PGP9.5, monoclonal antibody, mouse, 100 ul.
- Known as:
- PGP9.5, mab (anti-), mouse, 100 ul.
- Catalog number:
- MO25010-100
- Category:
- -
- Supplier:
- Neuromi
- Gene target:
- PGP9.5 monoclonal antibody mouse 100 .
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- The ketogenic diet (KD), a high-fat, low-carbohydrate diet, can effectively regulate energy metabolism in the brain. The regulation of cerebral energy metabolism in patients with Alzheimer's disease (AD) has attracted the attention of researchers. Recent studies have shown that ubiquitin carboxyl terminal hydrolase L1 (Uch-L1) deficiency leads to neurodegeneration by increasing energy demand and endoplasmic reticulum stress. However, the effect of Uch-L1 on AD remains to be explored. This study first combined Uch-L1 with cerebral energy metabolism to explore its role in long-term KD in AD. We found that AD mice with long-term KD showed better spatial recognition and working memory. KD promoted Uch-L1(C) and Mfn2 expression by inhibiting oxidative stress in the hippocampus of mice, improved mitochondrial function, increased ATP content, and significantly reduced neuronal apoptosis. In conclusion, KD can increase Uch-L1(C) and Mfn2 expression in the brain, and improve cerebral energy metabolism and cognitive function in AD mice. - Source: PubMed
Publication date: 2026/04/20
Bao NanaZhang MinTang MingShen ZiyiWang ShenglinJiang Guohui - Osteosarcoma is an aggressive bone malignancy with limited treatment options. Ubiquitin carboxyl-terminal hydrolase L1 (UCHL1) is implicated in tumor progression, but its role in osteosarcoma remains unclear. This study investigates UCHL1's function and explores cryptochlorogenic acid (CCA) as a potential inhibitor. Bioinformatics analysis of GEO datasets (GSE19276, GSE152048) identified UCHL1 overexpression in osteosarcoma. In vitro experiments used Saos2 cells for UCHL1 knockdown (shRNA) and CCA treatment, assessing proliferation (CCK-8, EdU), migration (Transwell, wound healing), and apoptosis (Western blot). Co-immunoprecipitation and ubiquitination assays evaluated UCHL1-LDHB interaction. In vivo, subcutaneous xenograft models tested CCA and UCHL1-LDHB efficacy in mice. UCHL1 was overexpressed in osteosarcoma tissues and Saos2 cells. UCHL1 knockdown suppressed proliferation, migration, and upregulated apoptosis markers (Bax, caspase-8/9). Mechanistically, UCHL1 bound and deubiquitinated LDHB, stabilizing this metabolic enzyme. LDHB knockdown reversed UCHL1-driven oncogenesis. Virtual screening identified CCA as a UCHL1 inhibitor, forming hydrogen bonds with Cys90/Phe160. CCA treatment inhibited Saos2 proliferation, migration, and tumor growth in vivo. Xenografts showed reduced PCNA and elevated Bax expression with CCA. UCHL1 promotes osteosarcoma progression by stabilizing LDHB via deubiquitination. CCA, a natural UCHL1 inhibitor, demonstrates significant anti-tumor efficacy, offering a novel therapeutic strategy for osteosarcoma. - Source: PubMed
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