DEDD2 antibody
- Known as:
- DEDD2 (anti-)
- Catalog number:
- orb100592
- Product Quantity:
- EUR
- Category:
- -
- Supplier:
- Biorbyt biorb
- Gene target:
- DEDD2 antibody
Related genes to: DEDD2 antibody
- Gene:
- DEDD2 NIH gene
- Name:
- death effector domain containing 2
- Previous symbol:
- -
- Synonyms:
- FLAME-3
- Chromosome:
- 19q13.2
- Locus Type:
- gene with protein product
- Date approved:
- 2004-02-10
- Date modifiied:
- 2016-10-05
Related products to: DEDD2 antibody
Related articles to: DEDD2 antibody
- Bladder cancer (BLCA) has a poor prognosis and continues to pose a significant challenge for clinicians. Prior studies have demonstrated a close relationship of BLCA with macrophages. However, the key subpopulations and molecular functions of macrophages in BLCA have not been uncovered. It becomes possible to use single-cell sequencing technology to explore macrophage heterogeneity and identify new biomarkers. - Source: PubMed
Publication date: 2025/10/04
Che GuangliangZhao XuejunLuo RongtuanYu QuanfengGuo XiaofengGao KeChen KangyuZhang Erfeng - Glioblastoma multiforme, one of the most malignant types of brain tumor, heavily relies on glycolytic pathways and is significantly influenced by immune infiltration and its surrounding microenvironment. Growing evidence implies that increase in glycolysis can lead to lactate accumulation, which further contributed to histone lactylation, playing a crucial role in tumor development, maintenance, and therapeutic response. This study explores the prognostic and therapeutic potential of lactylation-related genes in glioblastoma multiforme. Using single-cell (GSE162631) and bulk transcriptome datasets (TCGA, CGGA, and GSE16011), we identified lactylation-related genes through ssGSEA and WGCNA. Moreover, a machine learning framework, incorporating 10 algorithms and 101 combinations, was used to establish an eight-gene lactylation-related signature (POLDIP3, MMP14, MDK, KDELR2, GSTK1, DEDD2, CD151, and BRI3) with robust predictive accuracy for patient survival. A nomogram with lactylation-related signature integration was developed as a quantitative prognostic instrument for clinical use. Moreover, patients classified by lactylation-related signature risk scores showed distinct immune status, tumor mutation burden, immunotherapy response, and drug sensitivity. The expression of those lactylation-related genes was further validated by quantitative PCR and functional experiment in normal and GBM cell lines. Overall, this study establishes a lactylation-related signature with significant potential for glioblastoma multiforme prognostic prediction, targeted prevention, and individualized therapy. - Source: PubMed
Publication date: 2025/05/23
Wen WenjieChen JiongxueDeng FuyinGuo DajiZuo YouChen XuewenLi YoujiaLi YiTang Yamei - Rotenone has potential chemical toxicity in the nervous system of both insects and mammals, but its deep molecular biological mechanisms have not been clarified. Here, the epigenetic regulatory mechanism underlying the toxicity of rotenone was studied using murine brain organoids (mBOs). Transmission electron microscopy indicated that rotenone destroyed mBOs'mitochondrial structure. RRBS-Seq showed that some promoter regions from the DLK1-DIO3 imprinted microRNA clusters were hypomethylated. But, rotenone stimulated hypermethylation significantly on the promoter DNA of miR-6991-3p. MiR-6991-3p in the rotenone-treated mBOs had the greatest decreased miRNA expression compared with the control. Meanwhile, luciferase report assay indicated that miR-6991-3p induced a decrease in luciferase activity via binding to specific sites on the 3'UTR of DEDD2 gene. To overexpression of miR-6991-3p attenuated mBO proliferated inhibition and cell death, accumulation for lipid peroxidation products significantly by rotenone inducing. Subsequently, results of cell staining and molecular biology experiment revealed that overexpression for miR-6991-3p significantly weakened expression levels of death-related genes (DEDD2, caspase-8, caspase-3, and caspase-1), but significantly elevated expression levels of cell proliferation-related genes (Ki67 and BCL2) in rotenone treated mBOs group. Here, we reveal a novel epigenetic mechanism of rotenone-induced neuronal death, in which rotenone induced promoter DNA hypermethylation of miR-6991-3p in the DLK1-DIO3 imprinted cluster. This caused miR-6991-3p transcriptional activity to be downregulated, which subsequently significantly increased the expression of its target gene, DEDD2, ultimately leading to neural organoid cell death. - Source: PubMed
Publication date: 2025/03/05
Cui ZeyuLiu XinGao XijinYu ZhihuaPan WeidongLiu Te - Hookworms are soil-transmitted parasitic nematodes that penetrate the host skin before migrating to the lungs. With an estimated 500-700 million people infected worldwide, hookworm infections are a neglected tropical disease and a significant cause of morbidity, particularly in children, pregnant women, and immunocompromised individuals. Although there is ample evidence that complement activation is pivotal to elicit a protective host immune response against invasive pathogens, its role in hookworm infection remains insufficiently explored. Here, we investigated the complement anaphylatoxin, C5a, during the early lung stage of infection with in C57BL/6J wild type and C5aR1 mice. Despite the previously reported ability of lung larvae to evade complement activation, C5a was detectable locally in lung tissue and bronchoalveolar lavages. Surprisingly, C5aR1 presence directly contributed to the pathogenicity of hookworm infection. The burden of viable parasites in the lungs was mitigated in C5aR1 mice, compared to C57BL/6J mice 48 hours post-infection. Additionally, C5aR1 mice showed significantly reduced lung injury, lower cytokine release, attenuated alveolar hemorrhage, and limited alveolar-capillary barrier disruption. Neutrophils were the most abundant and highest C5aR1-expressing cell type in the alveolar space after infection. Deficiency of C5aR1 reduced the influx of neutrophils, monocytes, and eosinophils to the pulmonary airways. RNA sequencing of alveolar neutrophils revealed C5aR1-dependent regulation of the novel nuclear protein, DEDD2. In conclusion, our findings highlight the impact of C5aR1 signaling in neutrophils during hookworm infection uncovering an unexpected downside of complement activation in parasitic infection. - Source: PubMed
Publication date: 2024/11/19
Walachowski SarahGaro LucienSharma ArjunJayaraman ArchanaNoon JasonReinhardt ChristophBosmann Markus - Overlapping genes were thought to be essentially absent from the human genome until the discovery of hundreds of translated, frameshifted internal open reading frames (iORFs) within annotated protein coding sequences (CDS). This would suggest that some human genes encode two completely different proteins; however, it is unclear how iORF-encoded proteins are translated, and whether they are broadly functional. We demonstrate that "non-coding" alternative transcripts lacking a complete protein coding sequence (CDS) are required for iORF translation. We also demonstrate that iORFs such as the conserved and antiapoptotic iORF encode proteins with functions distinct from the annotated proteins they overlap. This work thus provides a molecular and functional basis for dual coding of overlapping ORFs in human genes. - Source: PubMed
Publication date: 2025/05/08
Su HaomiaoKatz Samuel GSlavoff Sarah A