DAPK2 Antibody
- Known as:
- DAPK2 Antibody
- Catalog number:
- Y107988
- Product Quantity:
- 100 ug
- Category:
- -
- Supplier:
- ABM
- Gene target:
- DAPK2 Antibody
Related genes to: DAPK2 Antibody
- Gene:
- DAPK2 NIH gene
- Name:
- death associated protein kinase 2
- Previous symbol:
- -
- Synonyms:
- DRP-1, MGC119312
- Chromosome:
- 15q22.31
- Locus Type:
- gene with protein product
- Date approved:
- 1999-10-19
- Date modifiied:
- 2016-10-05
Related products to: DAPK2 Antibody
Related articles to: DAPK2 Antibody
- Although circular RNAs (circRNAs) have been implicated in acute kidney injury (AKI), their functional mechanisms beyond acting as miRNA sponges remain poorly understood, and the role of N6-methyladenosine (m6A) modification in circRNA-mediated regulation in AKI is yet to be explored. Here, we identify a novel mechanism by which the m6A-modified circRNA circNfix contributes to the regulation of septic AKI (SAKI). In tubular epithelial cells (TECs), downregulation of RBM47 reduces circNfix expression during SAKI. m6A-modified circNfix scaffolds the E3 ligase HECTD1 to induce K48-linked polyubiquitination and proteasomal degradation of the m6A reader YTHDF2. This stabilizes DAPK2 mRNA, a key target of YTHDF2, inhibiting NF-κB activation, thereby reducing TEC apoptosis and inflammation. In mouse models of SAKI and ischemia-reperfusion injury-AKI, AAV-mediated circNfix delivery lowered YTHDF2, suppressed inflammation, improved renal function, and attenuated damage. In septic AKI patients, circNfix levels in plasma and urine were significantly decreased, negatively correlated with serum creatinine. Urinary and plasma circNfix showed diagnostic potential. Our study reveals a mechanism where an m6A-modified circRNA contributes to AKI progression by degrading its reader protein, suggesting that circNfix may represent a potential therapeutic target and non-invasive biomarker. - Source: PubMed
Publication date: 2026/09/15
Ma TongtongZhang ZiqiYang YilinChen ChaopengLi ZhiyiLuo HuashengYu YanmeiHuang HeChen ZhongqingWang Peng - Death-associated protein kinase 1 (DAPK1) is a key regulator of apoptosis and immune responses; however, its prognostic significance in oral cancer remains insufficiently characterized. This study investigated the prognostic relevance of DAPK1 in oral squamous cell carcinoma (OSCC) and examined its associations with immune infiltration and apoptosis-related signaling pathways. - Source: PubMed
Publication date: 2026/08/28
Lai Hsiao-ChiChang Keng-MingLee Ching-Chih - Excess neutrophil apoptosis and the release of neutrophil extracellular traps (NETs) in systemic lupus erythematosus (SLE) lead to the accumulation of cell debris and the production of auto-antibodies targeting nuclear proteins and DNA. SLE neutrophil activation is regulated by changes in gene expression, notably expression of type I interferon-response genes and genes coding for granule proteins. This observational study measured both mRNA and small noncoding RNAs in SLE (n = 11) and healthy control (HC, n = 10) ultra-pure blood neutrophils to identify changes in expression that are involved in regulating neutrophil phenotype. Using RNAseq, we identified significant differential expression (DE) of 69 microRNAs, 63 other small noncoding RNAs, 236 piwiRNAs, and 83 tRNA fragments in SLE neutrophils compared to HC (false discovery rate [FDR] adj. P < 0.05). We also identified 78 significant alternative splicing events across 64 genes (FDR adj. P < 0.05, Δpercent spliced in (PSI) > 0.1 or < -0.1). Bioinformatic analysis of miRNA:mRNA DE genes predicted significant activation of autophagy, neutrophil degranulation, interferon alpha/beta signaling, and apoptosis pathways in SLE neutrophils. Translation and mRNA processing were predicted to be downregulated. microRNAs