CATD_PIG CTSD ELISA tesk kit
- Known as:
- CATD_PIG CTSD Enzyme-linked immunosorbent assay test tesk reagent
- Catalog number:
- gen16452
- Product Quantity:
- 1
- Category:
- Peptides
- Supplier:
- Other suppliers
- Gene target:
- CATD_PIG CTSD ELISA tesk kit
Related genes to: CATD_PIG 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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- Ceritinib, an anaplastic lymphoma kinase (ALK) inhibitor, is associated with cardiovascular adverse events, yet the mechanisms remain incompletely understood. Here, we show that ceritinib impairs left ventricular systolic function in mice and induces cardiomyocyte apoptosis, and identify AKT (Ser473) suppression as a key initiating event. Loss of AKT activity is paralleled by reduced phosphorylation of mTOR (Ser2448) and ULK1 (Ser757), consistent with enhanced autophagy initiation. Concurrently, loss of inhibitory GSK3β (Ser9) phosphorylation correlates with impaired lysosomal function, reflected by disrupted cathepsin D maturation and reduced lysosomal acidification. This mismatch between enhanced autophagy initiation and impaired lysosomal clearance impairs autophagic flux despite preserved autophagosome-lysosome fusion, and causes mitochondrial damage, evidenced by reduced TOMM20 and HSP60 expression and membrane potential loss. Transcriptomic and functional analyses identify AKT2 as a particularly vulnerable isoform in this network. Metformin co-treatment preserves cardiac function and attenuates apoptosis. Mechanistically, metformin increases AMPK (Thr172) phosphorylation and reduces TFEB (Ser122) phosphorylation, restores CTSD maturation, and decreases LC3-II accumulation. These protective effects occur without reversing the suppressed AKT (Ser473) or GSK3β (Ser9) phosphorylation. Together, these findings establish that AKT suppression drives ceritinib cardiotoxicity through autophagic flux impairment and mitochondrial injury, and position AMPK-driven, TFEB-associated lysosomal restoration as a mechanism-based cardioprotective strategy independent of AKT recovery. - Source: PubMed
Publication date: 2026/08/21
Jiang FengFu Huang-XiWang LanPan Ze-ZhengJiang Yan-QiLiu NingChen Xue-QinGao Zi-ZhengWu Wen-TongYan HaoYang Xiao-ChunYang BoHe Qiao-JunLuo Pei-HuaXu Zhi-Fei - This study proposes a 2π solid angle-based heuristic framework for non-coplanar volumetric modulated arc therapy (VMAT) in patients with multiple brain metastases (MBM) to automate treatment angle selection.
Approach: Fifty-two patients with MBM (2-8 targets) were retrospectively included. A hybrid heuristic framework was constructed: first, a volume-weighted cumulative tumor-skin distance (VW-CTSD) metric was introduced to quantify geometric requirements in the 2π solid angle space and to automatically identify non-coplanar trajectories minimizing normal brain exposure. Subsequently, a blocking factor (BF)-based sub-arc segmentation and collimator-angle selection strategy determined the sub-arc splitting and collimator angles. Using 30 Gy/5 fractions, three plans were generated for each patient: manual expert planning (Pref), VW-CTSD-guided trajectory selection alone (Ptsd), and the proposed combined heuristic strategy (Pcom). Dosimetric metrics and plan parameters were compared.
Main results: All plans met clinical goals. Ptsd achieved automated trajectory selection with plan quality comparable to Pref. Values are presented as median (P25-P75). Compared with Pref, Pcom improved CI [0.86 (0.85-0.89) to 0.89 (0.85-0.91)] and reduced GI [3.37 (3.17-3.79) to 3.09 (2.74-3.48)]. Pcom also reduced normal brain tissue (NBT) V12Gy, MU, and complexity metric (CM) from 92.45 (62.54-141.46) to 83.57 (50.30-125.10) cc, from 2391 (2144-2527) to 1938 (1845-2085), and from 0.22 (0.21-0.24) to 0.20 (0.19-0.21), respectively. Control-point aperture analysis showed X-axis narrowing [129.75 (110.60-146.35) to 101.91 (83.34-120.20) mm] and Y-axis expansion [98.70 (80.13-105.86) to 119.17 (103.38-133.48) mm] in Pcom. All Pcom-versus-Pref comparisons for these metrics were statistically significant (P < 0.001).
