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Structured Review

OriGene ki67
Summary of previous reports and present case.

Ki67, supplied by OriGene, used in various techniques. Bioz Stars score: 93/100, based on 46 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
https://www.bioz.com/product/mouse+monoclonal/Ki67+(MKI67)+Mouse+Monoclonal+Antibody/pmc13651789-80-7-14
Average 93 stars, based on 46 article reviews

ki67 - by Bioz Stars, 2026-10

93/100 stars

Images

1) Product Images from "Multiple Pulmonary Papillary Adenoma With Malignant Potential Accompanied by ERBIN–BRAF Gene Fusion and APC Mutation: A Case Report and Literature Review"

Article Title: Multiple Pulmonary Papillary Adenoma With Malignant Potential Accompanied by ERBIN–BRAF Gene Fusion and APC Mutation: A Case Report and Literature Review

Journal: Canadian Respiratory Journal

doi: 10.1155/carj/3589904

Figure Legend Snippet: Summary of previous reports and present case.

Techniques Used: Immunohistochemistry, Expressing, Mutagenesis, Membrane, Staining, Tissue

Immunohistochemical staining (magnification × 100). Tumor cells showed diffuse positive expression of CK7 (A), Napsin A (B), and TTF‐1 (C); the Ki‐67 proliferation index was approximately 8% (D). Abbreviations: CK, cytokeratin; TTF‐1, thyroid transcription factor‐1. All figures were derived from original clinical data and were not generated or edited by artificial intelligence tools.

Figure Legend Snippet: Immunohistochemical staining (magnification × 100). Tumor cells showed diffuse positive expression of CK7 (A), Napsin A (B), and TTF‐1 (C); the Ki‐67 proliferation index was approximately 8% (D). Abbreviations: CK, cytokeratin; TTF‐1, thyroid transcription factor‐1. All figures were derived from original clinical data and were not generated or edited by artificial intelligence tools.

Techniques Used: Immunohistochemical staining, Staining, Expressing, Derivative Assay, Generated

Immunohistochemistry:

Article Title: An idiosyncratic zonated stroma encapsulates desmoplastic liver metastases and originates from injured liver
Article Snippet: .. Anti-CD146: OriGene #UM800051 mouse monoclonal clone UMAB154 Recommended by the manufacturer for IHC on FFPE; validation data for IHC shown for human melanoma, endometrium adenocarcinoma, colon adenocarcinoma, pancreas carcinoma, thyroid carcinoma, liver carcinoma, lung carcinoma, lymph node, endometrium, pancreas, prostate, lymphoma, kidney, ovary, tonsil tissue on the manufacturer homepage; antibody homepage: https ://www. thermofisher .corn/anti body/prod u ct/M CAM-Anti body-clone-U MA B 154-M onoclo na 1/U M800051 This antibody is extensively used in clinical routine at the Department of Pathology, Karolinska University Hospital, Huddinge, Sweden. ..

Article Title: Adrenal steroid metabolites and bone status in patients with adrenal incidentalomas and hypercortisolism
Article Snippet: .. Antibodies (cytochrome P450 21A2 [CYP21A2]; rabbit polyclonal, 1:1000, Atlas Antibodies, Cat# HPA048979, RRID: AB_2,680,584 and cytochrome b5 type A [CYB5A]; mouse monoclonal, 1:1000, OriGene, Cat#AM31963PU-N, RRID: AB_2940799) were used for IHC staining. ..

Formalin-fixed Paraffin-Embedded:

Biomarker Discovery:

Chick Chorioallantoic Membrane Assay:

Immunohistochemical staining:

Article Title: Multi-omics analysis of diabetic pig lungs reveals molecular derangements underlying pulmonary complications of diabetes mellitus.
Article Snippet: Growing evidence shows that the lung is an organ prone to injury by diabetes mellitus.. However, the molecular mechanisms of these pulmonary complications have not yet been characterized comprehensively.. To systematically study the effects of insulin deficiency and hyperglycaemia on the lung, we combined proteomics and lipidomics with quantitative histomorphological analyses to compare lung tissue samples from a clinically relevant pig model for mutant INS gene induced diabetes of youth (MIDY) with samples from wild-type (WT) littermate controls.

Article Title: Urinary Biomarkers Associated With Pathogenic Pathways Reflecting Histologic Findings in Lupus Nephritis
Article Snippet: After deparaffinization, the renal tissues were stained with BOND Epitope Retrieval Solution 1 (AR9961, Leica Biosystems) for calgranulin B and BOND Epitope Retrieval Solution 2 for MCP‐1 and IGFBP‐5 (AR9640, Leica Biosystems). .. For immunohistochemical staining, the renal tissues were incubated with 1:2,000 diluted mouse monoclonal anti–calgranulin B (TA804091S, OriGene Technologies), 1:100 diluted mouse monoclonal anti–MCP‐1 (MAB 679, R&D Systems), and 1:50 diluted mouse monoclonal anti–IGFBP‐5 (MAB875, R&D Systems) antibodies. .. BOND Polymer Refine Detection (DS9800; Leica Biosystems) was used as the secondary antibody.

Avidin-Biotin Assay:

Incubation:

Article Title: ChemR23 activation reprograms macrophages toward a less inflammatory phenotype and dampens carcinoma progression.
Article Snippet: Threemicrometers-thick tissue sections of formalin-fixed, paraffinembedded (FFPE) breast cancers were treated with protease for 4min (Protease 1, Ventana, 760-2018) to achieve epitope retrieval. .. Samples were then incubated during 32min at 37°C with the antiChemR23 antibody at a dilution of 1:200 (clone 1A7, mouse monoclonal, Origene) and with the anti-Iba1 antibody at a dilution of 1:1000 (clone EPR16588, rabbit monoclonal, Abcam). .. Protein expression was detected with an OptiView DAB IHC Detection Kit (Roche Diagnostics, 760-700), optimized for automated immunohistochemistry (Benchmark GX stainer, Ventana Medical Systems, Roche Diagnostics).

Staining:

other:

Article Title: EpCAM sustains crypt mechanics and prevents aberrant remodeling
Article Snippet: Mouse monoclonal (#TA506627, IF dilution 1:100) antibody directed against human EpCAM was from Origene (Rockville, USA).

