CASP3 Antibody
- Known as:
- CASP3 Antibody
- Catalog number:
- 32018
- Product Quantity:
- USD
- Category:
- -
- Supplier:
- Signalway
- 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
- Pyroptosis, a form of inflammatory programmed cell death, plays a dual role in tumor progression and anti-tumor immunity. Its comprehensive clinical and biological significance in intrahepatic cholangiocarcinoma (iCCA) remains to be elucidated. - Source: PubMed
Publication date: 2026/05/07
Zhao BinhanZhu YongjiJin ZiyangLi XiangLin KainanWang YifanLu YunkunHua Wen - The dedifferentiation of chondrocytes significantly restricts their functional performance and practical applications. In our previous research, an easily preparable microcavitary alginate hydrogel (MCG) was shown to effectively promote the redifferentiation of dedifferentiated chondrocytes. Building on this, the present study further investigates the transcriptomic changes during chondrocyte dedifferentiation, utilizing high-throughput RNA sequencing to explore how MCG regulates passage-four dedifferentiated porcine chondrocytes over a 28-day period. Integrated analysis of transcriptomic profiling data across multiple time points identified the p53 signaling pathway as a potentially central regulatory node. Key findings validated by quantitative real-time polymerase chain reaction, Western blot, and Cell Counting Kit-8 assays demonstrated the following: (1) MCG arrested the progression of dedifferentiation, downregulated fibrosis/degeneration markers (COL1A1, WNT5A/B), and partially restored chondrogenic gene expression relative to P4; (2) Time-series analysis revealed MCG's influence on cell cycle regulation, extracellular matrix organization, DNA repair, and differentiation processes; (3) Crucially, MCG dynamically regulated the p53 pathway: early activation (TP53, p-p53 Ser15, MDM2) promoted DNA repair (RRM2B) and suppressed excessive inflammation/apoptosis (IL6/8, PMAIP1/CASP3), while subsequent attenuation of the pathway correlated with enhanced late-stage proliferation. In conclusion, the growth factor-free MCG microenvironment alleviates chondrocyte dedifferentiation and facilitates partial redifferentiation by orchestrating cellular behaviors through dynamic regulation of the p53 pathway-particularly via enhanced DNA repair-thereby offering a promising strategy for cell-based therapeutic approaches. - Source: PubMed
Publication date: 2026/05/07
Yao YongchangSu WeixianNie YupengSun HaoyangWang RuiLiu RixuDong Weiqiang - Acrylamide (ACR) is an environmental reproductive toxicant with unclear testicular toxicity mechanisms. Retinoids are a group of vitamin A-related compounds that function by activating retinoid receptors. We aimed in this study to further explore All-trans retinoic acid's (ATRA) protective response against an acrylamide-induced testicular insult model and the underlying possible mechanisms. Fifty male rats were allocated into control, DMSO, ACR (40 mg/kg bwt, i.p. daily for 14 days), ATRA (7.5 mg/kg bwt, i.p. daily), and ACR + ATRA groups. Body and testes weights, sperm parameters, testosterone level, and lactate dehydrogenase-X (LDH-X) activity were measured. In addition, testicular levels of glutathione (GSH), superoxide dismutase (SOD), catalase (CAT), malondialdehyde (MDA), tumor necrosis factor-alpha (TNF-α), interleukin-1β (IL-1β), interleukin-6 (IL-6), caspase-3, Bax, and Bcl-2 were determined. Also, tissues were examined for histopathologic changes and immune expression of retinoic acid receptor-alpha (RAR-α). ACR exposure led to reduced body and testicular weights, impaired sperm parameters, and suppressed reproductive hormones (testosterone, FSH, LH). Testicular LDH-X activity decreased, along with reduced testicular RAR-α expression. Oxidative stress resulted in GSH depletion, reduced CAT and SOD activities, and increased MDA. ACR also triggered inflammation and apoptosis, with elevated TNF-α, IL-1β, IL-6, caspase-3, Bax. In contrast, ATRA improved sperm parameters and levels of hormones, restored RAR-α expression, mitigated oxidative stress, and decreased inflammation and apoptosis markers. Morphometric and histopathologic studies supported these biochemical observations. Overall, RAR-α agonist (ATRA) is linked to attenuation against ACR-induced testicular damage, along with a reduction in oxidative stress, inflammation, and cell death. These findings suggest that retinoid signaling might serve as a possible therapeutic target for reproductive toxicities induced by ACR, necessitating further mechanistic exploration. - Source: PubMed
