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The BmMKLP1 domains exhibit divergent nuclear and cytoplasmic localization (A) Subcellular localization of transiently expressed <t>GFP-tagged</t> domains (green) in BmN4 cells. Representative merged bright-field and <t>GFP</t> fluorescence images acquired at 10×, scale bars, 100 μm, BmN4 cells expressing the indicated constructs were imaged by differential interference contrast (DIC) microscopy (left) to show cell morphology and by fluorescence microscopy (right) to detect GFP-tagged proteins. All images were acquired with a 40× objective lens. Scale bars, 20 μm. (B) Western blot analysis of protein extracts from transfected BmN4 cells probed with <t>an</t> <t>anti-GFP</t> antibody (1:1,000, Proteintech, Wuhan, China), confirming the production of each GFP-tagged domain at its expected molecular weight. The “control” lane corresponds to the cycle 3 GFP-bleo fusion protein (∼39–40 KDa) expressed from the pIZT/V5-His vector. A representative blot from three independent experiments is shown. The PageRuler Prestained Protein Ladder (10–180 kDa; Thermo Fisher Scientific, Waltham, MA, USA) was used as a molecular weight marker.
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CCL-18 do not mediate glioma recurrence following radiotherapy in vivo (A) Viability of GL261 cells after treatment with different concentrations of CCL-18. Data were presented as mean ± SEM (one-way ANOVA, F = 0.9, p = 0.48, ∗∗∗ p < 0.001). (B) Viability of GL261 cells after treatment with CCL-18 (100 ng/mL) and R243 (50, 100 μM). Data were presented as mean ± SEM (one-way ANOVA, F = 1.43, p = 0.28, ∗ p < 0.05, ∗∗∗ p < 0.001). (C) Representative immunoblot of <t>ACP5,</t> Akt, and phosphorylated Akt on GL261 cells after CCL-18 (100 ng/mL) treatment. (D) Schematic workflow for the cell-derived allograft experiment. (E) The bioluminescence value in mice receiving radiation on the indicated days. Data were presented as mean ± SEM (one-way ANOVA, in radiation: F = 2.48, p = 0.1, ∗ p < 0.05; in radiation with CCL-18 treatment: F = 1.41, p = 0.3, ∗ p < 0.05). (F) Representative pseudo-color bioluminescence images of intracranial allografts receiving radiation with or without CCL-18 administration. (G) Quantitative results from (F) on the indicated days. Data were presented as mean ± SEM (two-way ANOVA, F = 2.39, p = 0.04, ∗ p < 0.05, ∗∗ p < 0.01). (H) Kaplan-Meier curve showing the percent survival of mice receiving different treatment. Data were presented as median (∗∗∗ p < 0.001). (I) The percent of M1-TAM in glioma after radiation with or without CCL-18 treatment. (J) Quantitative results from (I). Data were presented as mean ± SD (one-way ANOVA, F = 1.46, p = 0.26). (K)The percent of M2-TAM in glioma after radiation with or without CCL-18 treatment. (L) Quantitative results from (K). Data were presented as mean ± SD (one-way ANOVA, F = 0.1, p = 0.9). Data were obtained from 3 independent experiments (A, C, and I–L), and 4 independent experiments (B). Data were obtained from ≥6 mice (E), ≥11 mice (G and H), and 3 mice (I–L).
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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 <t>PEX14.</t> 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 .
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Image Search Results


The BmMKLP1 domains exhibit divergent nuclear and cytoplasmic localization (A) Subcellular localization of transiently expressed GFP-tagged domains (green) in BmN4 cells. Representative merged bright-field and GFP fluorescence images acquired at 10×, scale bars, 100 μm, BmN4 cells expressing the indicated constructs were imaged by differential interference contrast (DIC) microscopy (left) to show cell morphology and by fluorescence microscopy (right) to detect GFP-tagged proteins. All images were acquired with a 40× objective lens. Scale bars, 20 μm. (B) Western blot analysis of protein extracts from transfected BmN4 cells probed with an anti-GFP antibody (1:1,000, Proteintech, Wuhan, China), confirming the production of each GFP-tagged domain at its expected molecular weight. The “control” lane corresponds to the cycle 3 GFP-bleo fusion protein (∼39–40 KDa) expressed from the pIZT/V5-His vector. A representative blot from three independent experiments is shown. The PageRuler Prestained Protein Ladder (10–180 kDa; Thermo Fisher Scientific, Waltham, MA, USA) was used as a molecular weight marker.