Image Search Results

Deletion of Pex19 impairs the growth of mESCs (A) Pex19 deficiency reduces the growth of mESCs. Equal numbers of WT and Pex19 KO 46C mESCs were seeded and cultured in ESGRO medium, and cell counts were analyzed on day 3 ( n = 3 biological replicates/group; data are presented as mean ± SEM; Student’s t test, ∗∗ p < 0.01). (B) Pex19 deficiency reduces the single-cell self-renewal capacity of mESCs. WT and Pex19 KO mESCs were cultured for colony formation for 5 days ( n = 3 biological replicates/group; data are presented as mean ± SEM, Student’s t test, ∗ p < 0.05). (C) Pex19 deficiency increases cell death and apoptosis of mESCs ( n = 3 biological replicates/group, Student’s t test, ∗∗ p < 0.01, ∗∗∗ p < 0.001). (D) Adding back PEX19 restores the peroxisomal targeting of PEX14. Scale bars, 5 μm. (E–G) Adding back PEX19 rescues defective cell growth and elevated cell death in Pex19 KO mESCs. E and F, n = 3–4 biological replicates/group; data are presented as mean ± SEM, one-way ANOVA, ∗q < 0.05, ∗∗q < 0.01, ∗∗∗q < 0.001, n.s., not significant). (H) Top enriched GSEA pathways in Pex19 KO vs. WT mESCs. Transcriptomes of WT and Pex19 KO 46C mESCs from the RNA-seq dataset were analyzed using GSEA as described in . NES, Normalized Enrichment Score; FDR, False Discovery Rate. See also .

Journal: iScience

Article Title: Peroxisome-dependent and -independent functions of PEX19 in mouse embryonic stem cells

doi: 10.1016/j.isci.2026.117658

Figure Lengend Snippet: Deletion of Pex19 impairs the growth of mESCs (A) Pex19 deficiency reduces the growth of mESCs. Equal numbers of WT and Pex19 KO 46C mESCs were seeded and cultured in ESGRO medium, and cell counts were analyzed on day 3 ( n = 3 biological replicates/group; data are presented as mean ± SEM; Student’s t test, ∗∗ p < 0.01). (B) Pex19 deficiency reduces the single-cell self-renewal capacity of mESCs. WT and Pex19 KO mESCs were cultured for colony formation for 5 days ( n = 3 biological replicates/group; data are presented as mean ± SEM, Student’s t test, ∗ p < 0.05). (C) Pex19 deficiency increases cell death and apoptosis of mESCs ( n = 3 biological replicates/group, Student’s t test, ∗∗ p < 0.01, ∗∗∗ p < 0.001). (D) Adding back PEX19 restores the peroxisomal targeting of PEX14. Scale bars, 5 μm. (E–G) Adding back PEX19 rescues defective cell growth and elevated cell death in Pex19 KO mESCs. E and F, n = 3–4 biological replicates/group; data are presented as mean ± SEM, one-way ANOVA, ∗q < 0.05, ∗∗q < 0.01, ∗∗∗q < 0.001, n.s., not significant). (H) Top enriched GSEA pathways in Pex19 KO vs. WT mESCs. Transcriptomes of WT and Pex19 KO 46C mESCs from the RNA-seq dataset were analyzed using GSEA as described in . NES, Normalized Enrichment Score; FDR, False Discovery Rate. See also .

Article Snippet: Mouse anti-PEX19 monoclonal antibody , Novus , NBP2-43544; RRID: AB_3307633.

Techniques: Cell Culture, Single Cell, Colony Assay, RNA Sequencing

Deletion of Pex19 induces oxidative stress and impairs mitochondrial function in mESCs (A) Pex19 KO 46C mESCs have increased ROS. Levels of total cellular ROS were measured by FACS analysis of cell-permeable deep red dye ( n = 3 biological replicates/group; data are presented as mean ± SEM, Student’s t test, ∗∗∗∗ p < 0.0001). Scale bars, 5 μm. (B) The abundance and distribution of mitochondrial SOD2 in WT and Pex19 KO 46C mESCs. Scale bars, 5 μm. (C) NAC treatment rescues the defective mitochondrial membrane potential in Pex19 KO mESCs. WT and Pex19 KO 46C mESCs were treated with or without 2 mM NAC for 16 h and stained with MitoTracker, then subjected to FACS analysis ( n = 3–4 biological replicates/group, data are presented as mean ± SEM, two-way ANOVA, ∗∗q < 0.01). (D) WT and Pex19 KO 46C mESCs have comparable levels of an outer mitochondrial membrane protein, TOMM20. Total cell lysates were analyzed for the abundance of TOMM20 by immunoblotting. (E) Pex19 KO mESCs have impaired mitochondrial respiration. The oxygen consumption rate (OCR) and the extracellular acidification rate (ECAR) of WT and Pex19 KO 46C mESCs were analyzed by Seahorse XFe24 Analyzer ( n = 6 biological replicates/group; data are presented as mean ± SEM). Omy, oligomycin; FCCP, carbonyl cyanide-4 (trifluoromethoxy) phenylhydrazone; ROT and AA, Rotenone and antimycin A; 2-DG, 2-deoxy-glucose. (F) NAC treatment partially restores the defective mitochondrial respiration of Pex19 KO mESCs. The OCR of WT, Pex19 KO, and Pex19 KO 46C mESCs treated with 2 mM NAC for 16 h were analyzed by Seahorse XFe24 Analyzer ( n = 6 biological replicates/group; data are presented as mean ± SEM). (G) NAC treatment partially rescues the colony formation ability but not cell growth of Pex19 KO mESCs. WT and Pex19 KO 46C mESCs treated with or without 2 mM NAC were analyzed for their growth and colony formation ability ( n = 3 biological replicates/group; data are presented as mean ± SEM; two-way ANOVA, ∗∗q < 0.01, ∗∗∗q < 0.001, ∗∗∗∗q < 0.0001, n.s, not significant). (H) NAC treatment partially reduces cell death of Pex19 KO mESCs. WT and Pex19 KO 46C mESCs treated with or without 2 mM NAC for 24 h were analyzed by FACS ( n = 3 biological replicates/group; data are presented as mean ± SEM; two-way ANOVA; ∗∗q < 0.01, ∗∗∗q < 0.001, ∗∗∗∗q < 0.0001).

Journal: iScience

Article Title: Peroxisome-dependent and -independent functions of PEX19 in mouse embryonic stem cells

