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Miltenyi Biotec apc anti human cd45 antibody
Apc Anti Human Cd45 Antibody, supplied by Miltenyi Biotec, used in various techniques. Bioz Stars score: 96/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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a) UMOD -/- have increased serum creatinine levels 24 hours following bilateral ischemia reperfusion of the kidneys with 22 minute clamp time (22IRI, n = 9 per group) b) Visualization of hypothesis that characterizing earlier timepoints following IRI surgery will identify early molecular events determining later injury c) Study design showing contribution of mouse genetic lines (UMOD -/- and UMOD +/+ ) and surgical models to multiplexed imaging and kidney total and Kidney <t>CD45</t> + single cell RNA-sequencing d) Clustering of cell types identified in kidney total single cell RNA-sequencing e) Marker gene expression in single cell RNA-sequencing clusters f) Representative image of whole mouse kidney slice following multiplexed imaging by CODEX g) Clustering of cell types identified by CODEX multiplexed imaging h) Violin plots of antibody signal from individual cell clusters derived from CODEX multiplexed imaging i) Comparison of cell types identified by Kidney Total scRNA-seq and CODEX UMOD – Uromodulin, IRI – ischemia-reperfusion injury, PT-S1 – S1 proximal tubule, PT-S2 – S2 proximal tubule, PT-S3 – S3 proximal tubule, LOH – Loop of Henle, DCT – distal convoluted tubule, CNT – connecting tubule, CD-PC – Collecting Duct – Principal Cell, CD-ICa – Collecting Duct – Intercalated Cell Type A, CD-ICb – Collecting Duct – Intercalated Cell Type B, LRP2 – LDL Receptor Related Protein 2, CD71 – Cluster of Differentiation 71, LY6G – Lymphocyte Antigen 6 Family Member G, CD74 – Cluster of Differentiation 74, CD3 – Cluster of Differentiation 3, CD31 – Cluster of Differentiation 31, VWF – Von Willebrand Factor, AQP2 – Aquaporin 2, KIM-1 – Kidney Injury Molecule 1, CD8a – Cluster of Differentiation 8a, αSMA – α Smooth Muscle Actin
Apc Conjugated Cd45 Antibody, supplied by Miltenyi Biotec, used in various techniques. Bioz Stars score: 96/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
https://www.bioz.com/result/apc conjugated cd45 antibody/product/Miltenyi Biotec
Average 96 stars, based on 1 article reviews
apc conjugated cd45 antibody - by Bioz Stars, 2026-04
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Miltenyi Biotec cd45 apc cy7
Pharmacological and genetic inhibition of CEBPA synergizes with VEN-induced apoptosis in TP53mut/mut-like AMLs (A) MOLM13 (VEN-sensitive) and KG1 (VEN-resistant) cells were treated for 72 h with increasing concentrations of VEN and GFC. Synergy was determined by Bliss coefficient (ZIP score >10 indicates synergism). (B and C) Drug-induced apoptosis (B) and viable cell counts (C) in MOLM13 shCEBPA/shScr cells treated with VEN alone or in combination with GFC (concentrations indicated in the plots, 72 h) detected by flow cytometry ( n = 4). (D and E) Apoptosis was detected by flow cytometry in gated human <t>CD45</t> dim CD34 + (or CD117 + cells for CD34 − AMLs) of ex vivo -treated AML samples categorized as TP53 mut-like ( n = 8) (D) and TP53 mut ( n = 9) (E) in a co-culture system using an FITC-annexin V/DAPI staining method. Cells were treated with vehicle, VEN (100 and 500 nM), and VEN+Aza (VEN 100 nM + 5′ Aza 1.5 μM), in the presence or absence of GFC (30 μM) for 72 h. Bar graphs represent the mean ± SEM of all the independent patients screened; each point represents a patient. (F and G) Mitochondrial membrane potential (F) (measured by TMRE staining, n = 18) and total cytoplasmatic ROS levels (G) (measured using the CellROX Red probe, via flow cytometry, n = 6) for the data included in (D) and (E). TP53 mut AMLs are depicted in red, and TP53 mut-like AMLs are depicted in black. APR-246, eprenetapopt. Data are reported as mean ± SEM for (B)–(G). The p values and cell types are indicated in the graphs; ∗ p < 0.05; ∗∗ p < 0.01; ∗∗∗ p < 0.001; ANOVA and Bonferroni post-test.
