Apaf1
- Known as:
- Apaf1
- Catalog number:
- 000054A
- Product Quantity:
- 250ul
- Category:
- -
- Supplier:
- ABM
- Gene target:
- Apaf1
Related genes to: Apaf1
- Gene:
- APAF1 NIH gene
- Name:
- apoptotic peptidase activating factor 1
- Previous symbol:
- -
- Synonyms:
- CED4, APAF-1
- Chromosome:
- 12q23.1
- Locus Type:
- gene with protein product
- Date approved:
- 1998-01-20
- Date modifiied:
- 2016-10-04
Related products to: Apaf1
adaptor molecule apoptotic peptidase activating factor 1,APAF1 ELISA Kit, HumanAngiotensin II_vasopressin receptor,Avr,NACHT, LRR and PYD domains-containing protein 6,Nalp6,Nlrp6,Pypaf5,PYRIN-containing APAF1-like protein 5-like,Rat,Rattus norvegicusAnserine Apoptotic Peptidase Activating Factor 1 Elisa Kit (APAF1)Anserine anti - Apoptotic Peptidase Activating Factor 1 Elisa Kit (APAF1)Anti APAF1 Monoclonal AntibodyAnti APAF1 Monoclonal Antibody (DISCONTINUED)Anti APAF1 Monoclonal Antibody *DISCONTINUEDanti-APAF1anti-APAF1anti-APAF1anti-APAF1anti-APAF1anti-APAF1anti-APAF1 APAF-1Anti-Apaf1 Antibody Related articles to: Apaf1
- H5N6 highly pathogenic avian influenza virus (HPAIV) poses a serious threat to both poultry and public health due to its ability to cross species barriers. Although interferon-stimulated genes (ISGs) are key components of the host's antiviral defense, a systematic identification and functional characterization of duck ISGs has not yet been conducted. In this study, we identified 815 potential duck ISGs induced by type II interferon (IFN-γ) in duck embryo fibroblasts (DEFs). The majority of these type II ISGs were enriched in immune-related pathways, including "cytokine-cytokine receptor interaction" and "influenza A". Functional validation using siRNA-mediated knockdown demonstrated that six ISGs, including duIFI35, promote H5N6 AIV replication when silenced. Through TUNEL assay, flow cytometry, and apoptotic pathway analysis, Our analysis revealed that H5N6 AIV infection markedly upregulates apoptotic genes such as Fas, FADD, caspase-8, BAK, cytochrome c, APAF1, caspase-9, and caspase-3 (P < 0.05), thereby promoting apoptosis in DEFs. In investigating the antiviral mechanism of duIFI35, it was found that overexpression of duIFI35 further enhanced H5N6-induced apoptosis, as evidenced by increased transcription of these apoptotic genes, whereas duIFI35 knockdown had the opposite effect. Importantly, the antiviral effect of duIFI35 was significantly diminished upon treatment with the caspase inhibitor Z-VAD-FMK (20 μM) (P < 0.05), indicating that its antiviral activity is mediated through apoptosis induction. Collectively, this study provides the first systematic identification of type II ISGs in ducks and reveals duIFI35-mediated apoptosis as a critical antiviral mechanism, offering foundational insights into ISG-driven innate immunity against AIV in waterfowl. - Source: PubMed
Publication date: 2026/04/16
Zhang TaoYang NaMa LuluXu FengxiangLin XiaobingHuang JiangwuGao FeiLiao MingFeng MinDai Manman - Cytochrome c (Cytc) becomes a crucial regulator, determining the fate of cells at the confluence of apoptosis and metabolism. From its primary origin as an electron transporter in the mitochondrial electron transport chain (ETC), Cytc has ascended to a crucial role in apoptosis, triggering cascades of cellular deathupon liberation from the mitochondria.The intricate interplay between Cytc and apoptosis protease-activating factor-1 (Apaf-1) culminates in the apoptosome formation and activation of the cascade of caspase, underscoring the significance of Cytc in regulating cell death pathways. Moreover, tale of Cytc is adorned with post-translational modifications, particularly phosphorylation, which fine-tune its functions in respiration and apoptosis, adding layers of complexity to its regulatory effectiveness. Cytc becomes a lighthouse in the intricate web of cancer, its expression patterns providing hints about prognosis and paths toward treatment. Nevertheless, the story becomes more complex as Cytc becomes entangled in the metabolic reprogramming of cancer cells, implying a crucial involvement in tumor progression and treatment resistance. Collectively, these findings highlight Cytc as a multifunctional regulator of cellular fate that integrates mitochondrial respiration, apoptotic signalling, and metabolic reprogramming, suggesting new opportunities for cancer diagnosis and therapeutic intervention. Even if progress has been made, the story of Cytc is far from over, demanding more investigation into its complexities and biological consequences related to cancer. It represents a therapeutic target in the fight against cancer considering its substantial role in tumor metabolism. It promises a future in which creative solutions to the challenges of cellular destiny will be found. In this review, we have tried to highlight the multidimensional realm of Cytc, connecting threads between apoptosis, metabolic reprogramming, and the Warburg effect in line with cancer. - Source: PubMed
Publication date: 2026/04/13