doi: 10.1016/j.isci.2026.117658

Figure Lengend Snippet: Deletion of Pex19 induces oxidative stress and impairs mitochondrial function in mESCs (A) Pex19 KO 46C mESCs have increased ROS. Levels of total cellular ROS were measured by FACS analysis of cell-permeable deep red dye ( n = 3 biological replicates/group; data are presented as mean ± SEM, Student’s t test, ∗∗∗∗ p < 0.0001). Scale bars, 5 μm. (B) The abundance and distribution of mitochondrial SOD2 in WT and Pex19 KO 46C mESCs. Scale bars, 5 μm. (C) NAC treatment rescues the defective mitochondrial membrane potential in Pex19 KO mESCs. WT and Pex19 KO 46C mESCs were treated with or without 2 mM NAC for 16 h and stained with MitoTracker, then subjected to FACS analysis ( n = 3–4 biological replicates/group, data are presented as mean ± SEM, two-way ANOVA, ∗∗q < 0.01). (D) WT and Pex19 KO 46C mESCs have comparable levels of an outer mitochondrial membrane protein, TOMM20. Total cell lysates were analyzed for the abundance of TOMM20 by immunoblotting. (E) Pex19 KO mESCs have impaired mitochondrial respiration. The oxygen consumption rate (OCR) and the extracellular acidification rate (ECAR) of WT and Pex19 KO 46C mESCs were analyzed by Seahorse XFe24 Analyzer ( n = 6 biological replicates/group; data are presented as mean ± SEM). Omy, oligomycin; FCCP, carbonyl cyanide-4 (trifluoromethoxy) phenylhydrazone; ROT and AA, Rotenone and antimycin A; 2-DG, 2-deoxy-glucose. (F) NAC treatment partially restores the defective mitochondrial respiration of Pex19 KO mESCs. The OCR of WT, Pex19 KO, and Pex19 KO 46C mESCs treated with 2 mM NAC for 16 h were analyzed by Seahorse XFe24 Analyzer ( n = 6 biological replicates/group; data are presented as mean ± SEM). (G) NAC treatment partially rescues the colony formation ability but not cell growth of Pex19 KO mESCs. WT and Pex19 KO 46C mESCs treated with or without 2 mM NAC were analyzed for their growth and colony formation ability ( n = 3 biological replicates/group; data are presented as mean ± SEM; two-way ANOVA, ∗∗q < 0.01, ∗∗∗q < 0.001, ∗∗∗∗q < 0.0001, n.s, not significant). (H) NAC treatment partially reduces cell death of Pex19 KO mESCs. WT and Pex19 KO 46C mESCs treated with or without 2 mM NAC for 24 h were analyzed by FACS ( n = 3 biological replicates/group; data are presented as mean ± SEM; two-way ANOVA; ∗∗q < 0.01, ∗∗∗q < 0.001, ∗∗∗∗q < 0.0001).

Article Snippet: Mouse anti-PEX19 monoclonal antibody , Novus , NBP2-43544; RRID: AB_3307633.

Techniques: Analysis, Membrane, Staining, Western Blot, Colony Assay

$Deletion of Pex19 impairs peroxisomal lipid metabolism and pluripotency in mESCs (A) Pex19 KO 46C mESCs have reduced AP staining. WT and Pex19 KO 46C mESCs were stained for AP activity using the fluorescent Alkaline Phosphatase Detection Kit. Scale bars, 100 μm. (B) The fraction of AP + colonies is reduced in Pex19 KO mESCs. WT and Pex19 KO 46C mESCs were stained for AP activity using the StemAb Alkaline Phosphatase Staining kit II, and the percentage of AP + colonies was quantified ( n = 15–18 random fields/group were analyzed; data are presented as mean ± SEM, two-way ANOVA, ∗∗∗∗q < 0.0001). Scale bars, 200 μm. (C and D) Pex19 KO mESCs have altered lipid metabolism. WT and Pex19 KO 46C mESCs were subject to a lipidomics analysis as described in . (C) Volcano plot of all annotated lipids with cutoffs of p < 0.05 and |FC|>2 (gray line and dotted lines). Red, significantly upregulated lipids; green, significantly downregulated lipids; Blue, all ether PE. (D) Heatmap of significantly changed lipids (cutoffs of p < 0.05 and |FC|>2). (E) Pex19 KO mESCs have an increased membrane fluidity. WT and Pex19 KO 46C mESCs were stained with 5 μM di-4-ANEPPDHQ for 30 min. The relative ordered fraction in each group was analyzed as described in ( n = 40 colonies/group; data are presented as violin plots; Student’s t test, ∗∗∗∗ p < 0.0001). (F) Treatment with plasmalogens partially restores the clumping morphology of Pex19 KO mESCs. WT and Pex19 KO 46C mESCs were treated with vehicle control (ethanol) or 30 μg/mL plasmalogens (PLs) for 2 days ( n = 25 WT ethanol, 25 WT PLs, 17 KO ethanol, and 19 KO PLs; random fields were analyzed; data are presented as mean ± SEM, two-way ANOVA, ∗∗∗q < 0.001, ∗∗∗∗q < 0.0001). Scale bars, 100 μm. (G) Treatment with plasmalogens partially rescues the AP activity in Pex19 KO mESCs. WT and Pex19 KO 46C mESCs were treated as in (F) and stained for AP activity ( n = 15–17 random fields/group were analyzed; data are presented as mean ± SEM, two-way ANOVA, ∗∗∗∗q < 0.0001). Scale bars, 100 μm. See also .$

Journal: iScience

Article Title: Peroxisome-dependent and -independent functions of PEX19 in mouse embryonic stem cells

doi: 10.1016/j.isci.2026.117658

Figure Lengend Snippet: Deletion of Pex19 impairs peroxisomal lipid metabolism and pluripotency in mESCs (A) Pex19 KO 46C mESCs have reduced AP staining. WT and Pex19 KO 46C mESCs were stained for AP activity using the fluorescent Alkaline Phosphatase Detection Kit. Scale bars, 100 μm. (B) The fraction of AP + colonies is reduced in Pex19 KO mESCs. WT and Pex19 KO 46C mESCs were stained for AP activity using the StemAb Alkaline Phosphatase Staining kit II, and the percentage of AP + colonies was quantified ( n = 15–18 random fields/group were analyzed; data are presented as mean ± SEM, two-way ANOVA, ∗∗∗∗q < 0.0001). Scale bars, 200 μm. (C and D) Pex19 KO mESCs have altered lipid metabolism. WT and Pex19 KO 46C mESCs were subject to a lipidomics analysis as described in . (C) Volcano plot of all annotated lipids with cutoffs of p < 0.05 and |FC|>2 (gray line and dotted lines). Red, significantly upregulated lipids; green, significantly downregulated lipids; Blue, all ether PE. (D) Heatmap of significantly changed lipids (cutoffs of p < 0.05 and |FC|>2). (E) Pex19 KO mESCs have an increased membrane fluidity. WT and Pex19 KO 46C mESCs were stained with 5 μM di-4-ANEPPDHQ for 30 min. The relative ordered fraction in each group was analyzed as described in ( n = 40 colonies/group; data are presented as violin plots; Student’s t test, ∗∗∗∗ p < 0.0001). (F) Treatment with plasmalogens partially restores the clumping morphology of Pex19 KO mESCs. WT and Pex19 KO 46C mESCs were treated with vehicle control (ethanol) or 30 μg/mL plasmalogens (PLs) for 2 days ( n = 25 WT ethanol, 25 WT PLs, 17 KO ethanol, and 19 KO PLs; random fields were analyzed; data are presented as mean ± SEM, two-way ANOVA, ∗∗∗q < 0.001, ∗∗∗∗q < 0.0001). Scale bars, 100 μm. (G) Treatment with plasmalogens partially rescues the AP activity in Pex19 KO mESCs. WT and Pex19 KO 46C mESCs were treated as in (F) and stained for AP activity ( n = 15–17 random fields/group were analyzed; data are presented as mean ± SEM, two-way ANOVA, ∗∗∗∗q < 0.0001). Scale bars, 100 μm. See also .

Article Snippet: Mouse anti-PEX19 monoclonal antibody , Novus , NBP2-43544; RRID: AB_3307633.

