CATD_RAT Ctsd ELISA tesk kit
- Known as:
- CATD_RAT Ctsd Enzyme-linked immunosorbent assay test tesk reagent
- Catalog number:
- gen16454
- Product Quantity:
- 1
- Category:
- Peptides
- Supplier:
- Other suppliers
- Gene target:
- CATD_RAT Ctsd ELISA tesk kit
Related genes to: CATD_RAT Ctsd ELISA tesk kit
- Gene:
- CTSD NIH gene
- Name:
- cathepsin D
- Previous symbol:
- CPSD
- Synonyms:
- CLN10
- Chromosome:
- 11p15.5
- Locus Type:
- gene with protein product
- Date approved:
- 1986-01-01
- Date modifiied:
- 2014-11-18
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- Alzheimer's disease (AD) is characterized by amyloid-β (Aβ) accumulation, impaired proteostatic clearance, and oxidative damage, all of which contribute to neuronal dysfunction and disease progression. Fucoxanthin (FX), a marine-derived carotenoid abundant in brown algae, has shown antioxidant and neuroprotective potential. However, its role in autophagy-lysosome dysfunction and ferroptosis-associated oxidative injury under amyloidogenic conditions remains unclear. In this study, the effects of FX were investigated in APP Swedish mutant-expressing Neuro2a (SweAPP N2a) cells treated with 0.1-5 μM FX and in 5XFAD transgenic mice orally administered FX at 200 mg kg. FX treatment increased LC3-II expression and reduced p62 accumulation in SweAPP N2a cells, indicating enhanced autophagic degradation. FX also increased the expression of the lysosomal markers LAMP1 and cathepsin D (CTSD), suggesting enhanced lysosome-associated degradative capacity. These responses were accompanied by AMPK activation and suppression of mTOR signaling, together with increased autophagic flux as confirmed by bafilomycin A1-based analysis. Moreover, FX significantly reduced intracellular ROS levels and lipid peroxidation marker 4-hydroxynonenal (4-HNE), while modulating ferroptosis-associated proteins, including GPX4 and FTH1. Consistent with the cellular findings, FX administration in 5XFAD mice modulated autophagy-lysosome-related and ferroptosis-associated proteins in the brain and significantly reduced ThS-positive amyloid plaque burden. Collectively, these findings demonstrate that FX enhances autophagy-lysosome-associated proteostatic regulation through AMPK/mTOR signaling and attenuates ferroptosis-linked oxidative injury under amyloidogenic conditions. These results provide mechanistic evidence supporting the role of FX as a marine-derived bioactive compound for modulating AD-related pathological processes. - Source: PubMed
Publication date: 2026/06/23
Lee NayoungYoun KumjuMoon MinhoLee Dong-SeokKim Dong HyunHo Chi-TangJun Mira - Our previous preclinical study determined artesunate as a candidate drug for hepatocellular carcinoma (HCC) and identified glucosylceramidase (GBA) as one of its direct targets. This research aimed to identify the binding sites of GBA with artesunate and the potential anti-HCC mechanisms, which remain unclear. Artesunate effectively suppressed cell viability and proliferation, and enhanced apoptosis of HCC cell lines with more sensitivity in HepG2 than MHCC-97H cells. Network calculation and a series of and experimental data demonstrated that the apoptosis-related GBA-ceramide-CTSD-BID-BAX signaling was one of the key putative target pathways by which artesunate may inhibit the malignant progression of HCC. Furthermore, through integrated computational and experimental approaches, we identified Y313, E340, and N396 as critical binding residues within the GBA active site. Mutagenesis studies revealed that these residues were indispensable for the interaction, with E340R and N396R mutations exhibiting the most pronounced impairment in binding affinity and enzymatic activity, respectively. Crucially, disrupting this binding interface abolished artesunate's ability to modulate the downstream apoptotic pathway. Our findings provide the first structural and mechanistic elucidation of artesunate's target engagement with GBA, unveiling a specific signaling cascade for its anti-HCC activity and establishing a foundational framework for developing novel GBA-targeted therapies. - Source: PubMed
Publication date: 2026/01/20
Mao XiaYan XiangyingChen YawenCai BingbingChen WenjiaLin YaLin NaZhang Yanqiong - Accumulating evidence has demonstrated a significant association between e-cigarette exposure and airway epithelial damage. Nevertheless, the molecular drivers orchestrating this pathology remain unclear. Here, we demonstrated that nicotine is the key component of e-cigarette aerosols that induced pathogenic changes, including apoptosis, oxidative stress, and mucus overproduction, in mouse airway epithelium and in human bronchial epithelial (HBE) cells. We further established that the nicotine of e-cigarette aerosols induced autophagosome formation via MTOR inhibition, while concurrently suppressing autolysosomal degradation through lysosomal membrane permeabilization (LMP). Restoration of lysosomal membrane integrity reversed e-cigarette aerosol-induced LMP and the subsequent macroautophagy/autophagy