Significance: The proposed combined heuristic framework reduced NBT dose, GI, MU, and CM, suggesting its potential as a practical automated approach for non-coplanar VMAT angle selection in patients with MBM. - Source: PubMed
Publication date: 2026/08/18
Huang ShixiongYang SonghuaDong YangHuang ShengLi Xiao-HuaZeng Biao - Hepatic insulin resistance (HIR), an early feature of prediabetic, plays a pivotal role in disrupting glucose homeostasis. Clarifying the mechanisms underlying HIR is critical for diabetes prevention. Our previous study has discovered the positive correlations between plasma cathepsin D (CTSD) activity and the degree of HIR in people with obesity. Accordingly, this study investigates the roles of CTSD in the underlying mechanisms involving HIR and impaired glucose homeostasis. - Source: PubMed
Publication date: 2026/08/12
Ding LinglingJiang PengZou YuxiChen YanyanChen TingWang ShujinHe ChanglongQian Hui - Pathological choroidal neovascularization underlies vision loss in neovascular age-related macular degeneration (nAMD), yet the molecular regulators coordinating vascular and immune components remain incompletely defined. Here, we investigated the role of the endolysosomal cation channel, two-pore channel 2 (TPC2) in choroidal angiogenesis. Loss of TPC2 in mice markedly reduced ex vivo choroidal sprouting, while pharmacological activation enhanced vascular growth. Mechanistically, Tpc2-deficiency led to downregulation of multiple microglia-derived pro-angiogenic factors and impaired the ability of the microglial secretome to stimulate neovascularization. In choroidal vascular cells, TPC2 loss attenuated NF-κB/MAPK signaling pathways. Tpc2-deficiency is also associated with lysosomal secretion of cathepsins, especially CTSD, resulting in decreased extracellular proteolytic activity and impaired paracrine regulation of angiogenesis. Extending these findings to human cells, TPC2 knockout in iPSC-derived endothelial cells impaired migration, tube formation, and CTSD activity in the secretome, mirroring the murine phenotype. Together, these results establish TPC2 as one of the regulators of lysosome-mediated choroidal angiogenesis, highlighting its potential as a therapeutic target in nAMD. - Source: PubMed
Publication date: 2026/08/12
Lu YiReschigna AliceKynast FranzYang ZhuoGerhardt MaximillianKielkowski PavelPriglinger SiegfriedBiel MartinMichalakis Stylianos - Cocaine abuse can damage various organ systems; however, the molecular mechanisms underlying its potential contribute to chronic obstructive pulmonary disease (COPD) remain poorly understood. In this study, an integrative computational framework was used to investigate the molecular links between cocaine exposure and COPD and to identify potential key targets and regulatory mechanisms. Cocaine‑associated targets and COPD‑related differentially expressed genes (DEGs) were collected from public databases and transcriptomic datasets, yielding 34 overlapping DEGs that may be associated with both cocaine exposure and COPD. Functional enrichment and protein-protein interaction network analyses indicated that DEGs were mainly involved in cancer-, inflammation-, and virus-related pathways. Three machine learning algorithms combined with network topology analysis identified cathepsin D (CTSD) as a core target associated with multiple immune cell types. Single-cell RNA sequencing analysis further showed that CTSD is highly expressed in macrophages. Virtual knockout analysis using scTenifoldKnk identified 113 consistently responsive genes, which were functionally enriched in autoimmune reactions, infection-induced immune activation, and antigen presentation pathways. Molecular docking and molecular dynamics simulations demonstrated strong binding affinity and stable interactions between cocaine and CTSD, supporting a potential mechanistic role in COPD related to cocaine exposure. Additionally, ten CTSD-associated drugs were identified from DSigDB and evaluated using molecular docking, pharmacokinetic analysis, and druglikeness assessment. Collectively, this study highlights CTSD as a candidate molecular target linking cocaine exposure to COPD and provides a theoretical basis for future experimental and toxicological investigations. - Source: PubMed
Publication date: 2026/08/04
Luo WeiHe Ming-KeGuo Mao-RunZhao Guo-JianHu Rui-Si