Techniques: Staining, Activity Assay, Analysis, Membrane, Morphology, Control

$Deletion of Pex19 induces mitotic block in mESCs (A) Deletion of Pex19 impairs cell cycle progression and induces polynuclear mESCs. WT, Pex19 KO, and Pex19 KO + PEX19 46C mESCs were stained with PI for DNA content, then subjected to FACS analysis ( n = 3 biological replicates/group; data are presented as mean ± SEM). (B) Deletion of Pex5 in mESCs fails to induce detectable defects in the cell cycle. WT, Pex5 KO, and Pex19 KO 46C mESCs were stained with DAPI for DNA content, then subjected to FACS analysis. (C) Deletion of Pex19 but not Pex5 induces a new fraction of polynuclear mitotic cells. WT, Pex5 KO, and Pex19 KO 46C mESCs treated with or without 50 ng/mL nocodazole were stained with an anti-H3pS10 antibody for detection of mitotic cells and DAPI for DNA content, then subjected to FACS analysis. The M-B population represents polynuclear mitotic cells arrested by deletion of Pex19 or treatment with nocodazole. (D and E) Deletion of Pex19 delays cell cycle progression of mESCs. WT and Pex19 KO 46C mESCs treated with 50 ng/mL nocodazole for 5 h were transferred into normal culture medium without nocodazole, and cell cycle progression was analyzed 15 and 25 min later (three groups of cells (80–250 cells/group) from randomly selected fields were analyzed for each time point for both WT and Pex19 KO mESCs; data are presented as mean ± SEM). Scale bars, 10 μm. See also .$

Journal: iScience

Article Title: Peroxisome-dependent and -independent functions of PEX19 in mouse embryonic stem cells

doi: 10.1016/j.isci.2026.117658

Figure Lengend Snippet: Deletion of Pex19 induces mitotic block in mESCs (A) Deletion of Pex19 impairs cell cycle progression and induces polynuclear mESCs. WT, Pex19 KO, and Pex19 KO + PEX19 46C mESCs were stained with PI for DNA content, then subjected to FACS analysis ( n = 3 biological replicates/group; data are presented as mean ± SEM). (B) Deletion of Pex5 in mESCs fails to induce detectable defects in the cell cycle. WT, Pex5 KO, and Pex19 KO 46C mESCs were stained with DAPI for DNA content, then subjected to FACS analysis. (C) Deletion of Pex19 but not Pex5 induces a new fraction of polynuclear mitotic cells. WT, Pex5 KO, and Pex19 KO 46C mESCs treated with or without 50 ng/mL nocodazole were stained with an anti-H3pS10 antibody for detection of mitotic cells and DAPI for DNA content, then subjected to FACS analysis. The M-B population represents polynuclear mitotic cells arrested by deletion of Pex19 or treatment with nocodazole. (D and E) Deletion of Pex19 delays cell cycle progression of mESCs. WT and Pex19 KO 46C mESCs treated with 50 ng/mL nocodazole for 5 h were transferred into normal culture medium without nocodazole, and cell cycle progression was analyzed 15 and 25 min later (three groups of cells (80–250 cells/group) from randomly selected fields were analyzed for each time point for both WT and Pex19 KO mESCs; data are presented as mean ± SEM). Scale bars, 10 μm. See also .

Article Snippet: Mouse anti-PEX19 monoclonal antibody , Novus , NBP2-43544; RRID: AB_3307633.

Techniques: Blocking Assay, Staining, Analysis

Deletion of Pex19 impairs mitotic spindle assembly in mESCs (A) PEX19, not peroxisomes, is enriched near the centrosomes in mitotic mESCs. Scale bars, 5 μm. (B) PEX19 is colocalized with acetyl-K40 α-tubulin at the spindle poles during mitosis. Scale bars, 10 μm. (C) PEX19 interacts with tubulins in mESCs. Total cell lysates from WT and Pex19 KO 46C mESCs were immunoprecipitated (IP) with anti-PEX19 antibodies. (D) Deletion of Pex19 reduces the abundance of α-tubulin and α-tubulin-K40ac in mESCs. WT and Pex19 KO 46C mESCs treated with or without 50 ng/mL nocodazole for 5 h were transferred into normal culture medium without nocodazole, and the abundance of tubulins was analyzed at 0 and 30 min after release into mitosis. (E) Deletion of Pex19 reduces the formation of mitotic spindles in mitotic mESCs. WT and Pex19 KO 46C mESCs were treated as in (D), and α-tubulin-K40ac was analyzed by immunofluorescence staining at 0, 15, and 30 min after release into mitosis. Scale bars, 10 μm. (F) Structural scheme of mouse PEX19 protein. The leucine triad (L18, L21, L22) and F29 in the N-terminal PEX3 binding motif are highlighted. (G) HA-tagged N-terminal PEX3 binding fragment of PEX19 (a.a. 1–49) is expressed in HEK293T cells. HEK293T cells overexpressing the HA-PEX19-N fragment were stained with anti-HA antibodies. Scale bars, 10 μm. (H) The N-terminal PEX3 binding motif of PEX19 interacts with α-tubulin in cells. Total cell lysates from HEK293T cells expressing the indicated HA-tagged PEX19 truncation fragments were analyzed for their interaction with endogenous α-tubulin by co-immunoprecipitation (IP-HA). Please note that HA-PEX19-N was too small to be detected in this immunoblot. See also .

Journal: iScience

Article Title: Peroxisome-dependent and -independent functions of PEX19 in mouse embryonic stem cells

doi: 10.1016/j.isci.2026.117658

Figure Lengend Snippet: Deletion of Pex19 impairs mitotic spindle assembly in mESCs (A) PEX19, not peroxisomes, is enriched near the centrosomes in mitotic mESCs. Scale bars, 5 μm. (B) PEX19 is colocalized with acetyl-K40 α-tubulin at the spindle poles during mitosis. Scale bars, 10 μm. (C) PEX19 interacts with tubulins in mESCs. Total cell lysates from WT and Pex19 KO 46C mESCs were immunoprecipitated (IP) with anti-PEX19 antibodies. (D) Deletion of Pex19 reduces the abundance of α-tubulin and α-tubulin-K40ac in mESCs. WT and Pex19 KO 46C mESCs treated with or without 50 ng/mL nocodazole for 5 h were transferred into normal culture medium without nocodazole, and the abundance of tubulins was analyzed at 0 and 30 min after release into mitosis. (E) Deletion of Pex19 reduces the formation of mitotic spindles in mitotic mESCs. WT and Pex19 KO 46C mESCs were treated as in (D), and α-tubulin-K40ac was analyzed by immunofluorescence staining at 0, 15, and 30 min after release into mitosis. Scale bars, 10 μm. (F) Structural scheme of mouse PEX19 protein. The leucine triad (L18, L21, L22) and F29 in the N-terminal PEX3 binding motif are highlighted. (G) HA-tagged N-terminal PEX3 binding fragment of PEX19 (a.a. 1–49) is expressed in HEK293T cells. HEK293T cells overexpressing the HA-PEX19-N fragment were stained with anti-HA antibodies. Scale bars, 10 μm. (H) The N-terminal PEX3 binding motif of PEX19 interacts with α-tubulin in cells. Total cell lysates from HEK293T cells expressing the indicated HA-tagged PEX19 truncation fragments were analyzed for their interaction with endogenous α-tubulin by co-immunoprecipitation (IP-HA). Please note that HA-PEX19-N was too small to be detected in this immunoblot. See also .