inhibition, thereby alleviating airway epithelial damage. Mechanistically, nicotine of e-cigarette aerosols permeabilized lysosomal membranes via calcium-dependent activation of PLA2G4A, which hydrolyzed the sn-2 ester bond of lysosomal glycerophospholipids, generating lysophospholipids. This process was initiated by nicotine binding to CHRNA3/α3 nAChR, a ligand-gated ion channel whose activation triggered intracellular Ca overload. Genetic or pharmaceutical inhibition of CHRNA3 reduced intracellular Ca content, abolishing PLA2G4A activation. This inhibited lysosomal glycerophospholipid hydrolysis, thereby attenuating LMP and subsequently resolving autophagic flux blockade and cytotoxicity in HBE cells. Moreover, the role of CHRNA3-mediated PLA2G4A activation in e-cigarette aerosol-induced autophagy-lysosome dysfunction and cellular toxicity was validated in human lung organoids. Overall, our study underscores the importance of CHRNA3 activation, as a molecular initiating event (MIE), in the regulation of PLA2G4A-mediated hydrolysis of glycerophospholipids and autophagic flux impairment, and CHRNA3 inhibition could serve as a potential therapy for airway disorders induced by e-cigarette aerosols.: AACOCF3: arachidonyl trifluoromethyl ketone; AB-PAS: Alcian Blue Periodic Acid Schiff; ANXA5: annexin V; AOP: adverse outcome pathway; ATG: autophagy related; BECN1: beclin 1; CASP3: caspase 3; CASP7: caspase 7; CASP9: caspase 9; CQ: chloroquine; CHRNA/nAChR: cholinergic receptor nicotinic alpha subunit; CTSD: cathepsin D; DHE: dihydroethidium; DMSO: dimethyl sulfoxide; E-cigarette: electronic cigarette; ENGASE/NAG: endo-beta-N-acetylglucosaminidase; FBS: fetal bovine serum; GA: geldanamycin; GSH: glutathione; HBE: human bronchial epithelial; HEX: hexamethonium; LAMP: lysosome associated membrane protein; LC-MS/MS: liquid chromatography-tandem mass spectrometry; LGALS3: galectin 3; LBD: ligand-binding domain; LMP: lysosomal membrane permeabilization; LPC: lysophosphatidylcholine; LPE: lysophosphatidylethanolamine; MAP1LC3/LC3B: microtubule associated protein 1 light chain 3 beta; MDA: malondialdehyde; MIE: molecular initiating event; MTBE: methyl tert-butyl ether; MTOR: mechanistic target of rapamycin kinase; mtROS: mitochondrial reactive oxygen species; NBR1: NBR1 autophagy cargo receptor; PBS: phosphate-buffered saline; PC: diacyl glycerophosphatidylcholine; PE: diacyl glycerophosphatidylethanolamine; Penh: pulmonary resistance; PG: propylene glycol; PLA2G4A/cPLA2: phospholipase A2 group IVA; PLA2G4E: phospholipase A2 group IVE; ROS: reactive oxygen species; siRNA: small interfering RNA; SOD: superoxide dismutase; SQSTM1/p62: sequestosome 1; TEM: transmission electron microscopy; TUNEL: terminal deoxynucleotidyl transferase dUTP nick end labeling; VG: vegetable glycerin. - Source: PubMed
Publication date: 2026/06/21
Yu YongquanXu ShuyuYang LiuShu ShugeZhou HaojieHua ZhenchengWang LiZhu YingranShi AimingXia RongChen ChaoWang Shou-Lin - - Source: PubMed
Publication date: 2026/06/11
Marth LenaMarques André R ANoachtar SoheylRémi JanWeidinger EndyErnst KatharinaSchöberl FlorianGnörich Johannes SBrendel MatthiasBiskup SaskiaHöglinger GünterLevin JohannesNuebling Georg - Backfat thickness is an economically important trait in pig production, yet the functional regulatory variants underlying it remain poorly characterized. Here, we performed a genome-wide association study (GWAS) for backfat thickness at 100 kg (BF100) in a large Landrace population (n = 5923) using 13.46 million imputed SNPs. We identified two significant quantitative trait loci (QTLs) on SSC2 (1.21-3.69 Mb; explaining 2.3% of phenotypic variance) and SSC12 (51.70-52.88 Mb; explaining 0.8% of phenotypic variance). While nonsynonymous SNPs were limited (16 variants), we prioritized functional non-coding variants by integrating high-resolution Hi-C interaction maps, epigenomic marks, and previously published enhancer and promoter annotation results from public backfat datasets. This multi-omics strategy revealed that the SSC2 QTL functions as an active three-dimensional regulatory hub, with over 20 enhancer-promoter loops physically engaging the promoters of IGF2, CTSD, TSPAN32, and TSSC4. Similarly, the SSC12 QTL formed more than 10 long-range interactions with the promoters of ASGR1, YBX2, GPS2, MDPU1, and TP53. Focusing on SSC2, we prioritized two tightly linked SNPs (2-1280617 and 2-1280654) located within a putative enhancer, representing two major haplotypes. Dual-luciferase reporter assays in PK15 and 3T3-L1 cells confirmed that the GG haplotype drives significantly higher transcriptional activity than the AT haplotype (p < 0.001). Consistently, pigs carrying the GG haplotype exhibited significantly lower backfat thickness. By integrating multi-omics and functional assays, this study not only decodes the regulatory architecture of two backfat QTLs but also provides new molecular markers for genetic improvement in Landrace breeding. - Source: PubMed
Feng XigangZhou XiuqiLiang HaoLi JingjinYu MeiZhao ShuhongLi XinyunLi Xiaoping