implicated in NETs production were miR-155-5p, miR-146a-5p, and miR-let-7b-5p (FDR adj. P < 0.05). SNORD89 was identified as a potential promoter of apoptosis in SLE neutrophils, along with alternative splicing of apoptosis genes myeloid cell leukemia-1 (MCL1), caspase-8 (CASP8), and death-associated protein kinase-2 (DAPK2) (FDR adj. P < 0.05). Our study, for the first time, describes dysregulated expression of small noncoding RNAs in SLE neutrophils and proposes noncoding RNA and alternative gene splicing as regulators of neutrophil-driven disease pathology in SLE. - Source: PubMed
Filbertine GraceChabronova AlzbetaLiu XuanHaldenby SamThomas Huw BattenMcLaren ZoePeffers Mandy JayneWright Helen Louise - Sepsis is associated with a pronounced but poorly understood endoplasmic reticulum stress (ERS) response. In this study, we found that death-associated protein kinase 2 (DAPK2), a calcium/calmodulin-regulated serine/threonine kinase, exhibits elevated expression in macrophages from patients with sepsis and from septic mice. Macrophage DAPK2 expression is transcriptionally upregulated through the activation of the Toll-like receptor 4 (TLR4)-myeloid differentiation primary response 88 (MyD88)-nuclear factor-κB (NF-κB) pathway. Macrophage-specific deletion of DAPK2 attenuated sepsis severity and mitigated the ERS response. Using liquid chromatography-tandem mass spectrometry (LC-MS/MS), we identified heat shock protein family A member 5 (HSPA5) as a binding partner for DAPK2. Because DAPK2 function had been previously associated with the kinase activity, we speculated that it might control ERS of macrophages through HSPA5 phosphorylation. Further investigation indeed revealed that DAPK2 phosphorylates HSPA5 at serine-588, which promotes the proteasomal degradation of HSPA5 and subsequently leads to the activation of inositol-requiring enzyme 1α (IRE1α). Inhibition of HSPA5 exacerbated sepsis in mice with macrophage-specific DAPK2 deficiency; however, this effect was abrogated by the deactivation of IRE1α. In conclusion, our findings demonstrate that DAPK2 propagates macrophage ERS through the HSPA5-IRE1α axis during systemic infection, suggesting this pathway as a potential therapeutic target in sepsis. - Source: PubMed
Publication date: 2026/06/23
Ni YinTang Guo-ZhenQiu ChenZhu GeJin Shu-WenZhu Hai-PingMo Shi-JingFang Xiang-Ming - BackgroundmiRNAs are of interest due to have been involved in cancers such as colorectal cancer (CRC).ObjectiveTo explore the expression levels of miRNA-34a and miRNA-135b and whether they can be potential biomarker for early diagnosis of CRC.MethodsFifteen pairs newly diagnosed colorectal cancer and normal involved in the measurement of tissue and serum levels of miRNAs 34a and 135b and their target genes of SIRT1 and DAPK-1. We assessed the predictive value of these miRNAs utilizing the receiver operating characteristic curve.ResultsThe findings have shown that the miRNA-34a expression was significantly downregulated and miRNA-135b was upregulated in CRC tissues in comparison to their expression in adjacent normal tissue. This was additionally observed in the serum of the same CRC cases when compared to individuals without CRC. Furthermore, we found a significant increase in the level of SIRT-1 and a significant reduction in the expression level of DAPK-1 in CRC tissues compared to the adjacent normal tissue. The value of AUC was considerably high for the timely detection of CRC.ConclusionsWe found these miRNAs acting as potential non-invasive biomarkers for the early detection of CRC and in assessing the CRC risk within the general population. - Source: PubMed
Publication date: 2026/06/10
Karami RoyaNajafi ElahehBabaei AnahitaShahdoust ErfanShaghaghi AliAmiri-Dashatan NasrinMotlagh BehroozKoushki MehdiKhodabandehloo Hadi