Article Snippet: Mouse anti-PEX19 monoclonal antibody , Novus , NBP2-43544; RRID: AB_3307633.

Techniques: Immunoprecipitation, Immunofluorescence, Staining, Binding Assay, Expressing, Co-Immunoprecipitation Assay, Western Blot

Pex19 KO mESCs have reduced exit from pluripotency during the early stage of neural differentiation (A) Morphology of WT and Pex19 KO 46C mESCs after three days of in vitro neural differentiation. Scale barss, 100 μm. (B) Deletion of Pex19 delays the reduction of pluripotency genes during early neural differentiation. The expression of indicated genes was analyzed before and after three days of in vitro neural differentiation by qPCR ( n = 3 biological replicates/group; data are presented as mean ± SEM; two-way ANOVA, ∗∗∗q < 0.001, ∗∗∗∗q < 0.0001, n.s., not significant). (C) The protein level of Nanog in WT and Pex19 KO cells after three days of in vitro neural differentiation. Scale bars, 20 μm. (D) Adding back PEX19 restores the differentiation-induced reduction of pluripotency protein in Pex19 KO cells. The levels of indicated proteins were analyzed in WT, Pex19 KO (KO), and Pex19 KO + PEX19 (KO + PEX19) 46C mESCs before and after three days of in vitro neural differentiation by immunoblotting. (E) Treatment with DMSO partially increases G1 phase in Pex19 KO cells after three days of in vitro neural differentiation. WT and Pex19 KO 46C mESCs after three days of in vitro neural differentiation with or without 0.1% DMSO were stained with an anti-H3pS10 antibody for detection of mitotic cells and DAPI for DNA content, then subjected to FACS analysis ( n = 3 biological replicates/group; data are presented as mean ± SEM, two-way ANOVA, ∗q < 0.05, ∗∗q < 0.01, n.s., not significant). (F) Adding back PEX19 or treatment with DMSO partially rescues the differentiation defects in Pex19 KO cells. The levels of indicated genes were analyzed in WT, Pex19 KO (KO), or Pex19 KO + PEX19 (KO + P19) 46C mESCs after three days of in vitro neural differentiation with or without 0.1% DMSO by qPCR ( n = 3 biological replicates/group, data are presented as mean ± SEM, two-way ANOVA, ∗q < 0.05, ∗∗q < 0.01, ∗∗∗q < 0.001, and ∗∗∗∗q < 0.0001). (G) Treatment with DMSO partially restores the pluripotency exit defect in Pex19 KO cells. (H) Treatment with a low dose of nocodazole decreases the G1 population in WT cells after three days of in vitro neural differentiation. WT 46C mESCs before (D0) or after three days of in vitro neural differentiation with or without 12.5 ng/mL nocodazole were analyzed for G1 population as in (E) ( n = 3 biological replicates/group; data are presented as mean ± SEM; one-way ANOVA; ∗q < 0.05, ∗∗q < 0.01, n.s., not significant). (I) Treatment with a low dose of nocodazole delays the reduction of pluripotency genes in WT cells after three days of in vitro neural differentiation. The levels of indicated pluripotency genes were analyzed in WT 46C mESCs treated as in (H) ( n = 3 biological replicates/group; data are presented as mean ± SEM, one-way ANOVA, ∗ q < 0.05, ∗∗ q < 0.01, ∗∗∗ q < 0.001, ∗∗∗∗ q < 0.0001, n.s., not significant). See also .

Journal: iScience

Article Title: Peroxisome-dependent and -independent functions of PEX19 in mouse embryonic stem cells

doi: 10.1016/j.isci.2026.117658

Figure Lengend Snippet: Pex19 KO mESCs have reduced exit from pluripotency during the early stage of neural differentiation (A) Morphology of WT and Pex19 KO 46C mESCs after three days of in vitro neural differentiation. Scale barss, 100 μm. (B) Deletion of Pex19 delays the reduction of pluripotency genes during early neural differentiation. The expression of indicated genes was analyzed before and after three days of in vitro neural differentiation by qPCR ( n = 3 biological replicates/group; data are presented as mean ± SEM; two-way ANOVA, ∗∗∗q < 0.001, ∗∗∗∗q < 0.0001, n.s., not significant). (C) The protein level of Nanog in WT and Pex19 KO cells after three days of in vitro neural differentiation. Scale bars, 20 μm. (D) Adding back PEX19 restores the differentiation-induced reduction of pluripotency protein in Pex19 KO cells. The levels of indicated proteins were analyzed in WT, Pex19 KO (KO), and Pex19 KO + PEX19 (KO + PEX19) 46C mESCs before and after three days of in vitro neural differentiation by immunoblotting. (E) Treatment with DMSO partially increases G1 phase in Pex19 KO cells after three days of in vitro neural differentiation. WT and Pex19 KO 46C mESCs after three days of in vitro neural differentiation with or without 0.1% DMSO were stained with an anti-H3pS10 antibody for detection of mitotic cells and DAPI for DNA content, then subjected to FACS analysis ( n = 3 biological replicates/group; data are presented as mean ± SEM, two-way ANOVA, ∗q < 0.05, ∗∗q < 0.01, n.s., not significant). (F) Adding back PEX19 or treatment with DMSO partially rescues the differentiation defects in Pex19 KO cells. The levels of indicated genes were analyzed in WT, Pex19 KO (KO), or Pex19 KO + PEX19 (KO + P19) 46C mESCs after three days of in vitro neural differentiation with or without 0.1% DMSO by qPCR ( n = 3 biological replicates/group, data are presented as mean ± SEM, two-way ANOVA, ∗q < 0.05, ∗∗q < 0.01, ∗∗∗q < 0.001, and ∗∗∗∗q < 0.0001). (G) Treatment with DMSO partially restores the pluripotency exit defect in Pex19 KO cells. (H) Treatment with a low dose of nocodazole decreases the G1 population in WT cells after three days of in vitro neural differentiation. WT 46C mESCs before (D0) or after three days of in vitro neural differentiation with or without 12.5 ng/mL nocodazole were analyzed for G1 population as in (E) ( n = 3 biological replicates/group; data are presented as mean ± SEM; one-way ANOVA; ∗q < 0.05, ∗∗q < 0.01, n.s., not significant). (I) Treatment with a low dose of nocodazole delays the reduction of pluripotency genes in WT cells after three days of in vitro neural differentiation. The levels of indicated pluripotency genes were analyzed in WT 46C mESCs treated as in (H) ( n = 3 biological replicates/group; data are presented as mean ± SEM, one-way ANOVA, ∗ q < 0.05, ∗∗ q < 0.01, ∗∗∗ q < 0.001, ∗∗∗∗ q < 0.0001, n.s., not significant). See also .

