prmt1 inhibitor furamidine Search Results


furamidine  (MedChemExpress)
93
MedChemExpress furamidine
Effect of <t>furamidine</t> on proliferation of U87MG-derived GSCs in vitro and in vivo. ( A ) Protein expression levels of <t>PRMT1</t> in U87MG adherent and tumorsphere cells. Protein levels were detected by Western blotting and quantified by densitometry. β-Actin levels were used as a loading control. * p < 0.05. ( B ) Effect of furamidine on the proliferation and tumorsphere formation in U87MG-derived GSCs. Cells were treated with furamidine at various concentrations (0–100 μM) for 7 days. Cell proliferation was measured using the CellTiter-Glo ® luminescent assay system. Formed tumorspheres were counted under an optical microscope. ** p < 0.005, *** p < 0.001 vs. the control. ( C ) Effect of furamidine on tumor growth derived by U87MG GSCs in a CAM model. U87MG-derived GSCs were mixed with ECM gel in the absence or presence of the furamidine (10 µg/egg) and placed onto the CAM surface of fertilized chick eggs. After incubation for 7 days, the size and weight of the formed tumors were calculated. * p < 0.05 vs. the control.
Furamidine, supplied by MedChemExpress, used in various techniques. Bioz Stars score: 93/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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furamidine dihydrochloride  (Bio-Techne corporation)
89
Bio-Techne corporation furamidine dihydrochloride
Effect of <t>furamidine</t> on proliferation of U87MG-derived GSCs in vitro and in vivo. ( A ) Protein expression levels of <t>PRMT1</t> in U87MG adherent and tumorsphere cells. Protein levels were detected by Western blotting and quantified by densitometry. β-Actin levels were used as a loading control. * p < 0.05. ( B ) Effect of furamidine on the proliferation and tumorsphere formation in U87MG-derived GSCs. Cells were treated with furamidine at various concentrations (0–100 μM) for 7 days. Cell proliferation was measured using the CellTiter-Glo ® luminescent assay system. Formed tumorspheres were counted under an optical microscope. ** p < 0.005, *** p < 0.001 vs. the control. ( C ) Effect of furamidine on tumor growth derived by U87MG GSCs in a CAM model. U87MG-derived GSCs were mixed with ECM gel in the absence or presence of the furamidine (10 µg/egg) and placed onto the CAM surface of fertilized chick eggs. After incubation for 7 days, the size and weight of the formed tumors were calculated. * p < 0.05 vs. the control.
Furamidine Dihydrochloride, supplied by Bio-Techne corporation, used in various techniques. Bioz Stars score: 89/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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prmt-1 inhibitor furamidine  (Tocris)
90
Tocris prmt-1 inhibitor furamidine
Effect of <t>furamidine</t> on proliferation of U87MG-derived GSCs in vitro and in vivo. ( A ) Protein expression levels of <t>PRMT1</t> in U87MG adherent and tumorsphere cells. Protein levels were detected by Western blotting and quantified by densitometry. β-Actin levels were used as a loading control. * p < 0.05. ( B ) Effect of furamidine on the proliferation and tumorsphere formation in U87MG-derived GSCs. Cells were treated with furamidine at various concentrations (0–100 μM) for 7 days. Cell proliferation was measured using the CellTiter-Glo ® luminescent assay system. Formed tumorspheres were counted under an optical microscope. ** p < 0.005, *** p < 0.001 vs. the control. ( C ) Effect of furamidine on tumor growth derived by U87MG GSCs in a CAM model. U87MG-derived GSCs were mixed with ECM gel in the absence or presence of the furamidine (10 µg/egg) and placed onto the CAM surface of fertilized chick eggs. After incubation for 7 days, the size and weight of the formed tumors were calculated. * p < 0.05 vs. the control.
Prmt 1 Inhibitor Furamidine, supplied by Tocris, used in various techniques. Bioz Stars score: 90/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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prmt1 inhibitor db75  (Millipore)
90
Millipore prmt1 inhibitor db75
Upon TPO stimulation, human umbilical cord blood CD34+ cells differentiate into mature megakaryocytes. (A) FACS analysis of CD41 and CD42 double-positive cells cultured in medium containing high TPO on days 7, 10, 13 and 18. (B) Changes to RBM15 and <t>PRMT1</t> expression at 12, 24, 48 and 72 h of TPO treatment. The mRNA levels were calculated as the mean ± standard deviation from three independent experiments. (C) Intracellular immunostaining with anti-PRMT1 and anti-RBM15 antibodies (magnification, ×400). (D) PRMT1 and RBM15 protein levels were detected by FACS analysis in the course of megakaryocyte differentiation. Results are displayed as histogram overlays. **P<0.01 vs. 0 h. CD, cluster of differentiation; FACS, fluorescence-activated cell sorting; RBM15, RNA binding motif protein 15; PRMT1, protein arginine methyltransferase 1; PRMT1V2, PRMT1 V2 isoform; DAPI, 4,6-diamidino-2-phenylindole; TPO, thrombopoitin.
Prmt1 Inhibitor Db75, supplied by Millipore, used in various techniques. Bioz Stars score: 90/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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Image Search Results


