384 well v bottom polypropylene plate (Greiner Bio)
Greiner Bio is a verified supplier 
96
Structured Review
Greiner Bio
384 well v bottom polypropylene plate
384 Well V Bottom Polypropylene Plate, supplied by Greiner Bio, used in various techniques. Bioz Stars score: 96/100, based on 206 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
https://www.bioz.com/product/384+well+v+bottom+polypropylene+plate/Microplate+384+Well+Pp+Small+Volume/pm41872176-347-13-18
Average 96 stars, based on 206 article reviews
384 Well V Bottom Polypropylene Plate, supplied by Greiner Bio, used in various techniques. Bioz Stars score: 96/100, based on 206 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
https://www.bioz.com/product/384+well+v+bottom+polypropylene+plate/Microplate+384+Well+Pp+Small+Volume/pm41872176-347-13-18
Average 96 stars, based on 206 article reviews
384 well v bottom polypropylene plate - by Bioz Stars,
2026-09
96/100 stars
Images
Related Articles
Recombinant:Article Title: Structure-Based Exploration of Selectivity for ATM Inhibitors in Huntington's Disease. Article Snippet: Our group has recently shown that brain-penetrant ataxia telangiectasia-mutated (ATM) kinase inhibitors may have potential as novel therapeutics for the treatment of Huntington’s disease (HD).. However, the previously described pyranonethioxanthenes (e.g., 4) failed to afford selectivity over a vacuolar protein sorting 34 (Vps34) kinase, an important kinase involved with autophagy.. Given that impaired autophagy has been proposed as a pathogenic mechanism of neurodegenerative diseases such as HD, achieving selectivity over Vps34 became an important objective for our program. Article Title: ATM kinase inhibitors and compositions and methods of use thereof Article Snippet: .. ATM: Recombinant, full length human FLAG-tagged ATM activity (Eurofins 14-933) was measured in an ELISA for p53 S15 phosphorylation, in a Article Title: Optimization of Potent and Selective Ataxia Telangiectasia-Mutated Inhibitors Suitable for a Proof-of-Concept Study in Huntington’s Disease Models Article Snippet: Genetic and pharmacological evidence indicates that reduction of ataxia telangiectasiamutated (ATM) kinase activity can ameliorate mutant huntingtin (mHTT) toxicity in cellular and animal models of Huntington’s disease (HD), suggesting that selective inhibition of ATM could provide a novel clinical intervention to treat HD.. Here we describe the development and characterization of ATM inhibitor molecules to enable in vivo proof-of-concept studies in HD animal models.. Starting from previously reported ATM inhibitors, we aimed with few modifications to increase brain exposure by decreasing P-glycoprotein (P-gp) liability, while maintaining potency and selectivity. Activity Assay:Article Title: Structure-Based Exploration of Selectivity for ATM Inhibitors in Huntington's Disease. Article Snippet: Our group has recently shown that brain-penetrant ataxia telangiectasia-mutated (ATM) kinase inhibitors may have potential as novel therapeutics for the treatment of Huntington’s disease (HD).. However, the previously described pyranonethioxanthenes (e.g., 4) failed to afford selectivity over a vacuolar protein sorting 34 (Vps34) kinase, an important kinase involved with autophagy.. Given that impaired autophagy has been proposed as a pathogenic mechanism of neurodegenerative diseases such as HD, achieving selectivity over Vps34 became an important objective for our program. Article Title: ATM kinase inhibitors and compositions and methods of use thereof Article Snippet: .. ATM: Recombinant, full length human FLAG-tagged ATM activity (Eurofins 14-933) was measured in an ELISA for p53 S15 phosphorylation, in a Article Title: Optimization of Potent and Selective Ataxia Telangiectasia-Mutated Inhibitors Suitable for a Proof-of-Concept Study in Huntington’s Disease Models Article Snippet: Genetic and pharmacological evidence indicates that reduction of ataxia telangiectasiamutated (ATM) kinase activity can ameliorate mutant huntingtin (mHTT) toxicity in cellular and animal models of Huntington’s disease (HD), suggesting that selective inhibition of ATM could provide a novel