Ask about this productRelated genes to: CASP3 Blocking Peptide
- 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
Related products to: CASP3 Blocking Peptide
Related articles to: CASP3 Blocking Peptide
- Ionizing radiation (IR) generates reactive oxygen species (ROS), resulting in oxidative imbalance and tissue injury. The nuclear factor erythroid 2-related factor 2 (Nrf2)-antioxidant response element (ARE) pathway regulates antioxidant gene expression; however, effective radiomodulatory agents remain limited. Resveratrol (RES), a natural antioxidant with anti-inflammatory and ROS-scavenging properties, has been proposed as a potential radioprotective compound. - Source: PubMed
Publication date: 2026/09/09
Fekry Hader OAbdelrahman Ibrahim YSoliman Saeed MAbdelkader Nour MEl-Sayed Wael M - Tumor Necrosis Factor-Induced Protein 1 (TNIP1) is a well-known ubiquitin-binding signaling molecule involved in innate and adaptive inflammatory processes. It has been implicated in diverse immunological diseases, but also associated with various neuro-psychiatric conditions, including Alzheimer's disease, glioma formation, and demyelination. However, a systematic analysis of TNIP1 expression and function in the central nervous system is missing. Here, we combine immunohistochemical staining, Western blotting, quantitative PCR and the re-analysis of publicly available single cell- and in situ hybridization-mRNA datasets to document the expression of TNIP1 in the developing and adult murine cerebellum. We document that TNIP1 is broadly expressed in cerebellar neurons and macroglial cells, where it is localized to discrete puncta within cell nuclei and somata, including Purkinje cell dendrites. Both TNIP1 and its mRNA are developmentally regulated in the early postnatal cerebellum, and levels of the latter vary systematically across the cell cycle. Consistently, overexpression of TNIP1 in human embryonic kidney cells inhibits proliferation and activates cleaved caspase-3 expression. These observations support a role for TNIP1 in neur(on)al development and function and establish a paradigm to study the mechanistic basis of its function in the normal and diseased nervous system. - Source: PubMed
Publication date: 2026/09/09
Göttsche Esperança Clara CarolinaMichael SpoelgenRoeser Sebastian PSchilling KarlBaader Stephan L - Glyphosate-based herbicides (GBHs) are widely used worldwide. Increasing evidence has raised concerns about their hepatotoxic effects. While oxidative stress, inflammation, and apoptosis contribute to glyphosate-induced liver damage, the roles of intracellular cyclic nucleotides and vascular endothelial growth factor (VEGF) are not fully understood. This study investigated the dose-dependent effects of glyphosate on liver function, oxidative status, intracellular cyclic nucleotides, inflammatory mediators, apoptotic markers, and VEGF in adult female Wistar rats. Twenty-eight female Wistar rats were randomly assigned to four groups (n = 7/group) and administered orally either distilled water (control) or glyphosate at doses of 250, 500, or 1000 mg/kg/day for 30 days. Serum aminotransferase activities and total antioxidant status (TAS), total oxidant status (TOS), oxidative stress index (OSI), cyclic adenosine monophosphate (cAMP), cyclic guanosine monophosphate (cGMP), tumor necrosis factor-α (TNF-α), interleukin-1β (IL-1β), caspase-3, VEGF, Bax/Bcl-2 immunoreactivity, and histopathological changes were evaluated. Dose-response relationships were assessed using polynomial trend analysis. Glyphosate exposure caused dose-dependent increases in AST, TOS, OSI, TNF-α, IL-1β, caspase-3, VEGF, and the Bax/Bcl-2 ratio, accompanied by decreases in TAS, cAMP, and cGMP, as well as progressive histopathological changes. Polynomial trend analysis showed significant linear dose-response relationships for all biomarkers, while OSI, caspase-3, VEGF, and the Bax/Bcl-2 ratio showed significant deviations from linearity at higher glyphosate doses. These findings suggest that glyphosate-induced hepatotoxicity is associated with coordinated alterations in oxidative status, intracellular cyclic nucleotide homeostasis, inflammatory responses, apoptosis, and hepatic VEGF levels. - Source: PubMed
Publication date: 2026/09/09
Gokdemir Gul SahikaDurmaz Sevda CanbayDemirtaş SelimBaksi NazanGokdemir Mehmet Tahir - Clinical co-occurrence of Parkinson's disease (PD) and age-related bone loss in elderly patients has garnered increasing attention, yet its molecular mechanisms remain incompletely elucidated. This study used an 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP)-induced PD model in Ace2 mice to investigate the regulatory mechanisms of bone-brain axis-related genes and signaling pathways. Behavioral tests assessed motor and non-motor symptoms. Immunohistochemistry, Western blot, and histopathological staining analyzed dopaminergic neuron activity, microglial activation, and bone metabolic abnormalities. GEO dataset transcriptomics and weighted gene co-expression network analysis (WGCNA) identified key hub genes, with receiver operating characteristic (ROC) curves evaluating their diagnostic value in public single-disease transcriptome data. MPTP significantly exacerbated motor dysfunction and depression-like behaviors; Ace2 deletion lowered total Wnt, β-catenin, BMP and IGF-1 protein abundance alongside reduced phosphorylation ratios of their downstream kinases in brain and bone, while upregulating RANKL/RANK/OPG-associated inflammatory mediators, accompanied by elevated total α-synuclein, Casp3 and Bax protein levels. The parallel reduction of these signaling proteins only suggests potential perturbation of related cascades; WGCNA identified 10 hub genes (e.g., DNM1, OCRL, OPA1), whose dysregulation was linked to synaptic dysfunction and inflammation. ROC analysis based on single-disease datasets showed high diagnostic accuracy for PD and `osteoporosis (OP) (AUC: 0.683-0.981), with core genes influencing synaptic, MAPK, Rap1, and Ras pathways. These preclinical findings indicate that Ace2 deficiency is associated with concurrent pathological abnormalities in the brain and transient bone metabolic disturbance under short-term MPTP treatment in growing young male mice; coordinated dysregulation of shared signaling pathways was observed in the two tissues, consistent with a potential bone-brain axis pathological phenotype, though causal bidirectional tissue cross-talk cannot be confirmed in the current experimental design, providing candidate targets that warrant further validation. - Source: PubMed
Publication date: 2026/09/09
Liu TingtingRen YuhengTian XinghuaWei Jianshe - Hepatitis C virus (HCV) has developed multiple means to disrupt host innate immune response to promote its replication. Protein kinase D1 (PKD1) is a serine/threonine kinase involved in cell proliferation and lipid metabolism. By analyzing the effect of PKD1 on HCV replication, we found that HCV activated PKD1 via protein kinase C (PKC) early in infection and induced the cleavage of PKD1 at later timepoints of infection via caspase-3. PKD1 silencing had no effect on HCV entry, but it reduced HCV RNA levels in cells, indicating an important role of PKD1 in promoting HCV replication. PKD1 silencing also induced the expression of interferons (IFNs) and IFN-stimulated genes (ISGs) and augmented the HCV-induced TNF-α expression, which enhanced the IFN response. Interestingly, the induction of inflammasomes was compromised in HCV-infected cells in the absence of PKD1, indicating an important role of PKD1 in promoting the inflammasomal response. Taken together, our results indicated that HCV activated PKD1 to suppress the IFN response and TNF-α signaling and in the meantime induce the inflammasomal response. Our results, thus, revealed an interesting interplay between HCV and host innate immune responses and an important role of PKD1 in this intricate interplay. - Source: PubMed
Publication date: 2026/09/09
Lee JiyoungChuang Yu-ChenLee Johanna AhnOu J-H James