softmaxpro 3.1.1 software (SoftMax Inc)
90
Structured Review
SoftMax Inc
softmaxpro 3.1.1 software
Softmaxpro 3.1.1 Software, supplied by SoftMax 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/softmaxpro+software/softmaxpro+3+1+1+software/pm16771835-97-13-16
Average 90 stars, based on 1 article reviews
Softmaxpro 3.1.1 Software, supplied by SoftMax 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/softmaxpro+software/softmaxpro+3+1+1+software/pm16771835-97-13-16
Average 90 stars, based on 1 article reviews
softmaxpro 3.1.1 software - by Bioz Stars,
2026-10
90/100 stars
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Fluorescence:Article Title: Induction of Bcl-2 by functional regulation of G-protein coupled receptors protects from oxidative glutamate toxicity by increasing glutathione. Article Snippet: Glutamate treatment depletes hippocampal HT22 cells of glutathione, which renders the cells incapable to reduce reactive oxygen species and ultimately cumulates in cell death by oxidative stress.. HT22 cells resistant to glutamate displayed increased phosphorylation of cAMP-response-element binding (CREB) and decreased ERK1/2 suggestive of differences in signal transmission.. We investigated the amount of candidate G-protein-coupled receptors involved in this resistance and found an increase in mRNA for receptors activated by the vasoactive intestinal peptide VIP (VPAC2, 12.6-fold) and glutamate like the metabotropic glutamate receptor mGlu1 (5.3-fold). Article Title: Cooperative action of glutamate transporters and cystine/glutamate antiporter system Xc- protects from oxidative glutamate toxicity. Article Snippet: Oxidative glutamate toxicity in the neuronal cell line HT22 is a model for cell death by oxidative stress.. In this paradigm, an excess of extracellular glutamate blocks the glutamate/cystine-antiporter system X c , depleting the cell of cysteine, a building block of the antioxidant glutathione.. Loss of glutathione leads to the accumulation of reactive oxygen species and eventually cell death. Software:Article Title: Induction of Bcl-2 by functional regulation of G-protein coupled receptors protects from oxidative glutamate toxicity by increasing glutathione. Article Snippet: Glutamate treatment depletes hippocampal HT22 cells of glutathione, which renders the cells incapable to reduce reactive oxygen species and ultimately cumulates in cell death by oxidative stress.. HT22 cells resistant to glutamate displayed increased phosphorylation of cAMP-response-element binding (CREB) and decreased ERK1/2 suggestive of differences in signal transmission.. We investigated the amount of candidate G-protein-coupled receptors involved in this resistance and found an increase in mRNA for receptors activated by the vasoactive intestinal peptide VIP (VPAC2, 12.6-fold) and glutamate like the metabotropic glutamate receptor mGlu1 (5.3-fold). Article Title: Cooperative action of glutamate transporters and cystine/glutamate antiporter system Xc- protects from oxidative glutamate toxicity. Article Snippet: Oxidative glutamate toxicity in the neuronal cell line HT22 is a model for cell death by oxidative stress.. In this paradigm, an excess of extracellular glutamate blocks the glutamate/cystine-antiporter system X c , depleting the cell of cysteine, a building block of the antioxidant glutathione.. Loss of glutathione leads to the accumulation of reactive oxygen species and eventually cell death. |