annexin v binding buffer (Miltenyi Biotec)
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annexin v binding buffer
Annexin V Binding Buffer, supplied by Miltenyi Biotec, used in various techniques. Bioz Stars score: 97/100, based on 88 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
https://www.bioz.com/product/binding+buffer/Annexin+V+Binding+Buffer/pmc13087468-52-7-22
Average 97 stars, based on 88 article reviews
Annexin V Binding Buffer, supplied by Miltenyi Biotec, used in various techniques. Bioz Stars score: 97/100, based on 88 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
https://www.bioz.com/product/binding+buffer/Annexin+V+Binding+Buffer/pmc13087468-52-7-22
Average 97 stars, based on 88 article reviews
annexin v binding buffer - by Bioz Stars,
2026-09
97/100 stars
Images
1) Product Images from "Targeting the G-protein–coupled estrogen receptor: a novel therapeutic strategy in cutaneous T-cell lymphoma ∗ "
Article Title: Targeting the G-protein–coupled estrogen receptor: a novel therapeutic strategy in cutaneous T-cell lymphoma
Journal: Blood Neoplasia
doi: 10.1016/j.bneo.2026.100213
Figure Legend Snippet: G-1 induces apoptosis in CTCL cells. (A) For a 48-hour period, CTCL cells were exposed to either 500nM G-1 or DMSO. Cells were then stained for 20 minutes with Annexin V-FITC and 7-AAD. Annexin V–positive cells were analyzed by flow cytometry. Representative data shown from n = 3 independent experiments (left panel) and mean value of n = 3 independent experiments with SD (right panel). (B) The activation of caspase-3/7 by G-1 was assessed using the Caspase-Glo 3/7 assay. Cells were treated for 24 hours with 500nM G-1. The resulting caspase activity was normalized against cells treated with DMSO, which served as the untreated control. Mean values of n = 3 independent experiments with SD are plotted. (C) Different durations of treatment with DMSO or 500nM G-1 were applied to HuT and MyLa cells. Western blot analysis was used to evaluate protein expression levels. GAPDH served as a loading control. Representative plot of n = 3 independent experiments. Western blots were imaged digitally. Brightness and contrast were adjusted globally for each blot to improve clarity; no individual lanes were modified or removed. (D) Densitometric quantification of western blots shown in panel C. Band intensities were quantified using Image Studio, normalized to the loading control and expressed as fold change relative to DMSO (set to 1). Bars represent mean ± SD of n = 3 independent experiments. 7-AAD, 7-aminoactinomycin D; cIAP1, cellular inhibitor of apoptosis protein-1; DMSO, dimethyl sulfoxide; FITC, fluorescein isothiocyanate; GAPDH, glyceraldehyde-3-phosphate dehydrogenase; PARP, poly(ADP-ribose) polymerase; SD, standard deviation.
Techniques Used: Staining, Flow Cytometry, Activation Assay, Caspase-Glo Assay, Activity Assay, Control, Western Blot, Expressing, Modification, Standard Deviation
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![PGCs are more sensitive to DNA double-strand breaks than somatic cells. (A) Cell viability curves after 24 h treatment with increasing concentrations of etoposide (ETP; x-axis shows log 10 [ETP]). PGC viability dropped sharply even at low ETP doses, whereas CEF cells were more tolerant (viability data are mean ± SD of triplicates). (B) Apoptosis detection in PGCs treated with low-dose ETP. The proportion of Annexin V + /PI + cells (late apoptosis) was significantly elevated even at 0.03 µM ETP. (C) Western blot analysis of γ-H 2 AX protein in PGCs treated with varying ETP concentrations (left panel; β-actin as loading control). The bar graph (right) shows the ratio of γ-H 2 AX to β-actin band intensity, with a marked increase at 3 µM ETP (p-values are indicated in the figure). (D) Quantification of γ-H 2 AX foci per cell in THP-1 cells, male PGCs, and female PGCs after exposure to X-ray doses of 0, 2, 4, 6, and 8 Gy. After 48 h recovery, γ-H 2 AX foci increased significantly with higher radiation in THP-1, male PGCs, and female PGCs. Female PGC data points are red squares; male PGCs are blue squares; THP-1 are black circles. (E) Cell-cycle distribution of male vs. female PGCs after DNA damage. PGCs were irradiated (2, 4, 6 Gy), cultured 48 h, and analyzed by flow cytometry for cell-cycle phase (propidium iodide staining). Stacked bars show the percentage of cells in G 0 G 1 , S, and G 2 /M phases in untreated vs. irradiated cells. After damage, female PGCs predominantly arrested in G 2 /M (increased G 2 fraction), whereas male PGCs accumulated in S phase. Statistical significance by one-way ANOVA (p-values are indicated in the figure).](https://pub-med-central-images-cdn.bioz.com/pub_med_central_ids_ending_with_1053/pmc13011053/pmc13011053__gr3.jpg)