Journal: iScience

Article Title: Domain-autonomous MKLP1 modules divergently regulate mitotic fidelity and polyploidy in a holocentric system

doi: 10.1016/j.isci.2026.117149

Figure Lengend Snippet: The BmMKLP1 domains exhibit divergent nuclear and cytoplasmic localization (A) Subcellular localization of transiently expressed GFP-tagged domains (green) in BmN4 cells. Representative merged bright-field and GFP fluorescence images acquired at 10×, scale bars, 100 μm, BmN4 cells expressing the indicated constructs were imaged by differential interference contrast (DIC) microscopy (left) to show cell morphology and by fluorescence microscopy (right) to detect GFP-tagged proteins. All images were acquired with a 40× objective lens. Scale bars, 20 μm. (B) Western blot analysis of protein extracts from transfected BmN4 cells probed with an anti-GFP antibody (1:1,000, Proteintech, Wuhan, China), confirming the production of each GFP-tagged domain at its expected molecular weight. The “control” lane corresponds to the cycle 3 GFP-bleo fusion protein (∼39–40 KDa) expressed from the pIZT/V5-His vector. A representative blot from three independent experiments is shown. The PageRuler Prestained Protein Ladder (10–180 kDa; Thermo Fisher Scientific, Waltham, MA, USA) was used as a molecular weight marker.

Article Snippet: Scale bars, 20 μm. (B) Western blot analysis of protein extracts from transfected BmN4 cells probed with an anti-GFP antibody (1:1,000, Proteintech, Wuhan, China), confirming the production of each GFP-tagged domain at its expected molecular weight.

Techniques: Fluorescence, Expressing, Construct, Microscopy, Morphology, Western Blot, Analysis, Transfection, Molecular Weight, Control, Plasmid Preparation, Marker

The head and stalk domains induce G2/M arrest, whereas the tail promotes polyploidization (A) Representative flow cytometry histograms showing DNA content profiles (top) and polyploidy distributions (bottom) for control cells and cells expressing GFP-tagged BmMKLP1—full-length, head, -stalk, or -tail. Cell cycle phases (G0/G1, S, and G2/M) were determined by model-based fitting of propidium iodide (PI) fluorescence intensity histograms. Polyploidy histograms depict cells with DNA content exceeding 4 N. (B) Quantification of cell cycle distribution under each condition. Bars represent the mean ± SEM percentage of cells in G0/G1, S, and G2/M phases from at least three independent experiments. Different lowercase letters indicate significant differences (one-way ANOVA followed by Tukey’s HSD, p < 0.05). (C) Percentage of polyploid cells under each condition. Bars represent mean ± SEM, with statistical significance assessed as in (B).

Journal: iScience

Article Title: Domain-autonomous MKLP1 modules divergently regulate mitotic fidelity and polyploidy in a holocentric system

doi: 10.1016/j.isci.2026.117149

Figure Lengend Snippet: The head and stalk domains induce G2/M arrest, whereas the tail promotes polyploidization (A) Representative flow cytometry histograms showing DNA content profiles (top) and polyploidy distributions (bottom) for control cells and cells expressing GFP-tagged BmMKLP1—full-length, head, -stalk, or -tail. Cell cycle phases (G0/G1, S, and G2/M) were determined by model-based fitting of propidium iodide (PI) fluorescence intensity histograms. Polyploidy histograms depict cells with DNA content exceeding 4 N. (B) Quantification of cell cycle distribution under each condition. Bars represent the mean ± SEM percentage of cells in G0/G1, S, and G2/M phases from at least three independent experiments. Different lowercase letters indicate significant differences (one-way ANOVA followed by Tukey’s HSD, p < 0.05). (C) Percentage of polyploid cells under each condition. Bars represent mean ± SEM, with statistical significance assessed as in (B).

Article Snippet: Scale bars, 20 μm. (B) Western blot analysis of protein extracts from transfected BmN4 cells probed with an anti-GFP antibody (1:1,000, Proteintech, Wuhan, China), confirming the production of each GFP-tagged domain at its expected molecular weight.

Techniques: Flow Cytometry, Control, Expressing, Fluorescence

Journal: iScience

Article Title: Domain-autonomous MKLP1 modules divergently regulate mitotic fidelity and polyploidy in a holocentric system

doi: 10.1016/j.isci.2026.117149

Figure Lengend Snippet:

Article Snippet: Scale bars, 20 μm. (B) Western blot analysis of protein extracts from transfected BmN4 cells probed with an anti-GFP antibody (1:1,000, Proteintech, Wuhan, China), confirming the production of each GFP-tagged domain at its expected molecular weight.

