FLASH Antibody
- Known as:
- FLASH Antibody
- Catalog number:
- 2271
- Product Quantity:
- 0.1 mg
- Category:
- -
- Supplier:
- Prosci
- Gene target:
- FLASH Antibody
Related genes to: FLASH Antibody
- Gene:
- CASP8AP2 NIH gene
- Name:
- caspase 8 associated protein 2
- Previous symbol:
- -
- Synonyms:
- FLASH, CED-4, RIP25, FLJ11208, KIAA1315
- Chromosome:
- 6q15
- Locus Type:
- gene with protein product
- Date approved:
- 1999-12-10
- Date modifiied:
- 2014-11-19
Related products to: FLASH Antibody
Related articles to: FLASH Antibody
- Human embryonic kidney (HEK) 293 cells are widely used for recombinant protein production because of their efficient posttranslational modification capabilities. However, their large-scale culture is often limited by metabolic stress and early apoptosis, leading to insufficient protein yields. In this study, we aim to increase protein expression through the coordinated modulation of metabolic and apoptotic pathways. Using CRISPR/Cas9 technology, we target and knockout the genes of ornithine decarboxylase antizyme 1 (OAZ1), which regulates polyamine metabolism, and caspase 8-associated protein 2 (CASP8AP2), an apoptosis-related protein. We successfully construct an / double-knockout HEK293 cell line. Following transfection with the knockout vector and screening of single-cell clones, multiple levels of validation confirm the successful gene knockout. The results show that the double-knockout cells exhibit significantly reduced apoptosis rates. Furthermore, the production of recombinant secreted alkaline phosphatase (SEAP) and vitronectin (VN) increases by 2.1 folds and 2.9 folds, respectively, compared with those in wild-type cells. Metabolic profiling reveals that the cell cycle is arrested in the G1/G0 phase, accompanied by increased specific consumption and production rates of key metabolites. This study demonstrates that concurrent inhibition of apoptosis and optimization of metabolism effectively enhances recombinant protein production in HEK293 cells, suggesting a novel strategy for improving HEK293 cell-based expression. - Source: PubMed
Publication date: 2026/01/27
Zhang JunheZhang LiaoHou LuLi WeidongGeng ShaoleiWang XiaoyinWang Tianyun - Improved treatment of childhood acute lymphoblastic leukemia (ALL) depends on the identification of new molecular markers that can predict treatment response and clinical outcome. Examination of the expression patterns of a set of genes at the RNA level is one of these new modalities. The prognostic significance of caspase-8-associated protein 2 (CASP8AP2), an apoptosis-related gene, in pediatric ALL is controversial. - Source: PubMed
Publication date: 2025/12/11
Arafah OmarAshraf MarihameAbd Elsalam Ahmed MustafaElfishawi SallyHammad Mahmoud - Chinese hamster ovary (CHO) cells play a crucial role in biopharmaceutical production due to their ability to produce complex proteins. Enhancing the productivity of CHO cells is essential for meeting the growing demand for biologics. Caspase 8-Associated Protein 2 (CASP8AP2), a key regulator of apoptosis and cell survival, has been identified as a potential target to increase CHO cell productivity. To this end, CRISPR-mediated homology-independent targeted integration (HITI) was used to silence CASP8AP2. Results of the cell viability assay revealed that CASP8AP2-deficient clones (C2, C3, and C4) were more resistant to sodium butyrate (NaBu) compared to native cells, with IC50 values of 11.83, 12.77, 10.25, and 8.55 mM, respectively. Protein production assays showed a significant increase in JRed and luciferase expression in silenced clones (C2 and C4) compared to wild-type cells, with up to 1.2- and 1.9-fold increases for JRed, and 1.4- and 1.7-fold increases for luciferase, respectively. These findings could be attributed to the clones experiencing cell cycle arrest specifically during the S phase. While these results demonstrate proof-of-principle using reporter proteins, future validation with therapeutic biologics such as implementing monoclonal antibodies in bioreactor settings could confirm scalability for industrial bioprocessing. Transcriptomic analyses would further elucidate downstream effects on apoptosis and metabolism pathways. The results suggest that targeting CASP8AP2 could be a promising strategy for improving bioprocess efficiency and yield in CHO cell-based production systems. - Source: PubMed
Publication date: 2025/11/29
Kheirandish AliSorourian SoofiaBehbahani Abbas BehzadAhmadi Mohammad Karimi BabaDehbidi Gholamreza RafieiRahimi ElinaSafari Fatemeh - Manganese (Mn), a vital trace element for biological functions, has raised health concerns due to potential toxicity. Excessive Mn impairs male reproduction by reducing testosterone, inducing oxidative stress, and disrupting spermatogenesis. However, its mechanisms targeting Leydig and Sertoli cells remain unclear. This study investigates Mn's reproductive toxicity by utilizing Leydig cell line TM3 and Sertoli cell line TM4, MTT assays revealed median lethal concentrations of 230 μM (TM3) and 170 μM (TM4), with AO/EB/DAPI staining confirming condensed nuclei and enhanced fluorescence. Apoptosis inhibitor Z-VAD-FMK (20 μM) suppressed cell death in both cell lines, whereas ferroptosis inhibitor Ferrostatin-1 (10 μM) specifically attenuated TM4 cell death. Necrosis inhibitor Necrostatin-1 (10 μM) showed no protective effect. Mn triggered ROS elevation in TM4 cells, accompanied by upregulated , while downregulating . These findings reveal Mn activates apoptosis in TM3 cells and concurrent apoptosis/ferroptosis in TM4 cells through ROS-dependent dysregulation of apoptosis- and ferroptosis-related genes. These findings establish distinct toxic mechanisms in TM4 cells and highlight the axis as a therapeutic target to mitigate Mn-induced spermatogenic damage. - Source: PubMed
Publication date: 2025/07/24
He JiaqiLi TongciSu YueLiang YanTian YingCai RenlianZhang JidongLu XiangTan Jun - The therapeutic potential of presumed cardiac progenitor cells (CPCs) in heart regeneration has garnered significant interest, yet clinical trials have revealed limited efficacy due to challenges in cell survival, retention, and expansion. Priming CPCs to survive the hostile hypoxic environment may be key to enhancing their regenerative capacity. We demonstrate that microRNA-210 (miR-210), known for its role in hypoxic adaptation, significantly improves CPC survival by inhibiting apoptosis through the downregulation of , a ~40% reduction in caspase activity, and a ~90% decrease in DNA fragmentation. Contrary to the expected induction of Bnip3-dependent mitophagy by hypoxia, miR-210 did not upregulate , indicating a distinct anti-apoptotic mechanism. Instead, miR-210 reduced markers of mitophagy and increased mitochondrial biogenesis and oxidative metabolism, suggesting a role in metabolic reprogramming. Furthermore, miR-210 enhanced the secretion of paracrine growth factors from CPCs, with a ~1.6-fold increase in the release of stem cell factor and of insulin growth factor 1, which promoted in vitro endothelial cell proliferation and cardiomyocyte survival. These findings elucidate the multifaceted role of miR-210 in CPC biology and its potential to enhance cell-based therapies for myocardial repair by promoting cell survival, metabolic adaptation, and paracrine signalling. - Source: PubMed
Publication date: 2025/04/21
Alonaizan RitaPurnama UjangMalandraki-Miller SophiaGunadasa-Rohling MalaLewis AndrewSmart NicolaCarr Carolyn