Effect of furamidine on proliferation of U87MG-derived GSCs in vitro and in vivo. ( A ) Protein expression levels of PRMT1 in U87MG adherent and tumorsphere cells. Protein levels were detected by Western blotting and quantified by densitometry. β-Actin levels were used as a loading control. * p < 0.05. ( B ) Effect of furamidine on the proliferation and tumorsphere formation in U87MG-derived GSCs. Cells were treated with furamidine at various concentrations (0–100 μM) for 7 days. Cell proliferation was measured using the CellTiter-Glo ® luminescent assay system. Formed tumorspheres were counted under an optical microscope. ** p < 0.005, *** p < 0.001 vs. the control. ( C ) Effect of furamidine on tumor growth derived by U87MG GSCs in a CAM model. U87MG-derived GSCs were mixed with ECM gel in the absence or presence of the furamidine (10 µg/egg) and placed onto the CAM surface of fertilized chick eggs. After incubation for 7 days, the size and weight of the formed tumors were calculated. * p < 0.05 vs. the control.

Journal: International Journal of Molecular Sciences

Article Title: Inhibition of PRMT1 Suppresses the Growth of U87MG-Derived Glioblastoma Stem Cells by Blocking the STAT3 Signaling Pathway

doi: 10.3390/ijms25052950

Figure Lengend Snippet: Effect of furamidine on proliferation of U87MG-derived GSCs in vitro and in vivo. ( A ) Protein expression levels of PRMT1 in U87MG adherent and tumorsphere cells. Protein levels were detected by Western blotting and quantified by densitometry. β-Actin levels were used as a loading control. * p < 0.05. ( B ) Effect of furamidine on the proliferation and tumorsphere formation in U87MG-derived GSCs. Cells were treated with furamidine at various concentrations (0–100 μM) for 7 days. Cell proliferation was measured using the CellTiter-Glo ® luminescent assay system. Formed tumorspheres were counted under an optical microscope. ** p < 0.005, *** p < 0.001 vs. the control. ( C ) Effect of furamidine on tumor growth derived by U87MG GSCs in a CAM model. U87MG-derived GSCs were mixed with ECM gel in the absence or presence of the furamidine (10 µg/egg) and placed onto the CAM surface of fertilized chick eggs. After incubation for 7 days, the size and weight of the formed tumors were calculated. * p < 0.05 vs. the control.

Article Snippet: Furamidine (PRMT1 inhibitor), berbamine (CaMKIIγ inhibitor), and colivelin (STAT3 activator) were purchased from Tocris (Bristol, UK), Sigma-Aldrich (St. Louis, MO, USA), and MedChemExpress (Monmouth Junction, NJ, USA), respectively.

Techniques: Derivative Assay, In Vitro, In Vivo, Expressing, Western Blot, Control, Luminescence Assay, Microscopy, Incubation

Effect of furamidine on cell cycle and apoptosis in U87MG-derived GSCs. ( A – D ) U87MG-derived GSCs were treated with furamidine (10, 20, and 40 μM) for 48 h. ( A ) Cells were stained with Muse ® Cell Cycle reagent, and cell cycle distribution was measured using the Muse Cell Analyzer. ( B ) Cells were stained with Muse ® Annexin V and Dead Cell reagent, and apoptotic cells were detected using the Muse Cell Analyzer. ( C , D ) The expression levels of cell cycle and apoptosis-related proteins were detected by Western blotting and quantified by densitometry. β-Actin levels were used as a loading control. * p < 0.05 vs. the control.

Journal: International Journal of Molecular Sciences

Article Title: Inhibition of PRMT1 Suppresses the Growth of U87MG-Derived Glioblastoma Stem Cells by Blocking the STAT3 Signaling Pathway

doi: 10.3390/ijms25052950

Figure Lengend Snippet: Effect of furamidine on cell cycle and apoptosis in U87MG-derived GSCs. ( A – D ) U87MG-derived GSCs were treated with furamidine (10, 20, and 40 μM) for 48 h. ( A ) Cells were stained with Muse ® Cell Cycle reagent, and cell cycle distribution was measured using the Muse Cell Analyzer. ( B ) Cells were stained with Muse ® Annexin V and Dead Cell reagent, and apoptotic cells were detected using the Muse Cell Analyzer. ( C , D ) The expression levels of cell cycle and apoptosis-related proteins were detected by Western blotting and quantified by densitometry. β-Actin levels were used as a loading control. * p < 0.05 vs. the control.

