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Elabscience Biotechnology ferroptosis suppressor protein 1 fsp 1 inhibitor screening kit
Copper deprivation induced by SLC31A11 knockdown triggers the upregulation of SLC7A11. ( A ) Confocal imaging of Cu-probe and Mito-tracker in the NC and SLC31A1 knockdown AsPC-1 cells. Hoechst (blue) is used as a nuclear counterstain. Mean ± SD, n = 3. Statistical significance was determined using a two-way ANOVA test. Scale bar: 2 μm. ( B ) Total Fe level in the NC and SLC31A1 knockdown AsPC-1, MiaPaCa-2, and CFPAC-1 cells. Mean ± SD, n = 3. Statistical significance was determined using a one-way ANOVA test. ( C ) Volcano plot of gene expression (the SLC31A1 knockdown [shRNA#2] versus the control; log2(fold change) ≥1; p < 0.05 between SLC31A1 knockdown and NC AsPC-1 cells. ( D ) GO analysis of differentially expressed genes between SLC31A1 knockdown (shRNA#2) and NC AsPC-1 cells. ( E-G ) Western blot analysis of the indicated protein levels in the NC and SLC31A1 knockdown AsPC-1 (E), MiaPaCa-2 (F), and CFPAC-1 (G) cells. ( H and I ) GPX4 (H) <t>or</t> <t>FSP-1</t> activity (I) was tested in the NC and SLC31A1 knockdown AsPC-1 cells. Mean ± SD, n = 3. Statistical significance was determined using a one-way ANOVA test. ( J ) qPCR analysis of SLC31A1 and SLC7A11 gene expression in NC and SLC31A1 knockdown AsPC-1, MiaPaCa-2, and CFPAC-1 cells. Mean ± SD, n = 3. Statistical significance was determined using a one-way ANOVA test. ( K ) qPCR analysis of SLC31A1 and SLC7A11 gene expression in NC and SLC31A1 knockdown AsPC-1, MiaPaCa-2, and CFPAC-1 cells. Mean ± SD, n = 3. Statistical significance was determined using a one-way ANOVA test. ( L ) GSH level in the NC and SLC31A1 knockdown AsPC-1, MiaPaCa-2, and CFPAC-1 cells. Mean ± SD, n = 3. Statistical significance was determined using a one-way ANOVA test. ( M ) Cystine uptake level in the NC and SLC31A1 knockdown AsPC-1, MiaPaCa-2, and CFPAC-1 cells. Mean ± SD, n = 3. Statistical significance was determined using a one-way ANOVA test.
Ferroptosis Suppressor Protein 1 Fsp 1 Inhibitor Screening Kit, supplied by Elabscience Biotechnology, used in various techniques. Bioz Stars score: 94/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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Copper deprivation induced by SLC31A11 knockdown triggers the upregulation of SLC7A11. ( A ) Confocal imaging of Cu-probe and Mito-tracker in the NC and SLC31A1 knockdown AsPC-1 cells. Hoechst (blue) is used as a nuclear counterstain. Mean ± SD, n = 3. Statistical significance was determined using a two-way ANOVA test. Scale bar: 2 μm. ( B ) Total Fe level in the NC and SLC31A1 knockdown AsPC-1, MiaPaCa-2, and CFPAC-1 cells. Mean ± SD, n = 3. Statistical significance was determined using a one-way ANOVA test. ( C ) Volcano plot of gene expression (the SLC31A1 knockdown [shRNA#2] versus the control; log2(fold change) ≥1; p < 0.05 between SLC31A1 knockdown and NC AsPC-1 cells. ( D ) GO analysis of differentially expressed genes between SLC31A1 knockdown (shRNA#2) and NC AsPC-1 cells. ( E-G ) Western blot analysis of the indicated protein levels in the NC and SLC31A1 knockdown AsPC-1 (E), MiaPaCa-2 (F), and CFPAC-1 (G) cells. ( H and I ) GPX4 (H) <t>or</t> <t>FSP-1</t> activity (I) was tested in the NC and SLC31A1 knockdown AsPC-1 cells. Mean ± SD, n = 3. Statistical significance was determined using a one-way ANOVA test. ( J ) qPCR analysis of SLC31A1 and SLC7A11 gene expression in NC and SLC31A1 knockdown AsPC-1, MiaPaCa-2, and CFPAC-1 cells. Mean ± SD, n = 3. Statistical significance was determined using a one-way ANOVA test. ( K ) qPCR analysis of SLC31A1 and SLC7A11 gene expression in NC and SLC31A1 knockdown AsPC-1, MiaPaCa-2, and CFPAC-1 cells. Mean ± SD, n = 3. Statistical significance was determined using a one-way ANOVA test. ( L ) GSH level in the NC and SLC31A1 knockdown AsPC-1, MiaPaCa-2, and CFPAC-1 cells. Mean ± SD, n = 3. Statistical significance was determined using a one-way ANOVA test. ( M ) Cystine uptake level in the NC and SLC31A1 knockdown AsPC-1, MiaPaCa-2, and CFPAC-1 cells. Mean ± SD, n = 3. Statistical significance was determined using a one-way ANOVA test.
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Phenotypic differences between LMS-derived seeding (S3) and non-seeding (N3) cells. (A) Morphological differences were not observed between S3 and N3 under bright field microscope. (B) The graph shows that the proliferative capacity of S3 is slower than that of N3s <t>through</t> <t>High-Content</t> Screening <t>(HCS)</t> analysis. (C) The trans-well migration assay reveals that there was no significant difference in the migration ability between S3 and N3 (quantification graph). (D) Representative images from the trans-well migration assay. (E) Representative images of the wound-healing assay show that N3 filled the open area faster than S3. The white area is saturated with green color due to the overlapping of S3 without filling the wound gap. (F) Quantification graph of the wound-healing assay. (G) Adhesion of S3 and N3 cells to extracellular matrix (ECM) components, including fibronectin, collagen I, collagen IV, laminin I, and fibrinogen, was quantified after 24h of incubation. (H) Adhesion values were normalized to control conditions. All data are presented as mean ± SD from n = 3 independent experiments. Statistical comparisons between two groups were performed using a two-tailed Student’s t-test. *P < 0.05, **P < 0.01, ***P < 0.001.
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Phenotypic differences between LMS-derived seeding (S3) and non-seeding (N3) cells. (A) Morphological differences were not observed between S3 and N3 under bright field microscope. (B) The graph shows that the proliferative capacity of S3 is slower than that of N3s <t>through</t> <t>High-Content</t> Screening <t>(HCS)</t> analysis. (C) The trans-well migration assay reveals that there was no significant difference in the migration ability between S3 and N3 (quantification graph). (D) Representative images from the trans-well migration assay. (E) Representative images of the wound-healing assay show that N3 filled the open area faster than S3. The white area is saturated with green color due to the overlapping of S3 without filling the wound gap. (F) Quantification graph of the wound-healing assay. (G) Adhesion of S3 and N3 cells to extracellular matrix (ECM) components, including fibronectin, collagen I, collagen IV, laminin I, and fibrinogen, was quantified after 24h of incubation. (H) Adhesion values were normalized to control conditions. All data are presented as mean ± SD from n = 3 independent experiments. Statistical comparisons between two groups were performed using a two-tailed Student’s t-test. *P < 0.05, **P < 0.01, ***P < 0.001.
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Phenotypic differences between LMS-derived seeding (S3) and non-seeding (N3) cells. (A) Morphological differences were not observed between S3 and N3 under bright field microscope. (B) The graph shows that the proliferative capacity of S3 is slower than that of N3s <t>through</t> <t>High-Content</t> Screening <t>(HCS)</t> analysis. (C) The trans-well migration assay reveals that there was no significant difference in the migration ability between S3 and N3 (quantification graph). (D) Representative images from the trans-well migration assay. (E) Representative images of the wound-healing assay show that N3 filled the open area faster than S3. The white area is saturated with green color due to the overlapping of S3 without filling the wound gap. (F) Quantification graph of the wound-healing assay. (G) Adhesion of S3 and N3 cells to extracellular matrix (ECM) components, including fibronectin, collagen I, collagen IV, laminin I, and fibrinogen, was quantified after 24h of incubation. (H) Adhesion values were normalized to control conditions. All data are presented as mean ± SD from n = 3 independent experiments. Statistical comparisons between two groups were performed using a two-tailed Student’s t-test. *P < 0.05, **P < 0.01, ***P < 0.001.
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Image Search Results