Techniques: Transfection, Cloning, Imaging, Bicinchoninic Acid Protein Assay, Western Blot, Plasmid Preparation, Recombinant, Software

Journal: iScience

Article Title: M2 type tumor-associated macrophage-derived CCL-18 promotes glioma cell proliferation but does not mediates glioma recurrence after radiotherapy

doi: 10.1016/j.isci.2026.117695

Figure Lengend Snippet:

Article Snippet: Anti-p105/p50 rabbit antibody , Proteintech , 14220-1-AP; RRID: AB_2153393.

Techniques: Cell-Signaling, Virus, Tissue, Microarray, Recombinant, cDNA Synthesis, Enzyme-linked Immunosorbent Assay, Software, Biomarker Discovery, In Vivo Imaging

Journal: iScience

Article Title: Domain-autonomous MKLP1 modules divergently regulate mitotic fidelity and polyploidy in a holocentric system

doi: 10.1016/j.isci.2026.117149

Figure Lengend Snippet:

Article Snippet: rabbit anti-β-tubulin , Proteintech, Wuhan, China , Cat#10094-1-AP;RRID:AB_2210695.

Techniques: Transfection, Cloning, Imaging, Bicinchoninic Acid Protein Assay, Western Blot, Plasmid Preparation, Recombinant, Software

Journal: iScience

Article Title: TXNRD1-driven enteric glial remodeling promotes neuronal dysfunction in Hirschsprung disease

doi: 10.1016/j.isci.2026.117636

Figure Lengend Snippet:

Article Snippet: Rabbit anti-SPP1 , Proteintech , Cat# 22952-1-AP; RRID: AB_2783651.

Techniques: Model Organisms, Recombinant, CCK-8 Assay, Apoptosis Assay, ROS Assay, Calcium Assay, Enzyme-linked Immunosorbent Assay, Generated, Software, Genotyping

CCL-18 do not mediate glioma recurrence following radiotherapy in vivo (A) Viability of GL261 cells after treatment with different concentrations of CCL-18. Data were presented as mean ± SEM (one-way ANOVA, F = 0.9, p = 0.48, ∗∗∗ p < 0.001). (B) Viability of GL261 cells after treatment with CCL-18 (100 ng/mL) and R243 (50, 100 μM). Data were presented as mean ± SEM (one-way ANOVA, F = 1.43, p = 0.28, ∗ p < 0.05, ∗∗∗ p < 0.001). (C) Representative immunoblot of ACP5, Akt, and phosphorylated Akt on GL261 cells after CCL-18 (100 ng/mL) treatment. (D) Schematic workflow for the cell-derived allograft experiment. (E) The bioluminescence value in mice receiving radiation on the indicated days. Data were presented as mean ± SEM (one-way ANOVA, in radiation: F = 2.48, p = 0.1, ∗ p < 0.05; in radiation with CCL-18 treatment: F = 1.41, p = 0.3, ∗ p < 0.05). (F) Representative pseudo-color bioluminescence images of intracranial allografts receiving radiation with or without CCL-18 administration. (G) Quantitative results from (F) on the indicated days. Data were presented as mean ± SEM (two-way ANOVA, F = 2.39, p = 0.04, ∗ p < 0.05, ∗∗ p < 0.01). (H) Kaplan-Meier curve showing the percent survival of mice receiving different treatment. Data were presented as median (∗∗∗ p < 0.001). (I) The percent of M1-TAM in glioma after radiation with or without CCL-18 treatment. (J) Quantitative results from (I). Data were presented as mean ± SD (one-way ANOVA, F = 1.46, p = 0.26). (K)The percent of M2-TAM in glioma after radiation with or without CCL-18 treatment. (L) Quantitative results from (K). Data were presented as mean ± SD (one-way ANOVA, F = 0.1, p = 0.9). Data were obtained from 3 independent experiments (A, C, and I–L), and 4 independent experiments (B). Data were obtained from ≥6 mice (E), ≥11 mice (G and H), and 3 mice (I–L).

