Results 181 to 190 of about 1,020,842 (327)
SIRT1 Prevents Lens Epithelial Cell Senescence During Age‐Related Cataract via Regulating p66Shc
Schematic illustration of NMN‐mediated alleviation of age‐related cataract via SIRT1/p66Shc pathway–dependent inhibition of mitochondrial dysfunction and LEC senescence. ABSTRACT Lens epithelial cell (LEC) senescence is one of the key pathological processes of age‐related cataract (ARC) and is associated with oxidative stress, mitochondrial dysfunction,
Huirui Liu+8 more
wiley +1 more source
Importância da pesquisa da Beta-galactosidase na caracterização laboratorial da Neisserialactamica
Ilka Maria Landgraf Lee+4 more
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Transcriptomic and cellular analyses of BubR1 hypomorphic hearts reveal disruptions in key pathways and upregulation of markers linked to impaired cardiac structure and function. Comparative transcriptomic analysis shows that BubR1 insufficiency mirrors changes seen in aged and failing hearts. A key finding of this study is that BubR1 levels decline in
Renju Pun+13 more
wiley +1 more source
STUDIES ON BETA-N-ACETYLHEXOSAMINIDASE AND BETA-GALACTOSIDASE FROM TURBO CORNUTUS
KWOK-KAM YEUNG
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Healthy RPE cells produce AMPs and AMP precursors, including amyloid precursor protein (APP) and chemerin, and protect the neuroretina from blood‐borne pathogens and maintain homeostasis. When RPE cells undergo senescence, the antibacterial activity declines, and APP undergoes amylogenesis, leading to Aβ deposition.
Jian Liu+7 more
wiley +1 more source
The maintenance of aging mesenchymal stem cells (MSCs) on extracellular matrix synthesized by human amniotic fluid‐derived pluripotent stem cells (ECM Plus), a young microenvironment, remarkably restored their quantity and quality along with up‐regulating HLA‐DR and CD74.
Aaron O. Gonzalez+10 more
wiley +1 more source
Use of fluorescein-di-beta-D-galactopyranoside (FDG) and C12-FDG as substrates for beta-galactosidase detection by flow cytometry in animal, bacterial, and yeast cells [PDF]
Antonia Plovins+4 more
openalex +1 more source
Bifidobacterium pseudocatenulatum NCU‐08, isolated from the feces of centenarians, facilitated the entry of L‐tryptophan into hippocampal neurons of SAMP8 mice, where it was metabolized into NAD+. The increased NAD+ levels activated Sirt1 protein, thereby suppressing the expression of senescence‐associated proteins P53, P21, and Rb, ultimately delaying
Tangchang Xu+8 more
wiley +1 more source