mitochondrial dynamics antibody sampler kit ii Search Results


mitochondrial dynamics antibody sampler kit  (Cell Signaling Technology Inc)
93
Cell Signaling Technology Inc mitochondrial dynamics antibody sampler kit
High glucose increases <t>mitochondrial</t> fission in neurons and induces neuron apoptosis in HT22 (A-G, upper panel) and neurons (H-N, lower panel). Representative blots and densitometric quantification of DRP1, OPA1, and caspase proteins in HT22 (A–C) and neurons (H–J) . The phosphorylation of DRP1 (top blots) was normalized to total DRP1 protein (middle), and total DRP1 was normalized to β-ACTIN (bottom). Fluorescent signals and quantification of Mitotracker-Red CM-H2X ROS in HT22 (D–E) and primary neurons (K–L) stimulated with high glucose. (200 ×, Bar = 800 µm). Hoechst labeled the nuclei (blue), and Mitotracker-Red CM-H2X ROS was stained in red (Fluor 594). Fluorescent signals and quantification of TUNEL in HT22 (F–G) and primary neurons (M–N) stimulated with high glucose. (200 ×, Bar = 800 µm). DAPI labeled the nuclei (blue), and TUNEL was stained in red (Fluor 594). Data presented as means ± SEM, * p < 0.05 vs cells under control condition by One-way ANOVA.
Mitochondrial Dynamics Antibody Sampler Kit, supplied by Cell Signaling Technology Inc, used in various techniques. Bioz Stars score: 93/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
https://www.bioz.com/product/mitochondrial+dynamics+antibody+sampler+kit+ii/Mitochondrial+Dynamics+Antibody+Sampler+Kit+II/pmc08981993-79-0-18
Average 93 stars, based on 1 article reviews
mitochondrial dynamics antibody sampler kit - by Bioz Stars, 2026-09
93/100 stars
  Buy from Supplier

Image Search Results


High glucose increases mitochondrial fission in neurons and induces neuron apoptosis in HT22 (A-G, upper panel) and neurons (H-N, lower panel). Representative blots and densitometric quantification of DRP1, OPA1, and caspase proteins in HT22 (A–C) and neurons (H–J) . The phosphorylation of DRP1 (top blots) was normalized to total DRP1 protein (middle), and total DRP1 was normalized to β-ACTIN (bottom). Fluorescent signals and quantification of Mitotracker-Red CM-H2X ROS in HT22 (D–E) and primary neurons (K–L) stimulated with high glucose. (200 ×, Bar = 800 µm). Hoechst labeled the nuclei (blue), and Mitotracker-Red CM-H2X ROS was stained in red (Fluor 594). Fluorescent signals and quantification of TUNEL in HT22 (F–G) and primary neurons (M–N) stimulated with high glucose. (200 ×, Bar = 800 µm). DAPI labeled the nuclei (blue), and TUNEL was stained in red (Fluor 594). Data presented as means ± SEM, * p < 0.05 vs cells under control condition by One-way ANOVA.

Journal: Frontiers in Pharmacology

Article Title: Metformin Protects Against Diabetes-Induced Cognitive Dysfunction by Inhibiting Mitochondrial Fission Protein DRP1

doi: 10.3389/fphar.2022.832707

Figure Lengend Snippet: High glucose increases mitochondrial fission in neurons and induces neuron apoptosis in HT22 (A-G, upper panel) and neurons (H-N, lower panel). Representative blots and densitometric quantification of DRP1, OPA1, and caspase proteins in HT22 (A–C) and neurons (H–J) . The phosphorylation of DRP1 (top blots) was normalized to total DRP1 protein (middle), and total DRP1 was normalized to β-ACTIN (bottom). Fluorescent signals and quantification of Mitotracker-Red CM-H2X ROS in HT22 (D–E) and primary neurons (K–L) stimulated with high glucose. (200 ×, Bar = 800 µm). Hoechst labeled the nuclei (blue), and Mitotracker-Red CM-H2X ROS was stained in red (Fluor 594). Fluorescent signals and quantification of TUNEL in HT22 (F–G) and primary neurons (M–N) stimulated with high glucose. (200 ×, Bar = 800 µm). DAPI labeled the nuclei (blue), and TUNEL was stained in red (Fluor 594). Data presented as means ± SEM, * p < 0.05 vs cells under control condition by One-way ANOVA.

Article Snippet: Mitochondrial Dynamics Antibody Sampler Kit, p -AMPK, AMPK, caspase 3, cleaved caspase 3, ATG5, ATG7, β-actin purchased from Cell Signaling Technology (CST, Boston, MA), while Pink1 antibody was purchased from Novus Biologicals (Colorado, CO).

Techniques: Phospho-proteomics, Labeling, Staining, TUNEL Assay, Control

Inhibition of mitochondrial fission decreases oxidative stress and reduces apoptosis in HT22 ( (A–F) , upper panel) and neurons ( (G–L) , lower panel). Representative blots and densitometric quantification of phosphorylated DRP1 and caspase 3 in HT22 (A–B) and neurons (G–H) . The phosphorylation of DRP1 (top blots) was normalized to total DRP1 protein (middle), and total DRP1 was normalized to β-ACTIN (bottom). The cleaved of caspase3 (top blots) was normalized to caspase3 protein (middle), and caspase3 was normalized to β-ACTIN (bottom). Fluorescent signals and quantification of Mitotracker-Red CM-H2X ROS in HT22 (C–D) and primary neurons (I–J) stimulated with high glucose (200 ×, Bar = 800 µm). Fluorescent TUNEL signals and quantification in HT22 (E–F) and primary neurons (K–L) stimulated with high glucose. (200 ×, Bar = 800 µm). DAPI labeled the nuclei (blue), and TUNEL was stained in red (Fluor 594). Data presented as means ± SEM, * p < 0.05 vs cells under control condition, # p < 0.05 vs cells stimulated with high glucose by One-way ANOVA.