Journal: iScience

Article Title: M2 type tumor-associated macrophage-derived CCL-18 promotes glioma cell proliferation but does not mediates glioma recurrence after radiotherapy

doi: 10.1016/j.isci.2026.117695

Figure Lengend Snippet: CCL-18 do not mediate glioma recurrence following radiotherapy in vivo (A) Viability of GL261 cells after treatment with different concentrations of CCL-18. Data were presented as mean ± SEM (one-way ANOVA, F = 0.9, p = 0.48, ∗∗∗ p < 0.001). (B) Viability of GL261 cells after treatment with CCL-18 (100 ng/mL) and R243 (50, 100 μM). Data were presented as mean ± SEM (one-way ANOVA, F = 1.43, p = 0.28, ∗ p < 0.05, ∗∗∗ p < 0.001). (C) Representative immunoblot of ACP5, Akt, and phosphorylated Akt on GL261 cells after CCL-18 (100 ng/mL) treatment. (D) Schematic workflow for the cell-derived allograft experiment. (E) The bioluminescence value in mice receiving radiation on the indicated days. Data were presented as mean ± SEM (one-way ANOVA, in radiation: F = 2.48, p = 0.1, ∗ p < 0.05; in radiation with CCL-18 treatment: F = 1.41, p = 0.3, ∗ p < 0.05). (F) Representative pseudo-color bioluminescence images of intracranial allografts receiving radiation with or without CCL-18 administration. (G) Quantitative results from (F) on the indicated days. Data were presented as mean ± SEM (two-way ANOVA, F = 2.39, p = 0.04, ∗ p < 0.05, ∗∗ p < 0.01). (H) Kaplan-Meier curve showing the percent survival of mice receiving different treatment. Data were presented as median (∗∗∗ p < 0.001). (I) The percent of M1-TAM in glioma after radiation with or without CCL-18 treatment. (J) Quantitative results from (I). Data were presented as mean ± SD (one-way ANOVA, F = 1.46, p = 0.26). (K)The percent of M2-TAM in glioma after radiation with or without CCL-18 treatment. (L) Quantitative results from (K). Data were presented as mean ± SD (one-way ANOVA, F = 0.1, p = 0.9). Data were obtained from 3 independent experiments (A, C, and I–L), and 4 independent experiments (B). Data were obtained from ≥6 mice (E), ≥11 mice (G and H), and 3 mice (I–L).

Article Snippet: Anti-ACP5 rabbit antibody , Proteintech , 11594-1-AP; RRID: AB_2877781.

Techniques: In Vivo, Western Blot, Derivative Assay

Journal: iScience

Article Title: M2 type tumor-associated macrophage-derived CCL-18 promotes glioma cell proliferation but does not mediates glioma recurrence after radiotherapy

doi: 10.1016/j.isci.2026.117695

Figure Lengend Snippet:

Article Snippet: Anti-ACP5 rabbit antibody , Proteintech , 11594-1-AP; RRID: AB_2877781.

Techniques: Cell-Signaling, Virus, Tissue, Microarray, Recombinant, cDNA Synthesis, Enzyme-linked Immunosorbent Assay, Software, Biomarker Discovery, In Vivo Imaging

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: Rabbit anti-ESRRB polyclonal antibody , Proteintech , 22644-1-AP; RRID: AB_2879140.

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: iScience

Article Title: Domain-autonomous MKLP1 modules divergently regulate mitotic fidelity and polyploidy in a holocentric system

doi: 10.1016/j.isci.2026.117149

Figure Lengend Snippet:

Article Snippet: rabbit anti-γ-tubulin , Proteintech, Wuhan, China , Cat#15176-1-AP;RRID:AB_2878113.

Techniques: Transfection, Cloning, Imaging, Bicinchoninic Acid Protein Assay, Western Blot, Plasmid Preparation, Recombinant, Software

Journal: iScience

Article Title: Domain-autonomous MKLP1 modules divergently regulate mitotic fidelity and polyploidy in a holocentric system

doi: 10.1016/j.isci.2026.117149

Figure Lengend Snippet:

Article Snippet: mouse anti-α-tubulin , Proteintech, Wuhan, China , Cat#66031-1-Ig;RRID:AB_11042766.

Techniques: Transfection, Cloning, Imaging, Bicinchoninic Acid Protein Assay, Western Blot, Plasmid Preparation, Recombinant, Software

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: Rabbit anti-PEX14 polyclonal antibody , Proteintech , 10594-1-AP; RRID: AB_2252194.

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

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: Rabbit anti-PEX14 polyclonal antibody , Proteintech , 10594-1-AP; RRID: AB_2252194.

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