Article Snippet: Furamidine (PRMT1 inhibitor), berbamine (CaMKIIγ inhibitor), and colivelin (STAT3 activator) were purchased from Tocris (Bristol, UK), Sigma-Aldrich (St. Louis, MO, USA), and MedChemExpress (Monmouth Junction, NJ, USA), respectively.

Techniques: Derivative Assay, Staining, Expressing, Western Blot, Control

Effect of furamidine on features of mitochondria-mediated apoptosis in U87MG-derived GSCs. ( A – C ) U87MG-derived GSCs were treated with furamidine (10, 20, and 40 μM) for 48 h. ( A ) Changes in nuclear morphology were observed by DAPI staining under a fluorescence microscope. Condensed and fragmented nuclei were indicated by white arrows. ( B ) MMP was detected by TMRE staining. Fluorescent images were quantified with densitometry. ( C ) Intracellular ROS levels were detected by DCFH-DA staining. DCF fluorescence was quantified by densitometry. * p < 0.05, *** p < 0.001 vs. the control.

Journal: International Journal of Molecular Sciences

Article Title: Inhibition of PRMT1 Suppresses the Growth of U87MG-Derived Glioblastoma Stem Cells by Blocking the STAT3 Signaling Pathway

doi: 10.3390/ijms25052950

Figure Lengend Snippet: Effect of furamidine on features of mitochondria-mediated apoptosis in U87MG-derived GSCs. ( A – C ) U87MG-derived GSCs were treated with furamidine (10, 20, and 40 μM) for 48 h. ( A ) Changes in nuclear morphology were observed by DAPI staining under a fluorescence microscope. Condensed and fragmented nuclei were indicated by white arrows. ( B ) MMP was detected by TMRE staining. Fluorescent images were quantified with densitometry. ( C ) Intracellular ROS levels were detected by DCFH-DA staining. DCF fluorescence was quantified by densitometry. * p < 0.05, *** p < 0.001 vs. the control.

Article Snippet: Furamidine (PRMT1 inhibitor), berbamine (CaMKIIγ inhibitor), and colivelin (STAT3 activator) were purchased from Tocris (Bristol, UK), Sigma-Aldrich (St. Louis, MO, USA), and MedChemExpress (Monmouth Junction, NJ, USA), respectively.

Techniques: Derivative Assay, Staining, Fluorescence, Microscopy, Control

Effect of furamidine on STAT3 and stemness markers in U87MG-derived GSCs. ( A ) U87MG-derived GSCs were treated with furamidine (10, 20, and 40 μM) for 48 h. Protein levels were detected by Western blotting and quantified by densitometry. β-Actin levels were used as a loading control. * p < 0.05 vs. the control. ( B ) Effect of colivelin on the antiproliferative activity of furamidine in U87MG-derived GSCs. Cells were incubated for 7 days after treatment with colivelin and furamidine. The CellTiter-Glo ® luminescent assay was performed to measure cell proliferation. * p < 0.05, ** p < 0.005.

Journal: International Journal of Molecular Sciences

Article Title: Inhibition of PRMT1 Suppresses the Growth of U87MG-Derived Glioblastoma Stem Cells by Blocking the STAT3 Signaling Pathway

doi: 10.3390/ijms25052950

Figure Lengend Snippet: Effect of furamidine on STAT3 and stemness markers in U87MG-derived GSCs. ( A ) U87MG-derived GSCs were treated with furamidine (10, 20, and 40 μM) for 48 h. Protein levels were detected by Western blotting and quantified by densitometry. β-Actin levels were used as a loading control. * p < 0.05 vs. the control. ( B ) Effect of colivelin on the antiproliferative activity of furamidine in U87MG-derived GSCs. Cells were incubated for 7 days after treatment with colivelin and furamidine. The CellTiter-Glo ® luminescent assay was performed to measure cell proliferation. * p < 0.05, ** p < 0.005.

Article Snippet: Furamidine (PRMT1 inhibitor), berbamine (CaMKIIγ inhibitor), and colivelin (STAT3 activator) were purchased from Tocris (Bristol, UK), Sigma-Aldrich (St. Louis, MO, USA), and MedChemExpress (Monmouth Junction, NJ, USA), respectively.