Article Snippet: Mouse anti-PEX19 monoclonal antibody , Novus , NBP2-43544; RRID: AB_3307633.

Techniques: Morphology, In Vitro, Expressing, Western Blot, Staining, Analysis

Deletion of Pex19 in mESCs impairs neural differentiation (A and B) Pex19 deficiency alters transcriptomic response of mESCs during the first week of in vitro neural differentiation. WT and Pex19 KO mESCs were subject to in vitro neural differentiation and their transcriptomes at D0, D4, and D7 during differentiation were analyzed by RNA-seq as described in ( n = 3 independent cell clones/genotype). (A) Heatmaps of 2052 differentially expressed protein-coding genes between Pex19 KO vs. WT cells at different time points. (B) Top enriched GO pathways in different gene clusters in (A). (C) Pex19 KO cells have reduced expression of SOX1-GFP at day 6 after in vitro neural differentiation. Scale bars, 300 μm. The percentage of SOX1-GFP positive cells at Day 6 were analyzed by FACS ( n = 5 biological replicates/genotype; data are presented as mean ± SEM; Student’s t test, ∗∗∗∗ p < 0.0001). (D) Pex19 KO cells have reduced expression of different neural markers during three weeks of in vitro neural differentiation. The mRNA levels of indicated genes were analyzed by qPCR ( n = 3 biological replicates/group; data are presented as mean ± SEM; Student’s t test, ∗ p < 0.05, ∗∗ p < 0.01, ∗∗∗, p < 0.001, and ∗∗∗∗ p < 0.0001). (E) Defective neural differentiation of Pex19 KO 46C mESCs at day 21 (D21). The abundance, shape, and distribution of neural morphology marker TUBB3 and neural maturation marker MAP2 were determined by IF staining. Scale bars, 100 μm. See also .

Journal: iScience

Article Title: Peroxisome-dependent and -independent functions of PEX19 in mouse embryonic stem cells

doi: 10.1016/j.isci.2026.117658

Figure Lengend Snippet: Deletion of Pex19 in mESCs impairs neural differentiation (A and B) Pex19 deficiency alters transcriptomic response of mESCs during the first week of in vitro neural differentiation. WT and Pex19 KO mESCs were subject to in vitro neural differentiation and their transcriptomes at D0, D4, and D7 during differentiation were analyzed by RNA-seq as described in ( n = 3 independent cell clones/genotype). (A) Heatmaps of 2052 differentially expressed protein-coding genes between Pex19 KO vs. WT cells at different time points. (B) Top enriched GO pathways in different gene clusters in (A). (C) Pex19 KO cells have reduced expression of SOX1-GFP at day 6 after in vitro neural differentiation. Scale bars, 300 μm. The percentage of SOX1-GFP positive cells at Day 6 were analyzed by FACS ( n = 5 biological replicates/genotype; data are presented as mean ± SEM; Student’s t test, ∗∗∗∗ p < 0.0001). (D) Pex19 KO cells have reduced expression of different neural markers during three weeks of in vitro neural differentiation. The mRNA levels of indicated genes were analyzed by qPCR ( n = 3 biological replicates/group; data are presented as mean ± SEM; Student’s t test, ∗ p < 0.05, ∗∗ p < 0.01, ∗∗∗, p < 0.001, and ∗∗∗∗ p < 0.0001). (E) Defective neural differentiation of Pex19 KO 46C mESCs at day 21 (D21). The abundance, shape, and distribution of neural morphology marker TUBB3 and neural maturation marker MAP2 were determined by IF staining. Scale bars, 100 μm. See also .

Article Snippet: Mouse anti-PEX19 monoclonal antibody , Novus , NBP2-43544; RRID: AB_3307633.

Techniques: In Vitro, RNA Sequencing, Clone Assay, Expressing, Morphology, Marker, Staining

Journal: iScience

Article Title: Peroxisome-dependent and -independent functions of PEX19 in mouse embryonic stem cells

doi: 10.1016/j.isci.2026.117658

Figure Lengend Snippet:

Article Snippet: Mouse anti-PEX19 monoclonal antibody , Novus , NBP2-43544; RRID: AB_3307633.

Techniques: Cell-Signaling, Magnetic Beads, Virus, Recombinant, ROS Assay, Reverse Transcription, SYBR Green Assay, Staining, Plasmid Preparation, Flow Cytometry, Western Blot, Expressing, Control, Software

Journal: Canadian Respiratory Journal

Article Title: Multiple Pulmonary Papillary Adenoma With Malignant Potential Accompanied by ERBIN–BRAF Gene Fusion and APC Mutation: A Case Report and Literature Review

doi: 10.1155/carj/3589904

Figure Lengend Snippet: Summary of previous reports and present case.

Article Snippet: Cytokeratin 7 (CK7) (clone number: UMAB161) and Ki67 (clone number: UMAB107) were purchased from Beijing Zhongshan Golden Bridge Biotechnology Co., Ltd. CK5/6 (clone number: MX040), P40 (clone number: MXR010), P53 (clone number: MX008), thyroid transcription factor 1 (TTF‐1) (clone number: 8G7G3/1), Napsin A (aspartic proteinase A) (clone number: MX015), Chromogranin A (CgA) (clone number: RMA‐0548), synaptophysin (Syn) (clone number: MAB‐0742), and CD56 (neural cell adhesion molecule) (clone number: MX039) were obtained from Fuzhou Maixin Bio‐Tech Development Co., Ltd.

Techniques: Immunohistochemistry, Expressing, Mutagenesis, Membrane, Staining, Tissue

Journal: Canadian Respiratory Journal

Article Title: Multiple Pulmonary Papillary Adenoma With Malignant Potential Accompanied by ERBIN–BRAF Gene Fusion and APC Mutation: A Case Report and Literature Review

doi: 10.1155/carj/3589904

Figure Lengend Snippet: Immunohistochemical staining (magnification × 100). Tumor cells showed diffuse positive expression of CK7 (A), Napsin A (B), and TTF‐1 (C); the Ki‐67 proliferation index was approximately 8% (D). Abbreviations: CK, cytokeratin; TTF‐1, thyroid transcription factor‐1. All figures were derived from original clinical data and were not generated or edited by artificial intelligence tools.

Techniques: Immunohistochemical staining, Staining, Expressing, Derivative Assay, Generated

Real‐time monitoring of tumor progression and anti‐CD47 therapeutic efficiency. (A) Female BALB/c mice aged 8–10 weeks were implanted with dorsal skinfold window chambers. 4T1_PB3R‐RFP TNBC cells were transplanted into the subcutaneous tissue, and tumors were monitored using intravital imaging. (B) Detailed visualization of angiogenesis and tumor nodule formation in TNBC skinfold models compared with the isotype control group. (C, D) Conventional whole‐body bioluminescence imaging of mice bearing 4T1_PB3R‐RFP‐luc tumors revealed considerably decreased signals following anti‐CD47 immunotherapy administered over 5 days, beginning on day 9 for 5 days ( n = 7, p < 0.0001, 10 mg/kg, intravenous injection). Data are presented as the mean ± standard deviation (SD).