clinical intervention to treat HD.. Here we describe the development and characterization of ATM inhibitor molecules to enable in vivo proof-of-concept studies in HD animal models.. Starting from previously reported ATM inhibitors, we aimed with few modifications to increase brain exposure by decreasing P-glycoprotein (P-gp) liability, while maintaining potency and selectivity. Enzyme-linked Immunosorbent Assay:Article Title: Structure-Based Exploration of Selectivity for ATM Inhibitors in Huntington's Disease. Article Snippet: Our group has recently shown that brain-penetrant ataxia telangiectasia-mutated (ATM) kinase inhibitors may have potential as novel therapeutics for the treatment of Huntington’s disease (HD).. However, the previously described pyranonethioxanthenes (e.g., 4) failed to afford selectivity over a vacuolar protein sorting 34 (Vps34) kinase, an important kinase involved with autophagy.. Given that impaired autophagy has been proposed as a pathogenic mechanism of neurodegenerative diseases such as HD, achieving selectivity over Vps34 became an important objective for our program. Article Title: ATM kinase inhibitors and compositions and methods of use thereof Article Snippet: .. ATM: Recombinant, full length human FLAG-tagged ATM activity (Eurofins 14-933) was measured in an ELISA for p53 S15 phosphorylation, in a Article Title: Optimization of Potent and Selective Ataxia Telangiectasia-Mutated Inhibitors Suitable for a Proof-of-Concept Study in Huntington’s Disease Models Article Snippet: Genetic and pharmacological evidence indicates that reduction of ataxia telangiectasiamutated (ATM) kinase activity can ameliorate mutant huntingtin (mHTT) toxicity in cellular and animal models of Huntington’s disease (HD), suggesting that selective inhibition of ATM could provide a novel clinical intervention to treat HD.. Here we describe the development and characterization of ATM inhibitor molecules to enable in vivo proof-of-concept studies in HD animal models.. Starting from previously reported ATM inhibitors, we aimed with few modifications to increase brain exposure by decreasing P-glycoprotein (P-gp) liability, while maintaining potency and selectivity. Phospho-proteomics:Article Title: Structure-Based Exploration of Selectivity for ATM Inhibitors in Huntington's Disease. Article Snippet: Our group has recently shown that brain-penetrant ataxia telangiectasia-mutated (ATM) kinase inhibitors may have potential as novel therapeutics for the treatment of Huntington’s disease (HD).. However, the previously described pyranonethioxanthenes (e.g., 4) failed to afford selectivity over a vacuolar protein sorting 34 (Vps34) kinase, an important kinase involved with autophagy.. Given that impaired autophagy has been proposed as a pathogenic mechanism of neurodegenerative diseases such as HD, achieving selectivity over Vps34 became an important objective for our program. Article Title: ATM kinase inhibitors and compositions and methods of use thereof Article Snippet: .. ATM: Recombinant, full length human FLAG-tagged ATM activity (Eurofins 14-933) was measured in an ELISA for p53 S15 phosphorylation, in a Article Title: Optimization of Potent and Selective Ataxia Telangiectasia-Mutated Inhibitors Suitable for a Proof-of-Concept Study in Huntington’s Disease Models Article Snippet: Genetic and pharmacological evidence indicates that reduction of ataxia telangiectasiamutated (ATM) kinase activity can ameliorate mutant huntingtin (mHTT) toxicity in cellular and animal models of Huntington’s disease (HD), suggesting that selective inhibition of ATM could provide a novel clinical intervention to treat HD.. Here we describe the development and characterization of ATM inhibitor molecules to enable in vivo proof-of-concept studies in HD animal models.. Starting from previously reported ATM inhibitors, we aimed with few modifications to increase brain exposure by decreasing P-glycoprotein (P-gp) liability, while maintaining potency and selectivity. Glycoproteomics:Article Title: Unraveling cross-reactivity of anti-glycan IgG responses in filarial nematode infections Article Snippet: .. Briefly, fractions were aliquoted to a |