Shabir AishaSofi ShaziaJan NusratHaq Burhan UlQayoom HinaMir Manzoor A - BackgroundPhysical exercise shows neuroprotective and anti-inflammatory effects in Alzheimer's disease (AD) models, but whether it modulates neuroinflammation through regulation of peripheral T-cell activity is still unresolved.ObjectiveThe present study aimed to explore the mechanisms by which aerobic exercise regulates peripheral T cell-mediated immune responses and their potential contribution to neuroinflammation in AD.MethodsMale wild-type mice and APP/PS1 transgenic mice were divided into four groups: wild-type sedentary mice (WT-SE) group, wild-type exercise group (WT-EX), APP/PS1 transgenic AD sedentary mice (AD-SE) group, and APP/PS1 transgenic AD exercise mice (AD-EX) group. The sedentary groups received no exercise training, while the exercise groups underwent a 3-month treadmill aerobic exercise intervention. At the end of the intervention, T lymphocytes were isolated from spleens. Label-free proteomics combined with LC-MS/MS was used to identify differentially expressed proteins (DEPs) and perform functional and pathway enrichment analyses. Differentially expressed protein-coding genes were validated at the mRNA level using RT-qPCR.ResultsA total of 3399 proteins were quantified across the four groups. Applying a threshold of |log fold change| > 0.67 and < 0.05, 913 DEPs were identified. These DEPs were significantly enriched in biological processes including immune system processes, protein-containing complexes, and structural molecule activity, as well as signaling pathways including AD, TGF-β, and apoptosis.ConclusionsOverall, HSP90AB1, HSP90AA1, BAG5, DNAJC8, CTSD, and ANXA1 may play a role in peripheral T-cell immune dysregulation in AD, with potential implications for central neuroinflammation. Furthermore, the beneficial effects of aerobic exercise on AD-related peripheral immune alterations, and its potential modulation of neuroinflammation, may be associated with expression changes in DEPs including Ppp2r1b, Pde2a, Casp8, Apaf-1, Dnajb11, and Dnajc13. - Source: PubMed
Publication date: 2026/03/30
Ye XingHu KaiLiu Renyi - Chronic alcohol consumption exacerbates kidney injury, particularly in individuals with hepatitis B virus (HBV) infection. This study investigated the protective effects of boric acid supplementation against alcohol-induced renal damage in HBV transgenic mice. HBV transgenic mice were divided into four groups: control (C), boric acid (B), alcohol (A), and alcohol + boric acid (A + B). Renal injury was evaluated using H&E, PAS, TUNEL, and desmin staining. The expression of caspase-3, cytochrome c, and APAF-1 was analyzed by qRT-PCR. Biochemical analyses included BUN, creatinine, oxidative stress markers (ROS, MDA, TOS, OSI), total antioxidant status, and antioxidant enzyme activities (SOD, CAT, GPx). Histopathological findings showed activated parietal epithelial cells in all groups, indicating renal injury. Alcohol significantly increased tubular damage, podocyte desmin expression, apoptosis, cytochrome c and APAF-1 mRNA levels, and oxidative stress markers, while reducing antioxidant enzyme activities and BUN levels compared with controls. Boric acid supplementation significantly mitigated alcohol-induced tubular injury, apoptosis, oxidative stress, and serum creatinine levels, and improved BUN values. Boric acid treatment alone also alleviated glomerular and tubular injury and reduced tubular apoptosis compared with HBV control mice. Overall, boric acid exerts renoprotective effects in HBV-transgenic mice subjected to chronic alcohol exposure by inhibiting oxidative stress, apoptosis, and podocyte injury. - Source: PubMed
Publication date: 2026/03/03
Sevgin KubraErguven PelinTanrikulu-Kucuk SevdaDegirmencioglu SevginCetinalp PinarAksu SonerGun-Atak PalmetSogut Ibrahim - Tail resorption is a hallmark of amphibian metamorphosis, yet the underlying molecular mechanisms remain incompletely understood. To address these deficiencies, we integrated morphological, histological, transcriptomic, and metabolomic analyses to explore tail resorption in Fejervarya multistriata. Tadpole tail regressed during metamorphosis, whereas the limbs gradually developed to maturity. Correspondingly, the expression levels of genes encoding motor proteins were lower in the tail than in the hindlimbs, supporting a functional shift from tail to limb locomotion. Tail resorption is driven by three cellular processes: MMP mediated ECM degradation, autophagy, and apoptosis. Our transcriptomic analysis revealed key regulatory genes involved in these processes, including ECM-related genes (mmp9, mmp14, and mmp18), autophagy-related genes (atg4, gabarap, atg12, and atg16l), and apoptosis-related genes (bid, bax, apaf1, casp7, and casp9). Metabolomic data indicated palmitoylcarnitine and pAzPC as potential apoptosis indicators. Overall, our findings offer insights into the molecular basis of tail resorption and provide a multi-omics resource that will facilitate future studies of this process. - Source: PubMed
Publication date: 2026/03/21
Li WanzhuZhang JiahuiWang DahaiHe JinfanZhou XutingwenWang Hongyuan