Publication date: 2026/05/07
Mokhlis Hamada AhmedRashed Mohammed HelmySaleh Ibrahim GhalibEldeib Mahmoud GomaaEl-Husseiny Ahmed AKhidr Emad GamilGomaa Maher HGad Hesham SElnagar Mohamed RMokhtar Mahmoud MohamedAglan Ahmed - Tongue cancer is recognized globally as a prevalent oral cancer, with squamous cell carcinoma accounting for over 90% of oral cancer diagnoses. Tongue squamous cell carcinoma (SCC) has a poor survival rate and is highly invasive. The present study aimed to investigate the effect of the therapeutic agent gelsemine on SAS cells line derived from tongue squamous. Gelsemine was found to induce significant cell shrinkage and morphological changes. In addition, gelsemine significantly increased apoptosis, cytotoxicity and expression of signaling proteins related to apoptosis, namely cleaved PARP and caspase-3/-7, in dose-dependent maanner. Additionally, gelsemine increased the reactive oxygen species (ROS) generation, again depending on the dose. In terms of protein expression, pretreatment with the antioxidant N-acetyl-l-cysteine (NAC) reversed the increases in PARP and caspase-3/-7 caused by gelsemine. Gelsemine effectively increased the levels of JNK1/2 phosphorylation while not affecting ERK1/2 and p38 phosphorylation. Pretreatment with the specific JNK inhibitor SP600125 reversed the increases cleaved PARP and caspase-3/-7 caused by gelsemine. Both NAC and SP600125 reduced the increases in JNK1/2 phosphorylation, ROS generation and caspase-3/-7 activity caused by gelsemine. The results of the present study collectively suggested that gelsemine induces apoptosis through a ROS- and JNK1/2 -co-regulated pathway. To the best of our knowledge, this study is the first to demonstrate that gelsemine may be a potential therapeutic agent for tongue SCC. - Source: PubMed
Publication date: 2026/05/05
Wang Yao-ChienYeh Su-LingFang Kai-MinChen Ya-WenLiu Shing-HwaChang Kai-ChihChiang Su-YinHuang Chun-FaKuo Chun-YingSu Chin-Chuan - Different exercise intensities exert distinct effects on the knee joint. Overuse of the knee joint may lead to the early onset of osteoarthritis (OA), which is usually associated with injury to the superficial zone (SFZ) of articular cartilage. Proteoglycan 4 (PRG4), a representative marker of the SFZ, plays a pivotal role in articular cartilage lubrication and is mainly secreted by SFZ cells.In this study, Cre-dependent Prg4 tracing mice and wild-type mice were used, and all mice were subjected to treadmill running to induce forced movement. Additionally, the proliferation and pluripotency of SFZ cells were investigated, with relevant markers including Pcna, CD34, and others.As expected, the red fluorescence of Prg4 was significantly upregulated under moderate exercise but downregulated under excessive exercise. However, no significant changes were observed in proliferation- and stem cell-related markers, except for CD34 in the excessive exercise group. Furthermore, several anabolism and catabolism markers, such as Collagen 2, Aggrecan, and Mmp13, did not show significant changes during the exercise process.In summary, Prg4 expression increased under moderate exercise and slightly decreased under excessive exercise, which could provide guidance for formulating appropriate exercise patterns. Moreover, immunohistochemical analysis revealed that Caspase-3, one of the apoptosis markers, exhibited the same expression tendency as Prg4 during exercise.Collectively, this study demonstrated the expression patterns of Prg4 and other related markers under different exercise intensities, confirming that moderate exercise enhances Prg4 expression and that Prg4 maintains a relatively high level even under excessive exercise. Furthermore, Prg4 may regulate Caspase-3 expression through a specific signaling pathway. - Source: PubMed
Publication date: 2026/05/05
Tian PeichuSuo YaojunGuo LiLi PengcuiChen JiazhuZhang JiaweiMa YongshengZhang XuanpingWang ChunfangWei Xiaochun