Journal: Frontiers in Pharmacology

Article Title: Metformin Protects Against Diabetes-Induced Cognitive Dysfunction by Inhibiting Mitochondrial Fission Protein DRP1

doi: 10.3389/fphar.2022.832707

Figure Lengend Snippet: Inhibition of mitochondrial fission decreases oxidative stress and reduces apoptosis in HT22 ( (A–F) , upper panel) and neurons ( (G–L) , lower panel). Representative blots and densitometric quantification of phosphorylated DRP1 and caspase 3 in HT22 (A–B) and neurons (G–H) . The phosphorylation of DRP1 (top blots) was normalized to total DRP1 protein (middle), and total DRP1 was normalized to β-ACTIN (bottom). The cleaved of caspase3 (top blots) was normalized to caspase3 protein (middle), and caspase3 was normalized to β-ACTIN (bottom). Fluorescent signals and quantification of Mitotracker-Red CM-H2X ROS in HT22 (C–D) and primary neurons (I–J) stimulated with high glucose (200 ×, Bar = 800 µm). Fluorescent TUNEL signals and quantification in HT22 (E–F) and primary neurons (K–L) stimulated with high glucose. (200 ×, Bar = 800 µm). DAPI labeled the nuclei (blue), and TUNEL was stained in red (Fluor 594). Data presented as means ± SEM, * p < 0.05 vs cells under control condition, # p < 0.05 vs cells stimulated with high glucose by One-way ANOVA.

Article Snippet: Mitochondrial Dynamics Antibody Sampler Kit, p -AMPK, AMPK, caspase 3, cleaved caspase 3, ATG5, ATG7, β-actin purchased from Cell Signaling Technology (CST, Boston, MA), while Pink1 antibody was purchased from Novus Biologicals (Colorado, CO).

Techniques: Inhibition, Phospho-proteomics, TUNEL Assay, Labeling, Staining, Control

(A) Representative picture of mitochondria in hippocampal neurons (upper) and measurement of mitochondria short/long axis ratio (lower) (39 mitochondria from metformin treatment, 45 from Mdivi-1 treatment, n = 3, 200,00×, Bar = 0.5 µm) (B) Representative picture of a synaptic gap in the hippocampus (upper) and measurements of synaptic gap and PSD (lower) (30 synapses from metformin treatment, 26 from Mdivi-1 treatment, n = 3, 500,00×, Bar = 200 nm). (C) Representative picture of dendritic spines in the hippocampus (upper) and counts of dendritic spines per dendrite (lower) (23 dendrites from metformin treatment, 14 from Mdivi-1 treatment, n = 3, 500,00×, Bar = 200 nm). Metformin and Mdivi-1 protect against diabetes-induced cognitive dysfunction in short-term memory (D) , long-term memory (E) , and spatial disorientation (F) . Data presented as means ± SEM, * p < 0.05 vs m/m control, # p < 0.05 vs db -/- control by One-way ANOVA (G) Schematic diagram. High glucose increases mitochondrial fragments by activating DRP1 protein, resulting in elevated oxidative stress and cell apoptosis. Metformin inhibits DRP1 phosphorylation, reduces mitochondrial-derived oxidative stress, and prevents neuron loss.

Journal: Frontiers in Pharmacology

Article Title: Metformin Protects Against Diabetes-Induced Cognitive Dysfunction by Inhibiting Mitochondrial Fission Protein DRP1

doi: 10.3389/fphar.2022.832707

Figure Lengend Snippet: (A) Representative picture of mitochondria in hippocampal neurons (upper) and measurement of mitochondria short/long axis ratio (lower) (39 mitochondria from metformin treatment, 45 from Mdivi-1 treatment, n = 3, 200,00×, Bar = 0.5 µm) (B) Representative picture of a synaptic gap in the hippocampus (upper) and measurements of synaptic gap and PSD (lower) (30 synapses from metformin treatment, 26 from Mdivi-1 treatment, n = 3, 500,00×, Bar = 200 nm). (C) Representative picture of dendritic spines in the hippocampus (upper) and counts of dendritic spines per dendrite (lower) (23 dendrites from metformin treatment, 14 from Mdivi-1 treatment, n = 3, 500,00×, Bar = 200 nm). Metformin and Mdivi-1 protect against diabetes-induced cognitive dysfunction in short-term memory (D) , long-term memory (E) , and spatial disorientation (F) . Data presented as means ± SEM, * p < 0.05 vs m/m control, # p < 0.05 vs db -/- control by One-way ANOVA (G) Schematic diagram. High glucose increases mitochondrial fragments by activating DRP1 protein, resulting in elevated oxidative stress and cell apoptosis. Metformin inhibits DRP1 phosphorylation, reduces mitochondrial-derived oxidative stress, and prevents neuron loss.

Article Snippet: Mitochondrial Dynamics Antibody Sampler Kit, p -AMPK, AMPK, caspase 3, cleaved caspase 3, ATG5, ATG7, β-actin purchased from Cell Signaling Technology (CST, Boston, MA), while Pink1 antibody was purchased from Novus Biologicals (Colorado, CO).

Techniques: Control, Phospho-proteomics, Derivative Assay