Copper deprivation induced by SLC31A11 knockdown triggers the upregulation of SLC7A11. ( A ) Confocal imaging of Cu-probe and Mito-tracker in the NC and SLC31A1 knockdown AsPC-1 cells. Hoechst (blue) is used as a nuclear counterstain. Mean ± SD, n = 3. Statistical significance was determined using a two-way ANOVA test. Scale bar: 2 μm. ( B ) Total Fe level in the NC and SLC31A1 knockdown AsPC-1, MiaPaCa-2, and CFPAC-1 cells. Mean ± SD, n = 3. Statistical significance was determined using a one-way ANOVA test. ( C ) Volcano plot of gene expression (the SLC31A1 knockdown [shRNA#2] versus the control; log2(fold change) ≥1; p < 0.05 between SLC31A1 knockdown and NC AsPC-1 cells. ( D ) GO analysis of differentially expressed genes between SLC31A1 knockdown (shRNA#2) and NC AsPC-1 cells. ( E-G ) Western blot analysis of the indicated protein levels in the NC and SLC31A1 knockdown AsPC-1 (E), MiaPaCa-2 (F), and CFPAC-1 (G) cells. ( H and I ) GPX4 (H) or FSP-1 activity (I) was tested in the NC and SLC31A1 knockdown AsPC-1 cells. Mean ± SD, n = 3. Statistical significance was determined using a one-way ANOVA test. ( J ) qPCR analysis of SLC31A1 and SLC7A11 gene expression in NC and SLC31A1 knockdown AsPC-1, MiaPaCa-2, and CFPAC-1 cells. Mean ± SD, n = 3. Statistical significance was determined using a one-way ANOVA test. ( K ) qPCR analysis of SLC31A1 and SLC7A11 gene expression in NC and SLC31A1 knockdown AsPC-1, MiaPaCa-2, and CFPAC-1 cells. Mean ± SD, n = 3. Statistical significance was determined using a one-way ANOVA test. ( L ) GSH level in the NC and SLC31A1 knockdown AsPC-1, MiaPaCa-2, and CFPAC-1 cells. Mean ± SD, n = 3. Statistical significance was determined using a one-way ANOVA test. ( M ) Cystine uptake level in the NC and SLC31A1 knockdown AsPC-1, MiaPaCa-2, and CFPAC-1 cells. Mean ± SD, n = 3. Statistical significance was determined using a one-way ANOVA test.