Cd45 Apc Cy7, supplied by Miltenyi Biotec, used in various techniques. Bioz Stars score: 96/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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Pharmacological and genetic inhibition of CEBPA synergizes with VEN-induced apoptosis in TP53mut/mut-like AMLs (A) MOLM13 (VEN-sensitive) and KG1 (VEN-resistant) cells were treated for 72 h with increasing concentrations of VEN and GFC. Synergy was determined by Bliss coefficient (ZIP score >10 indicates synergism). (B and C) Drug-induced apoptosis (B) and viable cell counts (C) in MOLM13 shCEBPA/shScr cells treated with VEN alone or in combination with GFC (concentrations indicated in the plots, 72 h) detected by flow cytometry ( n = 4). (D and E) Apoptosis was detected by flow cytometry in gated human <t>CD45</t> dim CD34 + (or CD117 + cells for CD34 − AMLs) of ex vivo -treated AML samples categorized as TP53 mut-like ( n = 8) (D) and TP53 mut ( n = 9) (E) in a co-culture system using an FITC-annexin V/DAPI staining method. Cells were treated with vehicle, VEN (100 and 500 nM), and VEN+Aza (VEN 100 nM + 5′ Aza 1.5 μM), in the presence or absence of GFC (30 μM) for 72 h. Bar graphs represent the mean ± SEM of all the independent patients screened; each point represents a patient. (F and G) Mitochondrial membrane potential (F) (measured by TMRE staining, n = 18) and total cytoplasmatic ROS levels (G) (measured using the CellROX Red probe, via flow cytometry, n = 6) for the data included in (D) and (E). TP53 mut AMLs are depicted in red, and TP53 mut-like AMLs are depicted in black. APR-246, eprenetapopt. Data are reported as mean ± SEM for (B)–(G). The p values and cell types are indicated in the graphs; ∗ p < 0.05; ∗∗ p < 0.01; ∗∗∗ p < 0.001; ANOVA and Bonferroni post-test.
Apc Vio 770 Cd45, supplied by Miltenyi Biotec, used in various techniques. Bioz Stars score: 96/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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Pharmacological and genetic inhibition of CEBPA synergizes with VEN-induced apoptosis in TP53mut/mut-like AMLs (A) MOLM13 (VEN-sensitive) and KG1 (VEN-resistant) cells were treated for 72 h with increasing concentrations of VEN and GFC. Synergy was determined by Bliss coefficient (ZIP score >10 indicates synergism). (B and C) Drug-induced apoptosis (B) and viable cell counts (C) in MOLM13 shCEBPA/shScr cells treated with VEN alone or in combination with GFC (concentrations indicated in the plots, 72 h) detected by flow cytometry ( n = 4). (D and E) Apoptosis was detected by flow cytometry in gated human <t>CD45</t> dim CD34 + (or CD117 + cells for CD34 − AMLs) of ex vivo -treated AML samples categorized as TP53 mut-like ( n = 8) (D) and TP53 mut ( n = 9) (E) in a co-culture system using an FITC-annexin V/DAPI staining method. Cells were treated with vehicle, VEN (100 and 500 nM), and VEN+Aza (VEN 100 nM + 5′ Aza 1.5 μM), in the presence or absence of GFC (30 μM) for 72 h. Bar graphs represent the mean ± SEM of all the independent patients screened; each point represents a patient. (F and G) Mitochondrial membrane potential (F) (measured by TMRE staining, n = 18) and total cytoplasmatic ROS levels (G) (measured using the CellROX Red probe, via flow cytometry, n = 6) for the data included in (D) and (E). TP53 mut AMLs are depicted in red, and TP53 mut-like AMLs are depicted in black. APR-246, eprenetapopt. Data are reported as mean ± SEM for (B)–(G). The p values and cell types are indicated in the graphs; ∗ p < 0.05; ∗∗ p < 0.01; ∗∗∗ p < 0.001; ANOVA and Bonferroni post-test.
Anti Cd45 Apc Vio 770, supplied by Miltenyi Biotec, used in various techniques. Bioz Stars score: 96/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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Pharmacological and genetic inhibition of CEBPA synergizes with VEN-induced apoptosis in TP53mut/mut-like AMLs (A) MOLM13 (VEN-sensitive) and KG1 (VEN-resistant) cells were treated for 72 h with increasing concentrations of VEN and GFC. Synergy was determined by Bliss coefficient (ZIP score >10 indicates synergism). (B and C) Drug-induced apoptosis (B) and viable cell counts (C) in MOLM13 shCEBPA/shScr cells treated with VEN alone or in combination with GFC (concentrations indicated in the plots, 72 h) detected by flow cytometry ( n = 4). (D and E) Apoptosis was detected by flow cytometry in gated human <t>CD45</t> dim CD34 + (or CD117 + cells for CD34 − AMLs) of ex vivo -treated AML samples categorized as TP53 mut-like ( n = 8) (D) and TP53 mut ( n = 9) (E) in a co-culture system using an FITC-annexin V/DAPI staining method. Cells were treated with vehicle, VEN (100 and 500 nM), and VEN+Aza (VEN 100 nM + 5′ Aza 1.5 μM), in the presence or absence of GFC (30 μM) for 72 h. Bar graphs represent the mean ± SEM of all the independent patients screened; each point represents a patient. (F and G) Mitochondrial membrane potential (F) (measured by TMRE staining, n = 18) and total cytoplasmatic ROS levels (G) (measured using the CellROX Red probe, via flow cytometry, n = 6) for the data included in (D) and (E). TP53 mut AMLs are depicted in red, and TP53 mut-like AMLs are depicted in black. APR-246, eprenetapopt. Data are reported as mean ± SEM for (B)–(G). The p values and cell types are indicated in the graphs; ∗ p < 0.05; ∗∗ p < 0.01; ∗∗∗ p < 0.001; ANOVA and Bonferroni post-test.
Cd45 Apc, supplied by Miltenyi Biotec, used in various techniques. Bioz Stars score: 96/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
https://www.bioz.com/result/cd45 apc/product/Miltenyi Biotec
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Pharmacological and genetic inhibition of CEBPA synergizes with VEN-induced apoptosis in TP53mut/mut-like AMLs (A) MOLM13 (VEN-sensitive) and KG1 (VEN-resistant) cells were treated for 72 h with increasing concentrations of VEN and GFC. Synergy was determined by Bliss coefficient (ZIP score >10 indicates synergism). (B and C) Drug-induced apoptosis (B) and viable cell counts (C) in MOLM13 shCEBPA/shScr cells treated with VEN alone or in combination with GFC (concentrations indicated in the plots, 72 h) detected by flow cytometry ( n = 4). (D and E) Apoptosis was detected by flow cytometry in gated human <t>CD45</t> dim CD34 + (or CD117 + cells for CD34 − AMLs) of ex vivo -treated AML samples categorized as TP53 mut-like ( n = 8) (D) and TP53 mut ( n = 9) (E) in a co-culture system using an FITC-annexin V/DAPI staining method. Cells were treated with vehicle, VEN (100 and 500 nM), and VEN+Aza (VEN 100 nM + 5′ Aza 1.5 μM), in the presence or absence of GFC (30 μM) for 72 h. Bar graphs represent the mean ± SEM of all the independent patients screened; each point represents a patient. (F and G) Mitochondrial membrane potential (F) (measured by TMRE staining, n = 18) and total cytoplasmatic ROS levels (G) (measured using the CellROX Red probe, via flow cytometry, n = 6) for the data included in (D) and (E). TP53 mut AMLs are depicted in red, and TP53 mut-like AMLs are depicted in black. APR-246, eprenetapopt. Data are reported as mean ± SEM for (B)–(G). The p values and cell types are indicated in the graphs; ∗ p < 0.05; ∗∗ p < 0.01; ∗∗∗ p < 0.001; ANOVA and Bonferroni post-test.
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a) UMOD -/- have increased serum creatinine levels 24 hours following bilateral ischemia reperfusion of the kidneys with 22 minute clamp time (22IRI, n = 9 per group) b) Visualization of hypothesis that characterizing earlier timepoints following IRI surgery will identify early molecular events determining later injury c) Study design showing contribution of mouse genetic lines (UMOD -/- and UMOD +/+ ) and surgical models to multiplexed imaging and kidney total and Kidney CD45 + single cell RNA-sequencing d) Clustering of cell types identified in kidney total single cell RNA-sequencing e) Marker gene expression in single cell RNA-sequencing clusters f) Representative image of whole mouse kidney slice following multiplexed imaging by CODEX g) Clustering of cell types identified by CODEX multiplexed imaging h) Violin plots of antibody signal from individual cell clusters derived from CODEX multiplexed imaging i) Comparison of cell types identified by Kidney Total scRNA-seq and CODEX UMOD – Uromodulin, IRI – ischemia-reperfusion injury, PT-S1 – S1 proximal tubule, PT-S2 – S2 proximal tubule, PT-S3 – S3 proximal tubule, LOH – Loop of Henle, DCT – distal convoluted tubule, CNT – connecting tubule, CD-PC – Collecting Duct – Principal Cell, CD-ICa – Collecting Duct – Intercalated Cell Type A, CD-ICb – Collecting Duct – Intercalated Cell Type B, LRP2 – LDL Receptor Related Protein 2, CD71 – Cluster of Differentiation 71, LY6G – Lymphocyte Antigen 6 Family Member G, CD74 – Cluster of Differentiation 74, CD3 – Cluster of Differentiation 3, CD31 – Cluster of Differentiation 31, VWF – Von Willebrand Factor, AQP2 – Aquaporin 2, KIM-1 – Kidney Injury Molecule 1, CD8a – Cluster of Differentiation 8a, αSMA – α Smooth Muscle Actin

