CASP3 & DFFA Protein Protein Interaction Antibody Pair
- Known as:
- CASP3 & DFFA Protein Protein Interaction Antibody Pair
- Catalog number:
- DI0148
- Product Quantity:
- 1 Set
- Category:
- -
- Supplier:
- Abno
- Gene target:
- CASP3 & DFFA Protein Interaction Antibody Pair
Related genes to: CASP3 & DFFA Protein Protein Interaction Antibody Pair
- Gene:
- CASP3 NIH gene
- Name:
- caspase 3
- Previous symbol:
- -
- Synonyms:
- CPP32, CPP32B, Yama, apopain
- Chromosome:
- 4q35.1
- Locus Type:
- gene with protein product
- Date approved:
- 1996-07-22
- Date modifiied:
- 2016-10-05
- Gene:
- DFFA NIH gene
- Name:
- DNA fragmentation factor subunit alpha
- Previous symbol:
- -
- Synonyms:
- DFF-45, DFF45, ICAD, DFF1
- Chromosome:
- 1p36.22
- Locus Type:
- gene with protein product
- Date approved:
- 1997-10-27
- Date modifiied:
- 2016-10-05
Related products to: CASP3 & DFFA Protein Protein Interaction Antibody Pair
Related articles to: CASP3 & DFFA Protein Protein Interaction Antibody Pair
- (1) The cytotoxicity and antioxidant activity of different fractions as well as the pro-apoptotic activity of saponin fractions from L. in SKOV-3 was investigated. (2) In screening studies, the cytotoxicity of six fractions on SKOV-3 was examined by LDH and SRB assays. The most active fractions-triterpenoid saponins-were selected for further investigation. To determine the mechanism of saponin fractions' cytotoxicity, their ability to induce apoptosis was examined via Annexin V assay. The effect of the saponin fractions on caspase 3 activity was measured using a Caspase 3 Assay Kit. The expression of 84 apoptosis-related genes was investigated in cancer cells exposed to saponin fractions from the roots. The radical scavenging capacity of different fractions was determined via DPPH assay. (3) The pronounced cytotoxic effects in SKOV-3 were demonstrated by saponin fractions from the leaves and roots. Those saponin fractions were chosen for further investigation. The treatment of cancer cell lines with saponins obtained from the roots provoked a significant increase in apoptotic cells. In the SKOV-3 cells, saponins caused upregulation of pro-apoptotic genes and a decrease in anti-apoptotic genes. The activation of caspase 3 was correlated with an increased DFFA expression level in the treated SKOV-3 cells. The most active fractions were phenolic acids from the shoots and roots. (4) To the best of our knowledge, the current study is the first to demonstrate that the barrigenol-type triterpenoid saponin fraction from the roots of inhibits SKOV-3 cell proliferation and induces apoptosis, which may be regulated by the expression of genes mostly specific to a mitochondria-related pathway. - Source: PubMed
Publication date: 2023/06/29
Kikowska MałgorzataPiotrowska-Kempisty HannaKucińska MałgorzataMurias MarekBudzianowski JaromirBudzianowska AnnaKaczmarek MariuszKowalczyk MariuszStochmal AnnaThiem Barbara - Compared to other breast cancer types, triple-negative breast cancer (TNBC) has historically had few treatment alternatives. Therefore, exploring and pinpointing potentially implicated genes could be used for treating and managing TNBC. By doing this, we will provide essential data to comprehend how the genes are involved in the apoptotic pathways of the cancer cells to identify potential therapeutic targets. Analysis of a single genetic alteration may not reveal the pathogenicity driving TNBC due to the high genomic complexity and heterogeneity of TNBC. Therefore, searching through a large variety of gene interactions enabled the identification of molecular therapeutic genes. - Source: PubMed
Adinew Getinet MMesseha SamiaTaka EquarAhmed Shade ASoliman Karam F A - Neuronal apoptosis is considered to be a critical cause of Alzheimer's disease (AD). Recently, meloxicam has shown neuroprotective effects; however, the inherent mechanisms are highly overlooked. Using APP/PS1 transgenic (Tg) mice as in vivo animal models, we found that meloxicam inhibits apoptosis in neurons by deactivating tumor necrosis factor receptor superfamily member 25 (TNFRSF25), leading to the suppression of the expression of fas-associated protein with death domain (FADD) and the cleavage of DNA fragmentation factor subunit α (DFFA) and cysteine aspartic acid protease-3 (caspase 3) via β-amyloid protein (Aβ)-depressing mechanisms. Moreover, the meloxicam treatment blocked the effects of β-amyloid protein oligomers (Aβo) on stimulating the synthesis of tumor necrosis factor α (TNF-α) and TNF-like ligand 1A (TL1A) in neuroblastoma (N) 2a cells. TNF-α and TL1A induce apoptosis in neurons via TNFR- and TNFRSF25-dependent caspase 3-activating mechanisms, respectively. Knocking down the expression of TNFRSF25 blocked the effects of TL1A on inducing apoptosis in neurons by deactivating the signaling cascades of FADD, caspase 3, and DFFA. Consistently, TNFRSF25 shRNA blocked the effects of Aβo on inducing neuronal apoptosis, which was corroborated by the efficacy of meloxicam in inhibiting Aβo-induced neuronal apoptosis. By ameliorating neuronal apoptosis, meloxicam improved memory loss in APP/PS1 Tg mice. - Source: PubMed
Publication date: 2022/10/24
Guan PeipeiZhu DiWang Pu - Coumarin is a functional compound with a pronounced wide range of biological activities and has recently been shown to have anticancer effects on various human cancer cells. Cisplatin is widely used in treating many cancers, but its effectiveness is limited due to acquired resistance and dose-related side effects. - Source: PubMed
Güner AdemBektaş HakanMenteşe Emre - Dendritic cells (DCs) are critical for both innate and adaptive immunity. Meanwhile, nitric oxide (NO) is a member of reactive nitrogen species (RNS) generally considered to play a key role in the bactericidal process in innate immunity against Mycobacterium tuberculosis complex infection. The present study therefore investigated the mechanism of NO production in murine DCs induced by Mycobacterium bovis (M.bovis) and its attenuated strain Bacillus Calmette-Guérin (BCG) infection. The expression of genes Slc7A1, Slc7A2, iNOS, and ArgI essential to NO synthesis was up-regulated in M.bovis/BCG infected DCs. IFN-γ addition further increased, while the iNOS inhibitor L-NMMA significantly inhibited their expression. Accordingly, the end products of arginine metabolism, NO and urea, were found to be significantly increased. In addition, BCG induced significantly higher levels of apoptosis in DCs compared to M.bovis shown by higher levels of DNA fragmentation using flow cytometry and release of mitochondrial Cytochrome C, and up-regulation of the genes caspase-3, caspase-8, caspase-9 and dffa critical to apoptosis by qRT-PCR detection and western blot analysis. Furthermore, IFN-γ increased, but L-NMMA decreased apoptosis of M.bovis/BCG infected DCs. In addition, mycobacterial intracellular survival was significantly reduced by IFN-γ treatment in BCG infected DCs, while slightly increased by L-NMMA treatment. Taken altogether, our data show that NO synthesis was differentially increased and associated with apoptosis in M.bovis/BCG infected DCs. These findings may significantly contribute to elucidate the pathogenesis of M.bovis. - Source: PubMed
Publication date: 2020/06/03
Liu HanXiong XuekaiZhu TingtingZhu YifanPeng YongchongZhu XiaojieWang JieruChen HuanchunChen YingyuGuo Aizhen