computer program prism tm version 6.01 (GraphPad Software Inc)
GraphPad Software Inc is a verified supplier 
90
Structured Review
GraphPad Software Inc
computer program prism tm version 6.01
Computer Program Prism Tm Version 6.01, supplied by GraphPad Software Inc, used in various techniques. Bioz Stars score: 90/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
https://www.bioz.com/product/prism+tm+computer+program/computer+program+prism+tm+version+6+01/pmc11736643-118-0-24
Average 90 stars, based on 1 article reviews
Computer Program Prism Tm Version 6.01, supplied by GraphPad Software Inc, used in various techniques. Bioz Stars score: 90/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
https://www.bioz.com/product/prism+tm+computer+program/computer+program+prism+tm+version+6+01/pmc11736643-118-0-24
Average 90 stars, based on 1 article reviews
computer program prism tm version 6.01 - by Bioz Stars,
2026-11
90/100 stars
Images
Related Articles
other:Article Title: A Vicious NGF-p75 NTR Positive Feedback Loop Exacerbates the Toxic Effects of Oxidative Damage in the Human Retinal Epithelial Cell Line ARPE-19 Article Snippet: Data were analyzed using a Article Title: Mitochondrial oxygen consumption inhibition importance for TMT-dependent cell death in undifferentiated PC12 cells. Article Snippet: The evolving role of mitochondria as a target for different death-inducing noxae prompted us to investigate trimethyltin (TMT)-dependent effects on mitochondrial functionality.. For this purpose, we used a homogeneous cell culture model represented by undifferentiated PC12 cells.. Mitochondria isolated from PC12 cells treated with TMT for 6, 12 and 24 h, showed a time-dependent inhibition of ADP-stimulated oxygen consumption using succinate or glutamate/malate as substrate. IF-P:Article Title: Alzheimer's amyloid beta-peptide (1-42) induces cell death in human neuroblastoma via bax/bcl-2 ratio increase: an intriguing role for methionine 35. Article Snippet: The b amyloid (Ab), the major protein component of brain senile plaques in Alzheimer’s disease, is known to be directly responsible for the production of free radicals toxic to brain tissue and the redox state of Met-35 residue seems to play a particular and critical role in peptide’s neurotoxic actions.. In this study, we investigated, in human neuroblastoma cells (IMR-32), the relationship between the oxidative state of methionine, and both neurotoxic and pro-apoptotic actions induced by Ab-peptide, comparing the effects of native peptide, in which the Met-35 is present in the reduced state, with those of a modified peptide with oxidized Met-35 (Ab(1–42)), as well as an Ab-derivative with Met-35 substituted with norleucine (Ab(1–42)).. The obtained results show that Ab induces a time-dependent decrease in cell viability; Ab(1–42) was significantly less potent, though inducing a remarkable decrease in cell viability compared to control. |