Journal: bioRxiv

Article Title: Uromodulin promotes immune zonation and inhibits alternative inflammasome-mediated activation of immune-to-collecting duct inflammatory signaling in early acute kidney injury

doi: 10.64898/2026.02.26.708299

Figure Lengend Snippet: a) UMOD -/- have increased serum creatinine levels 24 hours following bilateral ischemia reperfusion of the kidneys with 22 minute clamp time (22IRI, n = 9 per group) b) Visualization of hypothesis that characterizing earlier timepoints following IRI surgery will identify early molecular events determining later injury c) Study design showing contribution of mouse genetic lines (UMOD -/- and UMOD +/+ ) and surgical models to multiplexed imaging and kidney total and Kidney CD45 + single cell RNA-sequencing d) Clustering of cell types identified in kidney total single cell RNA-sequencing e) Marker gene expression in single cell RNA-sequencing clusters f) Representative image of whole mouse kidney slice following multiplexed imaging by CODEX g) Clustering of cell types identified by CODEX multiplexed imaging h) Violin plots of antibody signal from individual cell clusters derived from CODEX multiplexed imaging i) Comparison of cell types identified by Kidney Total scRNA-seq and CODEX UMOD – Uromodulin, IRI – ischemia-reperfusion injury, PT-S1 – S1 proximal tubule, PT-S2 – S2 proximal tubule, PT-S3 – S3 proximal tubule, LOH – Loop of Henle, DCT – distal convoluted tubule, CNT – connecting tubule, CD-PC – Collecting Duct – Principal Cell, CD-ICa – Collecting Duct – Intercalated Cell Type A, CD-ICb – Collecting Duct – Intercalated Cell Type B, LRP2 – LDL Receptor Related Protein 2, CD71 – Cluster of Differentiation 71, LY6G – Lymphocyte Antigen 6 Family Member G, CD74 – Cluster of Differentiation 74, CD3 – Cluster of Differentiation 3, CD31 – Cluster of Differentiation 31, VWF – Von Willebrand Factor, AQP2 – Aquaporin 2, KIM-1 – Kidney Injury Molecule 1, CD8a – Cluster of Differentiation 8a, αSMA – α Smooth Muscle Actin

