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Proteintech rabbit anti pex14 polyclonal antibody
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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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 <t>Pex5</t> 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 .
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Image Search Results


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

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

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: Rabbit anti-PEX5 polyclonal antibody , Novus , NBP1-87185; RRID: AB_11023925.

Techniques: Blocking Assay, Staining, Analysis

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-PEX5 polyclonal antibody , Novus , NBP1-87185; RRID: AB_11023925.

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: 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-p65 rabbit antibody , Proteintech , 10745-1-AP; RRID: AB_2178878.

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