Journal: Cancer Medicine

Article Title: In Vivo Immunoscoring Technique to Monitor Anti‐ CD47 Immunotherapy Efficacy in Triple‐Negative Breast Cancer

doi: 10.1002/cam4.72232

Figure Lengend Snippet: Real‐time monitoring of tumor progression and anti‐CD47 therapeutic efficiency. (A) Female BALB/c mice aged 8–10 weeks were implanted with dorsal skinfold window chambers. 4T1_PB3R‐RFP TNBC cells were transplanted into the subcutaneous tissue, and tumors were monitored using intravital imaging. (B) Detailed visualization of angiogenesis and tumor nodule formation in TNBC skinfold models compared with the isotype control group. (C, D) Conventional whole‐body bioluminescence imaging of mice bearing 4T1_PB3R‐RFP‐luc tumors revealed considerably decreased signals following anti‐CD47 immunotherapy administered over 5 days, beginning on day 9 for 5 days ( n = 7, p < 0.0001, 10 mg/kg, intravenous injection). Data are presented as the mean ± standard deviation (SD).

Article Snippet: To evaluate the performance of the in vivo immunoscoring technique for the monitoring of anti‐CD47 immunotherapy efficacy, anti‐mouse CD47 monoclonal antibodies (specifically, anti‐CD47 mAbs, clone MIAP301, Rat IgG2a, κ, BioXcell, USA) and an IgG2a mAbs isotype control (clone 2A3, Rat IgG2a, κ, BioXcell, USA) were systemically and intravenously (IV) injected at a dosage of 10 mg/kg once a day for a duration of five consecutive days.

Techniques: Real-time Monitoring, Tissue, Imaging, Control, Injection, Standard Deviation

In vivo and in vitro validation of TNBC targeting by Dextran‐AF680. (A–C) The signals emitted by Dextran‐AF680 at various time intervals following intravenous injections exhibited significant differences between 10 and 180 min and between 180 and 360 min. (D, E) Dextran‐AF680 can be administrated for TNBC imaging with photoacoustic tomography, and the optimal imaging time is 3 h after dextran injection, indicating its potential as an imaging probe for enhancing TNBC visualization ( n = 7, p = 0.024, p = 0.004). (F, G) Longitudinal conventional fluorescence imaging of the anti‐CD47 immunotherapeutic response, in comparison with the isotype control treatment, demonstrated a significant change in the average radiant efficiency of Dextran AF680 following 5 days of treatment ( n = 12, p = 0.0022). (H, I) An evident shift in the population of Dextran‐AF680+ and RFP+ cells was observed after anti‐CD47 mAb immunotherapies ( n = 10, p = 0.0079). Data are presented as the mean ± standard deviation (SD).

Journal: Cancer Medicine

Article Title: In Vivo Immunoscoring Technique to Monitor Anti‐ CD47 Immunotherapy Efficacy in Triple‐Negative Breast Cancer

doi: 10.1002/cam4.72232

Figure Lengend Snippet: In vivo and in vitro validation of TNBC targeting by Dextran‐AF680. (A–C) The signals emitted by Dextran‐AF680 at various time intervals following intravenous injections exhibited significant differences between 10 and 180 min and between 180 and 360 min. (D, E) Dextran‐AF680 can be administrated for TNBC imaging with photoacoustic tomography, and the optimal imaging time is 3 h after dextran injection, indicating its potential as an imaging probe for enhancing TNBC visualization ( n = 7, p = 0.024, p = 0.004). (F, G) Longitudinal conventional fluorescence imaging of the anti‐CD47 immunotherapeutic response, in comparison with the isotype control treatment, demonstrated a significant change in the average radiant efficiency of Dextran AF680 following 5 days of treatment ( n = 12, p = 0.0022). (H, I) An evident shift in the population of Dextran‐AF680+ and RFP+ cells was observed after anti‐CD47 mAb immunotherapies ( n = 10, p = 0.0079). Data are presented as the mean ± standard deviation (SD).

Techniques: In Vivo, In Vitro, Biomarker Discovery, Imaging, Micro-PAT, Injection, Fluorescence, Comparison, Control, Standard Deviation

Intravital imaging of M2 macrophage targeting by Dextran‐AF680. (A) Dynamic in vivo distribution of intravenously injected Dextran‐AF680 in representative blood vessels of a skinfold TNBC model. The Dextran‐AF680 signal peaked at 3 h and dissipated from the vessels within 24 h. (B) Substantial colocalization was observed between Dextran‐AF680 targeted cells (red) and CD206‐FITC+ cells (green). (C) Antibody‐dependent cellular phagocytosis (ADCP) occured in rapid, brief waves between Dextran‐AF680‐labeled macrophages and CD47 inhibitor‐treated tumor cells in a skinfold TNBC model. (D) CD47 inhibitor‐treated cancer cells (green) were engulfed by macrophages labeled with the pan‐macrophage marker F4/80‐PE (red), underscoring the highly phagocytic nature of macrophages (scale bars, 25 μm). (E) Intravital imaging of the robust phagocytic capacity of F4/80+ macrophages (red) toward CD47 inhibitor‐treated tumor cells (green).

Journal: Cancer Medicine

Article Title: In Vivo Immunoscoring Technique to Monitor Anti‐ CD47 Immunotherapy Efficacy in Triple‐Negative Breast Cancer

doi: 10.1002/cam4.72232

Figure Lengend Snippet: Intravital imaging of M2 macrophage targeting by Dextran‐AF680. (A) Dynamic in vivo distribution of intravenously injected Dextran‐AF680 in representative blood vessels of a skinfold TNBC model. The Dextran‐AF680 signal peaked at 3 h and dissipated from the vessels within 24 h. (B) Substantial colocalization was observed between Dextran‐AF680 targeted cells (red) and CD206‐FITC+ cells (green). (C) Antibody‐dependent cellular phagocytosis (ADCP) occured in rapid, brief waves between Dextran‐AF680‐labeled macrophages and CD47 inhibitor‐treated tumor cells in a skinfold TNBC model. (D) CD47 inhibitor‐treated cancer cells (green) were engulfed by macrophages labeled with the pan‐macrophage marker F4/80‐PE (red), underscoring the highly phagocytic nature of macrophages (scale bars, 25 μm). (E) Intravital imaging of the robust phagocytic capacity of F4/80+ macrophages (red) toward CD47 inhibitor‐treated tumor cells (green).