Journal: Redox Biology

Article Title: Copper deprivation reprograms antioxidant defense to suppress ferroptosis via SLC7A11

doi: 10.1016/j.redox.2026.104130

Figure Lengend Snippet: Copper deprivation induced by SLC31A11 knockdown triggers the upregulation of SLC7A11. ( A ) Confocal imaging of Cu-probe and Mito-tracker in the NC and SLC31A1 knockdown AsPC-1 cells. Hoechst (blue) is used as a nuclear counterstain. Mean ± SD, n = 3. Statistical significance was determined using a two-way ANOVA test. Scale bar: 2 μm. ( B ) Total Fe level in the NC and SLC31A1 knockdown AsPC-1, MiaPaCa-2, and CFPAC-1 cells. Mean ± SD, n = 3. Statistical significance was determined using a one-way ANOVA test. ( C ) Volcano plot of gene expression (the SLC31A1 knockdown [shRNA#2] versus the control; log2(fold change) ≥1; p < 0.05 between SLC31A1 knockdown and NC AsPC-1 cells. ( D ) GO analysis of differentially expressed genes between SLC31A1 knockdown (shRNA#2) and NC AsPC-1 cells. ( E-G ) Western blot analysis of the indicated protein levels in the NC and SLC31A1 knockdown AsPC-1 (E), MiaPaCa-2 (F), and CFPAC-1 (G) cells. ( H and I ) GPX4 (H) or FSP-1 activity (I) was tested in the NC and SLC31A1 knockdown AsPC-1 cells. Mean ± SD, n = 3. Statistical significance was determined using a one-way ANOVA test. ( J ) qPCR analysis of SLC31A1 and SLC7A11 gene expression in NC and SLC31A1 knockdown AsPC-1, MiaPaCa-2, and CFPAC-1 cells. Mean ± SD, n = 3. Statistical significance was determined using a one-way ANOVA test. ( K ) qPCR analysis of SLC31A1 and SLC7A11 gene expression in NC and SLC31A1 knockdown AsPC-1, MiaPaCa-2, and CFPAC-1 cells. Mean ± SD, n = 3. Statistical significance was determined using a one-way ANOVA test. ( L ) GSH level in the NC and SLC31A1 knockdown AsPC-1, MiaPaCa-2, and CFPAC-1 cells. Mean ± SD, n = 3. Statistical significance was determined using a one-way ANOVA test. ( M ) Cystine uptake level in the NC and SLC31A1 knockdown AsPC-1, MiaPaCa-2, and CFPAC-1 cells. Mean ± SD, n = 3. Statistical significance was determined using a one-way ANOVA test.

