CASP9 polyclonal antibody
- Known as:
- CASP9 pab (anti-)
- Catalog number:
- PAB9830
- Product Quantity:
- 100 ug
- Category:
- -
- Supplier:
- Abno
- Gene target:
- CASP9 polyclonal antibody
Related genes to: CASP9 polyclonal antibody
- Gene:
- CASP9 NIH gene
- Name:
- caspase 9
- Previous symbol:
- -
- Synonyms:
- MCH6, ICE-LAP6, APAF-3, PPP1R56
- Chromosome:
- 1p36.21
- Locus Type:
- gene with protein product
- Date approved:
- 1996-11-11
- Date modifiied:
- 2016-04-25
Related products to: CASP9 polyclonal antibody
Related articles to: CASP9 polyclonal antibody
- (), a primary exacerbating factor in eczema, remains a prevalent pathogenic public-health threat. The mechanism of mast cell/basophil degranulation in the context of -exacerbated eczema remains unclear. We sought to investigate the direct effect of mast cell/basophil activation by isolated from patients with severe eczema undergoing topical steroid withdrawal (TSW) and understand the mechanism of berberine (BBR) in inhibiting this activation. Clinical strains (N = 8) were isolated from skin swabs of severe eczema patients and confirmed by sequencing. Human basophils (KU812), rat basophils (RBL-2H3) and murine mast cells (MC/9) were pre-treated with BBR for 48 h. and stimulated with heat-killed standard - and clinical strains for 45 min, and degranulation was measured. BBR's molecular-targets on basophils were identified by computational modeling and validated by qRT-PCR. BBR prevented degranulation following standard stimulation in KU812, RBL-2H3 and MC/9 cells. BBR dose-dependently inhibited degranulation in KU812. BBR inhibited TNF-α and IL-4 release, and markedly suppressed the expression of FcεR1 (α, β, γ), TNFα, MAPK1, MAPK3, AKT2, CASP9, and CCND1 following standard stimulation. BBR dose-dependently inhibited KU812 cell degranulation, markedly reduced TNF-α, IL-4, and MAPK1 and enhanced NFκB1A expression following clinical strain stimulation. BBR inhibition of -induced KU812 activation was at least associated with inhibition of MAPK-associated gene expression. This study provides novel insights into BBR's effect in preventing and human basophil interaction. - Source: PubMed
Publication date: 2026/09/03
Maskey Anish RKopulos DanielSpears MadisonWang Zhen-ZhenMo XianMusa IbrahimYang NanNowak-Wegrzyn AnnaChung DannaMaitland Anne LWang JulieTiwari Raj KSampson Hugh AGeliebter JanLi Xiu-Min - Estrogen deficiency after menopause is a major driver of osteoporosis and has been increasingly linked to dysregulated cellular stress responses, including autophagy and apoptosis, that affect bone remodeling and microarchitecture. - Source: PubMed
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Gao HongweiMa PengchengChen HuizhiZhang ZhengkaiDavtyan NaraZheng Jiachun - Tetraconazole, a triazole fungicide, is widely used in agriculture and is frequently detected in aquatic environments, where it may affect non‑target organisms. However, its developmental toxicity and the underlying mechanisms of action remain poorly understood. In this study, the effects of tetraconazole on zebrafish embryonic development were investigated based on physiological and behavioral changes as well as associated toxicological pathways. Tetraconazole exposure induced morphological abnormalities and mitochondrial dysfunction, as evidenced by decreased mitochondrial respiration, increased reactive oxygen species production, and reduced expression of antioxidant enzyme genes sod1, cat, gpx1a, and gpx1b. Furthermore, acridine orange and TUNEL staining revealed elevated apoptosis, which was supported by dysregulated expression of bcl2l1, bax, and casp9. In parallel, tetraconazole modulated Erk and Akt signaling and induced multiorgan toxicity, as demonstrated in transgenic reporter lines for the cardiovascular (cmlc2:dsRED and fli1a:EGFP), nervous (olig2:dsRED, gfap:EGFP, and gad1b:EGFP), and metabolic organs (fabp10a:dsRED, elastase:EGFP, and insulin:EGFP), revealing defects in cardiac function, neurobehavior, vascular development, and hepatopancreatic differentiation. Collectively, these findings indicate that tetraconazole functions as a potent developmental toxicant in zebrafish embryos by inducing mitochondrial dysfunction‒mediated oxidative stress and interfering with physiological and behavioral processes, ultimately disrupting Erk/Akt-dependent signaling networks and leading to widespread organ-level abnormalities. - Source: PubMed
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Hong TaeyeonLee HojunJeong WooyoungSong GwonhwaLim Whasun - Glioblastoma (GBM) is the most aggressive primary brain tumor in adults, with limited therapeutic options and poor survival. Resistance to standard temozolomide (TMZ) therapy remains a major challenge, necessitating novel agents. Tropolone derivatives, particularly the synthetic trichlorotropolone JO-122(2), have shown broad preclinical antitumor activity. This study aimed to determine whether JO-122(2), alone or combined with TMZ, can suppress GBM growth in vivo and to define the accompanying changes in the p53/MDM2/Bcl-2 apoptotic axis. - Source: PubMed
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Kit Oleg IMaksimov Aleksey YuGolovinov Igor VKuznetsova Natalia SKaplieva Irina VKhodakova Daria VSagakyants Alexander BGalina Anastasia VShulga Anna AGurova Sofya VBondarenko Elena SRostorguev Eduard ESayapin Yurii AGusakov Eugeny A - Corneal crosslinking (CXL) using riboflavin and ultraviolet A (UV-A) illumination is widely used to stabilize progressive ectatic corneal disorders such as keratoconus. However, the photochemical reaction generates oxidative stress and may induce apoptosis, while potential differences between healthy human corneal fibroblasts (HCF) and human corneal fibroblasts derived from keratoconus corneas (KC-HCF) remain insufficiently understood. This study examined in-vitro changes in pro- and anti-apoptotic markers in HCF and KC-HCF following riboflavin-UV-A illumination. - Source: PubMed
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