Techniques: Imaging, In Vivo, Injection, Labeling, Marker

In vivo and in vitro validation of TNBC targeting by MCP1‐FITC. (A, B) Following intravenous injection of MCP1‐FITC, fluorescence signals in TNBC tissue peaked at 4 min and rapidly declined within 2 h ( n = 6, p = 0.0313). (C, D) Ex vivo imaging of dissected organs from subcutaneous xenograft models revealed a noticeable difference in fluorescence signal intensity between TNBC tumors and normal organs at 4 min after intravenous injection of MCP1‐FITC ( n = 6, p = 0.0095). (E, F) The average radiant efficiency of MCP1‐FITC in resected TNBC tissues was quantitively compared between the anti‐CD47 monoclonal antibody (mAb) and isotype control (ISO) treatment groups ( n = 16, p = 0.0499). (G) A significant difference in the M1/M2 ratio, based on the average radiant efficiency, was observed between anti‐CD47 mAb‐treated and ISO‐treated mice ( n = 12, p = 0.0022). (H) A pronounced shift in the population of MCP1‐FITC targeted cells was observed following repeated immunotherapy. (I, J) Significant differences in the M1/M2 ratio, based on the MCP‐1 FITC+ cells, is observed between anti‐CD47 mAb‐treated and ISO‐treated mice ( n = 16, p = 0.0104), ( n = 10, p = 0.0079). (K) A correlation analysis indicated that there is a strong correlation between the flow cytometry‐derived M1/M2 ratio and the imaging‐derived M1/M2 ratio. Data are presented as the mean ± standard deviation (SD).

Journal: Cancer Medicine

Article Title: In Vivo Immunoscoring Technique to Monitor Anti‐ CD47 Immunotherapy Efficacy in Triple‐Negative Breast Cancer

doi: 10.1002/cam4.72232

Figure Lengend Snippet: In vivo and in vitro validation of TNBC targeting by MCP1‐FITC. (A, B) Following intravenous injection of MCP1‐FITC, fluorescence signals in TNBC tissue peaked at 4 min and rapidly declined within 2 h ( n = 6, p = 0.0313). (C, D) Ex vivo imaging of dissected organs from subcutaneous xenograft models revealed a noticeable difference in fluorescence signal intensity between TNBC tumors and normal organs at 4 min after intravenous injection of MCP1‐FITC ( n = 6, p = 0.0095). (E, F) The average radiant efficiency of MCP1‐FITC in resected TNBC tissues was quantitively compared between the anti‐CD47 monoclonal antibody (mAb) and isotype control (ISO) treatment groups ( n = 16, p = 0.0499). (G) A significant difference in the M1/M2 ratio, based on the average radiant efficiency, was observed between anti‐CD47 mAb‐treated and ISO‐treated mice ( n = 12, p = 0.0022). (H) A pronounced shift in the population of MCP1‐FITC targeted cells was observed following repeated immunotherapy. (I, J) Significant differences in the M1/M2 ratio, based on the MCP‐1 FITC+ cells, is observed between anti‐CD47 mAb‐treated and ISO‐treated mice ( n = 16, p = 0.0104), ( n = 10, p = 0.0079). (K) A correlation analysis indicated that there is a strong correlation between the flow cytometry‐derived M1/M2 ratio and the imaging‐derived M1/M2 ratio. Data are presented as the mean ± standard deviation (SD).

Techniques: In Vivo, In Vitro, Biomarker Discovery, Injection, Fluorescence, Tissue, Ex Vivo, Imaging, Xenograft Assay, Control, Analysis, Flow Cytometry, Derivative Assay, Standard Deviation

ONS76 ( A ) and UW228-3 ( B ) cells were exposed to the indicated doses γIR and harvested at day 4, 5 and 6 after irradiation. Protein extracts were analyzed by western blotting for the expression of p53, p21, and Bcl-2, as well as actin as a housekeeper control. Please note that the ONS76 sample at day 5 after 9 Gy γIR was included on the UW228-3 blot ( B ) for a better comparison of protein expression levels between these two cell lines. This demonstrates the much lower p21 protein expression in irradiated p53-mutated UW228 cells when compared to irradiated p53 wild-type ONS76 cells. ( C–E ) ONS76 cells were transfected with ON-TARGET plus siRNA pools directed against p53 or p21, or with a nontargeting pool (siCon) as a control. 24 h after transfection, cells were divided equally and either left untreated (day 0) or were irradiated with 16 Gy γIR. At days 3 and 5 after irradiation, the cells were harvested and analyzed by western blotting ( C ) and flow cytometrical determination of Zombie-violet-( D ) and GLF16-positive cells ( E ). For ( D, E ), the mean % of positive cells ± S.D. of three independent experiments is shown. Individual data points are displayed in the bar charts by small filled circles. ** p < 0.01, *** p < 0.001. For ( A–C ), the western blots shown are representative of three to four independent experiments. Densitometric analyses of these blots can be found in Supplementary Fig. ( A–F ).

Journal: Cell Death Discovery

Article Title: p53 wild-type/low c-Myc-expressing ONS76 pediatric medulloblastoma cells become senescent after gamma-irradiation and can be eliminated by senolytic substances

doi: 10.1038/s41420-026-03404-4

Figure Lengend Snippet: ONS76 ( A ) and UW228-3 ( B ) cells were exposed to the indicated doses γIR and harvested at day 4, 5 and 6 after irradiation. Protein extracts were analyzed by western blotting for the expression of p53, p21, and Bcl-2, as well as actin as a housekeeper control. Please note that the ONS76 sample at day 5 after 9 Gy γIR was included on the UW228-3 blot ( B ) for a better comparison of protein expression levels between these two cell lines. This demonstrates the much lower p21 protein expression in irradiated p53-mutated UW228 cells when compared to irradiated p53 wild-type ONS76 cells. ( C–E ) ONS76 cells were transfected with ON-TARGET plus siRNA pools directed against p53 or p21, or with a nontargeting pool (siCon) as a control. 24 h after transfection, cells were divided equally and either left untreated (day 0) or were irradiated with 16 Gy γIR. At days 3 and 5 after irradiation, the cells were harvested and analyzed by western blotting ( C ) and flow cytometrical determination of Zombie-violet-( D ) and GLF16-positive cells ( E ). For ( D, E ), the mean % of positive cells ± S.D. of three independent experiments is shown. Individual data points are displayed in the bar charts by small filled circles. ** p < 0.01, *** p < 0.001. For ( A–C ), the western blots shown are representative of three to four independent experiments. Densitometric analyses of these blots can be found in Supplementary Fig. ( A–F ).

Article Snippet: From Santa Cruz (Heidelberg, Germany) was the mouse monoclonal Bcl-2 antibody (clone C-2; # sc-7382; AB_626736).

Techniques: Irradiation, Western Blot, Expressing, Control, Comparison, Transfection

Review

ki67 (OriGene)

Structured Review

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1) Product Images from "Multiple Pulmonary Papillary Adenoma With Malignant Potential Accompanied by ERBIN–BRAF Gene Fusion and APC Mutation: A Case Report and Literature Review"

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