Article Snippet: Ferroptosis Suppressor Protein-1 (FSP-1) Inhibitor Screening Kit , Elabscience , E-BC-D008.

Techniques: Knockdown, Imaging, Gene Expression, shRNA, Control, Western Blot, Activity Assay

Phenotypic differences between LMS-derived seeding (S3) and non-seeding (N3) cells. (A) Morphological differences were not observed between S3 and N3 under bright field microscope. (B) The graph shows that the proliferative capacity of S3 is slower than that of N3s through High-Content Screening (HCS) analysis. (C) The trans-well migration assay reveals that there was no significant difference in the migration ability between S3 and N3 (quantification graph). (D) Representative images from the trans-well migration assay. (E) Representative images of the wound-healing assay show that N3 filled the open area faster than S3. The white area is saturated with green color due to the overlapping of S3 without filling the wound gap. (F) Quantification graph of the wound-healing assay. (G) Adhesion of S3 and N3 cells to extracellular matrix (ECM) components, including fibronectin, collagen I, collagen IV, laminin I, and fibrinogen, was quantified after 24h of incubation. (H) Adhesion values were normalized to control conditions. All data are presented as mean ± SD from n = 3 independent experiments. Statistical comparisons between two groups were performed using a two-tailed Student’s t-test. *P < 0.05, **P < 0.01, ***P < 0.001.

Journal: Translational Oncology

Article Title: Overcoming the leptomeningeal seeding of medulloblastoma by targeting HSP70

doi: 10.1016/j.tranon.2026.102695

Figure Lengend Snippet: Phenotypic differences between LMS-derived seeding (S3) and non-seeding (N3) cells. (A) Morphological differences were not observed between S3 and N3 under bright field microscope. (B) The graph shows that the proliferative capacity of S3 is slower than that of N3s through High-Content Screening (HCS) analysis. (C) The trans-well migration assay reveals that there was no significant difference in the migration ability between S3 and N3 (quantification graph). (D) Representative images from the trans-well migration assay. (E) Representative images of the wound-healing assay show that N3 filled the open area faster than S3. The white area is saturated with green color due to the overlapping of S3 without filling the wound gap. (F) Quantification graph of the wound-healing assay. (G) Adhesion of S3 and N3 cells to extracellular matrix (ECM) components, including fibronectin, collagen I, collagen IV, laminin I, and fibrinogen, was quantified after 24h of incubation. (H) Adhesion values were normalized to control conditions. All data are presented as mean ± SD from n = 3 independent experiments. Statistical comparisons between two groups were performed using a two-tailed Student’s t-test. *P < 0.05, **P < 0.01, ***P < 0.001.

Article Snippet: Cell proliferation was monitored and quantified consecutively for 64 hours using a high-content screening (HCS) system (Operetta CLS, PerkinElmer).

Techniques: Derivative Assay, Microscopy, High Content Screening, Migration, Wound Healing Assay, Incubation, Control, Two Tailed Test