Article Snippet: To label the cells with CD45 antibody, 10 μL (1.5 μg) APC conjugated CD45 antibody (clone 30F11, Miltenyi) was added to the 100 μL suspension and incubated for 30 minutes at 4°C.

Techniques: Imaging, Single Cell, RNA Sequencing, Marker, Gene Expression, Derivative Assay, Comparison

a) Representative image of mouse kidney slice following multiplexed imaging by CODEX with selected immune cell markers b) Clustering of CD45 + cell types identified by CODEX multiplexed imaging c) Dotplot of antibody signal from individual CD45 + cell clusters derived from CODEX multiplexed imaging d) Cluster overlay of CD45 + cell clusters onto identical images from (a) e) Distribution of myeloid cell type clusters by region in UMOD +/+ sham kidney slices (n = 3) f) Representative whole kidney slice from UMOD +/+ sham kidney with selected markers g) Representative image of dendritic cell CD11c hi population in UMOD +/+ sham kidney h) Representative image of dendritic cell CD11lo i population in UMOD +/+ sham kidney i) Representative image of macrophage Mac (C) population in UMOD +/+ sham kidney j) Representative image of macrophage Mac (E) population in UMOD +/+ sham kidney UMOD – Uromodulin, DC – dendritic cell, mac - macrophage

Journal: bioRxiv

Article Title: Uromodulin promotes immune zonation and inhibits alternative inflammasome-mediated activation of immune-to-collecting duct inflammatory signaling in early acute kidney injury

doi: 10.64898/2026.02.26.708299

Figure Lengend Snippet: a) Representative image of mouse kidney slice following multiplexed imaging by CODEX with selected immune cell markers b) Clustering of CD45 + cell types identified by CODEX multiplexed imaging c) Dotplot of antibody signal from individual CD45 + cell clusters derived from CODEX multiplexed imaging d) Cluster overlay of CD45 + cell clusters onto identical images from (a) e) Distribution of myeloid cell type clusters by region in UMOD +/+ sham kidney slices (n = 3) f) Representative whole kidney slice from UMOD +/+ sham kidney with selected markers g) Representative image of dendritic cell CD11c hi population in UMOD +/+ sham kidney h) Representative image of dendritic cell CD11lo i population in UMOD +/+ sham kidney i) Representative image of macrophage Mac (C) population in UMOD +/+ sham kidney j) Representative image of macrophage Mac (E) population in UMOD +/+ sham kidney UMOD – Uromodulin, DC – dendritic cell, mac - macrophage

Article Snippet: To label the cells with CD45 antibody, 10 μL (1.5 μg) APC conjugated CD45 antibody (clone 30F11, Miltenyi) was added to the 100 μL suspension and incubated for 30 minutes at 4°C.

