA sequencing (scRNA-seq) dataset (GSE147287) were downloaded. Differentially expressed genes (DEGs) between OP patients and controls were identified. Candidate genes were obtained by intersecting DEGs with ER stress-related genes and programmed cell death (PCD)-related genes. Machine learning was used to screen intersection genes, and biomarkers were determined via expression level analysis. Gene set enrichment analysis (GSEA), immune cell infiltration analysis, drug prediction and molecular docking, scRNA-seq analysis, key cell screening, cell communication analysis, and pseudotime analysis were performed. Finally, reverse transcription quantitative polymerase chain reaction (RT-qPCR) were further conducted. A total of 28 candidate genes were obtained by intersection. CAMKK2 and DAPK3 were confirmed as biomarkers, and were consistently down-regulated in both datasets and verified by RT-qPCR. GSEA analysis revealed that biomarkers were enriched in cytokine-cytokine receptor interaction. Correlations between biomarkers and activated dendritic cells were found via immune cell infiltration analysis. Preliminary computational analyses indicated that drugs including calcitriol and danazol may potentially interact with the biomarkers in a stable manner. Bone marrow-derived mesenchymal stem cells (BM-MSCs) were identified as potential key cells via scRNA-seq analysis. Complex interactions involving BM-MSCs, such as ANGPTL4-CDH11 mediating BM-MSC self-communication, were revealed by cell communication analysis. Dynamic expression of biomarkers during BM-MSC differentiation was shown by pseudotime analysis: CAMKK2 fluctuated with differentiation stages, while DAPK3 shifted from high to low then high expression. CAMKK2 and DAPK3 were confirmed as diagnostic biomarkers for OP, providing insights into OP diagnosis and potential therapeutic targets. - Source: PubMed
Publication date: 2026/03/30
Xia YifengPeng ZhongyuZhao LingruiLong YuanChen RenweiDong JiahaoChu MeixiangYu WeijieChen Tao - Quercetin, a dietary flavonoid, has been implicated in obesity prevention; however, its role in adipocyte differentiation and adipose tissue remodeling remains incompletely defined. In HFD-fed C57BL/6 mice, quercetin dose-dependently attenuated body weight gain and reduced white adipose tissue expansion without altering food intake. Histological analysis revealed decreased adipocyte hypertrophy and improved adipose tissue architecture, indicating enhanced tissue remodeling. In differentiating 3T3-L1 adipocytes, quercetin markedly suppressed lipid droplet accumulation during the early stage of adipogenesis and enhanced autophagic flux, as evidenced by increased LC3-II conversion, P62 degradation, and autolysosome formation. Mechanistically, quercetin activated the AMPK-DAPK3-ULK1 signaling axis, promoting lipophagy and limiting LD formation during adipocyte differentiation. Proteomic analysis demonstrated cell-type-specific regulation: DAPK1 predominated in whole adipose tissue under metabolic stress, whereas DAPK3 was selectively upregulated in metabolically active differentiating adipocytes, aligning with its role in promoting lipophagy. Collectively, these findings demonstrate that quercetin suppresses adipocyte differentiation and promotes adipose tissue remodeling through DAPK3-mediated lipophagy, identifying DAPK3 as a key regulatory factor in adipogenesis. - Source: PubMed
Publication date: 2026/03/20
Chen ZihanPeng BaoyingZhao LeiHuang ZhibiaoChen MeifenZheng SuishengJiang YujiaZhou LiangLi Xin