Trypsin is a serine protease produced in the pancreas. Ethylenediaminetetraacetic acid (EDTA) is a chelating agent which sequesters metal ions such as Ca+2 and Mg+2, enhancing the trypsinization reaction. 0.05% Trypsin/EDTA (T/E) is a sterile, phosphate and HEPES-buffered saline solution with a pH of 7.4 at room temperature. It contains 0.05% trypsin and 0.5 mM EDTA.
胰蛋白酶（Trypsin）是一种由胰腺产生的丝氨酸蛋白酶。乙二胺四乙酸（EDTA）是一种螯合剂，可结合 Ca2+ 和 Mg2+ 等金属离子，从而增强胰蛋白酶消化反应。0.05% 胰蛋白酶/EDTA溶液（T/E）是一种无菌的磷酸盐和 HEPES 缓冲盐溶液，在室温下 pH 值为 7.4。其成分包含 0.05% 胰蛋白酶和 0.5 mM EDTA。
Product Sheets
0183
Search for a Certificate of Analysis by Lot Number below:
NAD⁺ homeostasis is vital for neuronal health, as demonstrated by the opposing roles of nicotinamide mononucleotide adenylyltransferase 2 (NMNAT2), a NAD⁺-synthesizin... More
NAD⁺ homeostasis is vital for neuronal health, as demonstrated by the opposing roles of nicotinamide mononucleotide adenylyltransferase 2 (NMNAT2), a NAD⁺-synthesizing enzyme, and sterile alpha and TIR motif-containing protein 1 (SARM1), a NAD⁺ hydrolase. Neurodegenerative insults that decrease NMNAT2 activate SARM1, leading to axon loss. To understand how the NMNAT2–SARM1 axis influences brain energy metabolism, multi-omics approaches are used to investigate the metabolic changes resulting from neuronal NMNAT2 loss. Loss of NMNAT2 in glutamatergic neurons leads to a significant metabolic shift in the cerebral cortex from glucose to lipid catabolism, reduced lipid abundance, and pronounced neurodegenerative phenotypes and motor behavioral deficits. These metabolic disturbances are accompanied by altered glial expression of enzymes regulating glucose and lipid metabolism, enhanced inflammatory signaling, and disrupted astrocytic transcriptomic profiles related to cholesterol synthesis and immune activation. Notably, SARM1 deletion in NMNAT2-deficient mice restored lipid metabolism, astrocyte transcriptomic profiles, and mitigated neurodegeneration and motor behaviors. These findings suggest that neuronal NAD⁺ depletion triggers maladaptive, SARM1-dependent metabolic reprogramming, shifting energy use from glucose to lipids, which in turn promotes inflammation and neurodegeneration. Less
ScienCell Research Laboratories (SRL) takes pride in being a resource for researchers all over the world. The publications listed here are not meant as an endorsement or confirmation of the reliability of the products.