Techniques: Imaging, Derivative Assay

Pharmacological and genetic inhibition of CEBPA synergizes with VEN-induced apoptosis in TP53mut/mut-like AMLs (A) MOLM13 (VEN-sensitive) and KG1 (VEN-resistant) cells were treated for 72 h with increasing concentrations of VEN and GFC. Synergy was determined by Bliss coefficient (ZIP score >10 indicates synergism). (B and C) Drug-induced apoptosis (B) and viable cell counts (C) in MOLM13 shCEBPA/shScr cells treated with VEN alone or in combination with GFC (concentrations indicated in the plots, 72 h) detected by flow cytometry ( n = 4). (D and E) Apoptosis was detected by flow cytometry in gated human CD45 dim CD34 + (or CD117 + cells for CD34 − AMLs) of ex vivo -treated AML samples categorized as TP53 mut-like ( n = 8) (D) and TP53 mut ( n = 9) (E) in a co-culture system using an FITC-annexin V/DAPI staining method. Cells were treated with vehicle, VEN (100 and 500 nM), and VEN+Aza (VEN 100 nM + 5′ Aza 1.5 μM), in the presence or absence of GFC (30 μM) for 72 h. Bar graphs represent the mean ± SEM of all the independent patients screened; each point represents a patient. (F and G) Mitochondrial membrane potential (F) (measured by TMRE staining, n = 18) and total cytoplasmatic ROS levels (G) (measured using the CellROX Red probe, via flow cytometry, n = 6) for the data included in (D) and (E). TP53 mut AMLs are depicted in red, and TP53 mut-like AMLs are depicted in black. APR-246, eprenetapopt. Data are reported as mean ± SEM for (B)–(G). The p values and cell types are indicated in the graphs; ∗ p < 0.05; ∗∗ p < 0.01; ∗∗∗ p < 0.001; ANOVA and Bonferroni post-test.

Journal: Cell Reports Medicine

Article Title: ΔNp73 isoform defines a TP53 -mutant-like poor-risk subgroup of acute myeloid leukemia

doi: 10.1016/j.xcrm.2025.102540

Figure Lengend Snippet: Pharmacological and genetic inhibition of CEBPA synergizes with VEN-induced apoptosis in TP53mut/mut-like AMLs (A) MOLM13 (VEN-sensitive) and KG1 (VEN-resistant) cells were treated for 72 h with increasing concentrations of VEN and GFC. Synergy was determined by Bliss coefficient (ZIP score >10 indicates synergism). (B and C) Drug-induced apoptosis (B) and viable cell counts (C) in MOLM13 shCEBPA/shScr cells treated with VEN alone or in combination with GFC (concentrations indicated in the plots, 72 h) detected by flow cytometry ( n = 4). (D and E) Apoptosis was detected by flow cytometry in gated human CD45 dim CD34 + (or CD117 + cells for CD34 − AMLs) of ex vivo -treated AML samples categorized as TP53 mut-like ( n = 8) (D) and TP53 mut ( n = 9) (E) in a co-culture system using an FITC-annexin V/DAPI staining method. Cells were treated with vehicle, VEN (100 and 500 nM), and VEN+Aza (VEN 100 nM + 5′ Aza 1.5 μM), in the presence or absence of GFC (30 μM) for 72 h. Bar graphs represent the mean ± SEM of all the independent patients screened; each point represents a patient. (F and G) Mitochondrial membrane potential (F) (measured by TMRE staining, n = 18) and total cytoplasmatic ROS levels (G) (measured using the CellROX Red probe, via flow cytometry, n = 6) for the data included in (D) and (E). TP53 mut AMLs are depicted in red, and TP53 mut-like AMLs are depicted in black. APR-246, eprenetapopt. Data are reported as mean ± SEM for (B)–(G). The p values and cell types are indicated in the graphs; ∗ p < 0.05; ∗∗ p < 0.01; ∗∗∗ p < 0.001; ANOVA and Bonferroni post-test.

Article Snippet: To analyze the cytotoxicity in the different fractions of the bulk treated AML cells, treated MNCs were blocked with human FcR blocking reagent (Miltenyi Biotec) for 5 min and stained with the following antibodies: CD45-APC-Cy7, TMRE, CD14-PerCP, CD34-PE-Cy7 (or CD117-PE-Cy7 for CD34 − samples), and CD11b-APC for 20 min at 4°C.

Techniques: Inhibition, Flow Cytometry, Ex Vivo, Co-Culture Assay, Staining, Membrane