CASP3 Antibody
- Known as:
- CASP3 Antibody
- Catalog number:
- abx000602
- Product Quantity:
- EUR
- Category:
- -
- Supplier:
- Abbexa
- Gene target:
- CASP3 Antibody
Related genes to: CASP3 Antibody
- 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 Antibody
Related articles to: CASP3 Antibody
- This study aimed to determine whether repetitive transcranial magnetic stimulation (rTMS) is associated with changes in motor recovery and apoptosis-related pathways after spinal cord injury (SCI), and to characterize the temporal dependence of these effects. A rat model of SCI was established using Allen's method, and rTMS was initiated on day 2 post-injury. Western blot and immunofluorescence were used to quantify apoptosis-related execution-phase proteins, including caspase-3, cleaved caspase-3, caspase-7, PARP1, and cleaved PARP1, and to assess their cellular distribution. Double immunofluorescence of NeuN and cleaved caspase-3 was performed to identify the localization of apoptotic signals. TUNEL staining, HE staining, and BBB scores were used to assess apoptotic cell death, tissue injury, and motor recovery. rTMS was associated with time-dependent changes, with limited effects at early stages but reduced apoptosis-related signaling and improved tissue preservation and functional recovery at later time points. Co-localization of NeuN and cleaved caspase-3 indicated that apoptotic signaling was localized in neurons. These findings suggest that rTMS is associated with reduced activation of apoptosis-related execution-phase signaling after SCI in a time-dependent manner, together with enhanced tissue preservation and functional recovery. The caspase-3/caspase-7/PARP1 cleavage axis may be involved in the biological changes associated with rTMS treatment after SCI. - Source: PubMed
Publication date: 2026/05/24
Hu DandanXu QingqinLei QianHu MengxuanChen HemuLi JianChen YingGao Xiaoping - The skin barrier function is essential for maintaining skin health. Consequently, it is crucial to evaluate the protective and restorative effects of topical medications and cosmetics on the skin barrier. However, methods that can directly assess the skin barrier function in zebrafish beyond their regenerative capabilities are limited. Therefore, we aimed to develop an , , high-throughput screening model for assessing skin barrier function in zebrafish embryos. - Source: PubMed
Publication date: 2026/05/24
Tao QinqianHe MingjieZeng JiaqiWang YaxinChen XingmeiLi YingxinYan ErpingZhao Haishan - Intracerebral hemorrhage (ICH) is a devastating form of stroke with limited treatment options. Although exercise is beneficial in ischemic stroke, its preconditioning effects in hemorrhagic stroke remain unclear. We examined whether voluntary wheel running prior to ICH modulates acute outcomes and gene expression. Male ICR mice underwent three weeks of voluntary running or sedentary housing before ICH induction. Neurological function was assessed 3 days post-ICH, and perihematomal tissue was analyzed by quantitative PCR. ICH increased expression of Iba1, GFAP, C3, MMP9, TIMP1, and Caspase3, while reducing BDNF expression. Exercise preconditioning did not improve acute behavioral deficits at the group level. However, running distance strongly predicted molecular and pathological responses. BDNF expression correlated positively with exercise volume, whereas C3 showed a negative correlation, with a similar trend for GFAP. Caspase3 and Bax expression were negatively correlated with running distance. Although hematoma volume did not differ significantly between groups, greater running distance was associated with smaller hematoma volume within the exercise group. These findings indicate that habitual voluntary exercise does not attenuate acute functional deficits after ICH but induces dose-dependent molecular adaptations related to neuroplasticity, glial inflammation, and cell death, potentially priming the brain for enhanced recovery in later phases. - Source: PubMed
Oka YuichiroSugiyama TakuyaChen KeTakamura HanaLiu YushanDing YuanShishido GinjiroMaejima Hiroshi - Glioblastoma (GB) is one of the most aggressive brain tumours, with low survival rates despite combined radiation and chemotherapy. The blood-brain barrier (BBB) limits the delivery and efficacy of many chemotherapeutic agents, highlighting the need for more effective and alternative therapeutic strategies. 5-Ethynyl-2-deoxyuridine (EdU), a thymidine analogue capable of crossing the BBB, has recently been investigated for its effects on cellular processes in glioma, particularly in relation to replication stress and DNA damage responses. This study aimed to investigate the effects of EdU on apoptosis, autophagy, and cell cycle regulation in U87-MG glioma cells (PTEN mutant, p53 wild-type) using both 2D monolayer and 3D spheroid culture models. EdU exposure significantly reduced glioma cell proliferation and migration, was associated with increased apoptotic markers including cleaved caspase-3, and modulated autophagy-related markers including LC3A, LAMP2A, and HSC70 expression. Moreover, EdU exposure was associated with alterations in epithelial-mesenchymal transition (EMT) markers, including decreased N-cadherin and β-catenin and increased E-cadherin levels, and with reduced nuclear translocation of Hsp70.In 3D spheroid cultures, 50 μM EdU significantly reduced spheroid growth and migration, supporting its biological activity in a physiologically relevant model. These findings suggest that EdU-induced cellular stress responses may represent a potential area for further investigation in glioblastoma, particularly in relation to autophagy and apoptosis. Further studies are warranted to better understand the underlying mechanisms and potential applications of EdU in glioblastoma. - Source: PubMed
Publication date: 2026/05/23
Gencel-Güler CerenÖnay Uçar Evren - High temperature stress is the main cause of mass summer mortality in the Yesso scallop (Patinopecten yessoensis). Among the various cellular responses upon high temperature stress, apoptosis serves as a critical regulatory process, with cysteinyl aspartate specific proteinase-3 (Caspase-3) acting as a central executor. In the present study, a Caspase-3 homolog PyCaspase-3 with a typical CASc domain was identified in P. yessoensis. PyCaspase-3 mRNA was constitutively expressed in all examined scallop tissues, with the highest expression level observed in the haemocytes. The mRNA expression of PyCaspase-3 was significantly induced by high temperature, which peaked at 12 h with a 5.09-fold increase relative to 0 h (p < 0.01). Overexpression of PyCaspase-3 in HEK293T cells significantly enhanced the Caspase-3-like activity and promoted apoptosis. Conversely, knockdown of PyCaspase-3 by RNAi markedly suppressed haemocyte apoptosis under high temperature with the apoptosis rate was reduced to 0.30 times that of the EGFP group (p < 0.01). Notably, the knockdown of PyCaspase-3 enabled scallops to maintain robust physiological condition under high temperature stress, with no obvious tissue abnormalities, whereas scallops in the control group displayed pronounced mantle atrophy and tissue lesion. These findings suggested that PyCaspase-3 mediated the haemocyte apoptosis of scallop in response to high temperature stress, with important insights for further understanding the occurrence of summer mortality in scallop aquaculture. - Source: PubMed
Publication date: 2026/05/23
Hao WentongWang BoLi XiangQiao XinFeng LixinKong NingWang LinglingSong Linsheng