DAPK2 Pre-design Chimera RNAi
- Known as:
- DAPK2 Pre-design Chimera RNAi
- Catalog number:
- H00023604-R02
- Product Quantity:
- 20 nmol
- Category:
- -
- Supplier:
- Abno
- Gene target:
- DAPK2 Pre-design Chimera RNAi
Related genes to: DAPK2 Pre-design Chimera RNAi
- 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 Pre-design Chimera RNAi
Related articles to: DAPK2 Pre-design Chimera RNAi
- 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 - Psoriasis is a chronic, immune-mediated disorder with an unmet need for effective treatments. To systematically prioritize therapeutic targets, we integrated proteome-wide Mendelian randomization (MR) with expression validation in blood/skin, genetic susceptibility analysis in the UK Biobank, differential gene expression (DGE) from bulk and single-cell RNA sequencing (scRNA-seq), colocalization, pathway enrichment, and protein-protein interaction analyses. - Source: PubMed
Publication date: 2026/05/28
Si ShuchengWang XiaoxiaoZhan Siyan - Alzheimer's disease (AD) is a chronic progressive neurocognitive disorder manifested by increased production and deposition of amyloid beta (Aβ), abnormal tau phosphorylation, and formation of neurofibrillary tangles (NFTs). In addition, the disease progression is found to be associated with neuronal cell death, elevated levels of reactive oxygen species, mitochondrial dysfunction, and loss of synaptic plasticity in specific regions of the brain. AD is seventh leading cause of death and over more than 70%-80% of 57 million people having dementia develop AD worldwide. The disease population is also severely increasing at an alarming rate globally. The currently available treatment strategies remain insufficient to cure the disease because AD involves very complex pathways during its progression. Death-associated protein kinase 1 (DAPK1) is identified as a promising next-generation therapeutic drug target for the management of AD. It belongs to a family of serine/threonine kinases that influences different hypotheses involved in AD pathogenesis, such as tauopathies, Aβ hypothesis, redox, and autophagy pathways. In this review, we highlight the involvement of DAPK1 in various molecular pathways associated with AD pathogenesis and the crosstalk between DAPK1 and synaptic dysfunction and neuronal cell death implicated in AD. Moreover, the various small molecules, microRNAs, and phytoconstituents have been discussed, which have the potential to be developed as a treatment strategy targeting DAPK1-related pathological pathways in AD. - Source: PubMed
Publication date: 2026/05/22
Shukla ShashikeshSingh Rakesh Kumar - Alzheimer's disease (AD) is a neurodegenerative disorder that is caused by multiple factors, characterized by a progressive decline in cognitive ability, extracellular amyloid-β (Aβ) plaques, and intracellular neurofibrillary tangles composed of hyperphosphorylated tau. Current treatment strategies can provide only symptomatic treatment or limited efficacy, highlighting the need to intervene in the upstream regulatory factors that drive both amyloid and tau pathologies. Death-associated protein kinase 1 (DAPK1) is a key driver upstream of both amyloid precursor protein processing and tau phosphorylation, simultaneously promoting amyloidogenesis and tau-mediated pathology in AD. In this study, we developed CP1, a bifunctional proteolysis-targeting chimera (PROTAC), to recruit E3 ubiquitin ligase to DAPK1, thereby inducing the ubiquitination and proteasomal degradation of DAPK1. CP1 efficiently eliminated the DAPK1 protein in primary cortical neurons without affecting its mRNA level, resulting in reduced Aβ generation and tau hyperphosphorylation. , upon systemic administration, CP1 effectively crossed the blood-brain barrier, degraded DAPK1, and consequently reduced the Aβ plaque burden and mitigated neuroinflammation in female 5xFAD mice. In a AAV-hTau-P301L tauopathy model, CP1 treatment suppressed tau hyperphosphorylation, preserved NeuN- and MAP2-positive neurons, attenuated astrocytic and microglial activation, and ultimately restored learning and memory abilities in both male and female mice. In summary, these findings demonstrate that degrading DAPK1 via a PROTAC strategy simultaneously mitigates both amyloid and tau pathology, indicating that CP1 is an effective candidate for disease-modifying therapy. - Source: PubMed
Publication date: 2026/04/23
Li RuomengYao JingPeng WenZheng LizhenWu XueyinShui XindongZheng XiaoqingTian WujinWang LongZhou YingRuan XinglinPan XiaodongZhang TaoLiu YangLee Tae HoChen Dongmei - Disuse osteoporosis, a consequence of prolonged mechanical unloading, is characterized by bone loss and elevated fracture susceptibility. Although melatonin exhibits bone‑anabolic properties, its mechanistic role in the context of mechanical unloading remains elusive. Our findings demonstrate that melatonin promotes osteogenic differentiation and suppresses osteoblast apoptosis, collectively mitigating unloading‑induced osteoporotic bone loss in hindlimb unloading (HLU) mice. Moreover, unloading suppressed YTHDF3 expression in osteoblasts and bone tissue, which was effectively rescued by melatonin administration. Functionally, YTHDF3 potentiated osteoblast differentiation and matrix mineralization while inhibiting apoptotic cell death. At the molecular level, YTHDF3 directly recognized mA‑modified Dapk2 transcripts and promoted their decay. DAPK2 was characterized as a negative regulator that impedes osteoblast differentiation and survival. Genetic analyses established that melatonin‑driven suppression of DAPK2 and functional recovery of osteoblasts are contingent upon YTHDF3. In summary, we delineate a melatonin/YTHDF3/DAPK2 protective axis that safeguards against unloading‑induced bone deterioration via post‑transcriptional regulation of Dapk2, thereby unveiling new mechanistic perspectives and therapeutic opportunities for disuse osteoporosis. - Source: PubMed
Sun QuanXu LiqunLi ZhikuiZhang JunfeiZhao XiranZhang LijunZhang XiaoyanZhao JiangdongTan YingjunWang LuyaoZhang GeHu ZebingZhang ShuShi Fei