Techniques: Derivative Assay, Western Blot, Control, Activity Assay, Incubation, Luminescence Assay

Effect of PRMT1 knockdown on proliferation of U87MG-derived GSCs in vitro and in vivo. ( A ) U87MG-derived GSCs were transfected with either PRMT1 siRNA (200 nM) or negative control siRNA for 48 h. The knockdown of the PRMT1 gene was confirmed by Western blotting. β-Actin levels were used as an internal control. ( B ) Following genetic knockdown, cell proliferation was measured using the CellTiter-Glo ® luminescent assay system. ( C ) Effect of PRMT1 knockdown on tumor growth derived by U87MG GSCs in a CAM model. * p < 0.05 vs. the control.

Journal: International Journal of Molecular Sciences

Article Title: Inhibition of PRMT1 Suppresses the Growth of U87MG-Derived Glioblastoma Stem Cells by Blocking the STAT3 Signaling Pathway

doi: 10.3390/ijms25052950

Figure Lengend Snippet: Effect of PRMT1 knockdown on proliferation of U87MG-derived GSCs in vitro and in vivo. ( A ) U87MG-derived GSCs were transfected with either PRMT1 siRNA (200 nM) or negative control siRNA for 48 h. The knockdown of the PRMT1 gene was confirmed by Western blotting. β-Actin levels were used as an internal control. ( B ) Following genetic knockdown, cell proliferation was measured using the CellTiter-Glo ® luminescent assay system. ( C ) Effect of PRMT1 knockdown on tumor growth derived by U87MG GSCs in a CAM model. * p < 0.05 vs. the control.

Article Snippet: Furamidine (PRMT1 inhibitor), berbamine (CaMKIIγ inhibitor), and colivelin (STAT3 activator) were purchased from Tocris (Bristol, UK), Sigma-Aldrich (St. Louis, MO, USA), and MedChemExpress (Monmouth Junction, NJ, USA), respectively.

Techniques: Knockdown, Derivative Assay, In Vitro, In Vivo, Transfection, Negative Control, Western Blot, Control, Luminescence Assay

Effect of PRMT1 knockdown on STAT3 and stemness markers in U87MG-derived GSCs. ( A ) Effect of PRMT1 knockdown on the cell cycle. ( B ) Effect of PRMT1 knockdown on apoptotic cell death. ( C ) Effect of PRMT1 knockdown on the protein expression levels of GSC markers. * p < 0.05 vs. the control. ( D ) Effect of colivelin on the antiproliferative activity of PRMT1 knockdown in U87MG-derived GSCs. *** p < 0.001.

Journal: International Journal of Molecular Sciences

Article Title: Inhibition of PRMT1 Suppresses the Growth of U87MG-Derived Glioblastoma Stem Cells by Blocking the STAT3 Signaling Pathway

doi: 10.3390/ijms25052950

Figure Lengend Snippet: Effect of PRMT1 knockdown on STAT3 and stemness markers in U87MG-derived GSCs. ( A ) Effect of PRMT1 knockdown on the cell cycle. ( B ) Effect of PRMT1 knockdown on apoptotic cell death. ( C ) Effect of PRMT1 knockdown on the protein expression levels of GSC markers. * p < 0.05 vs. the control. ( D ) Effect of colivelin on the antiproliferative activity of PRMT1 knockdown in U87MG-derived GSCs. *** p < 0.001.

Article Snippet: Furamidine (PRMT1 inhibitor), berbamine (CaMKIIγ inhibitor), and colivelin (STAT3 activator) were purchased from Tocris (Bristol, UK), Sigma-Aldrich (St. Louis, MO, USA), and MedChemExpress (Monmouth Junction, NJ, USA), respectively.

Techniques: Knockdown, Derivative Assay, Expressing, Control, Activity Assay

Effect of combined treatment of furamidine and berbamine on proliferation of U87MG-derived GSCs. ( A ) Effect of combined treatment with furamidine and berbamine for 7 days on the proliferation and tumorsphere formation in U87MG-derived GSCs. ( B , C ) Effect of combined treatment with furamidine and berbamine for 48 h on ( B ) the cell cycle and ( C ) apoptotic cell death in U87MG-derived GSCs. * p < 0.05, *** p < 0.001 vs. the compound alone.

Journal: International Journal of Molecular Sciences

Article Title: Inhibition of PRMT1 Suppresses the Growth of U87MG-Derived Glioblastoma Stem Cells by Blocking the STAT3 Signaling Pathway

doi: 10.3390/ijms25052950

Figure Lengend Snippet: Effect of combined treatment of furamidine and berbamine on proliferation of U87MG-derived GSCs. ( A ) Effect of combined treatment with furamidine and berbamine for 7 days on the proliferation and tumorsphere formation in U87MG-derived GSCs. ( B , C ) Effect of combined treatment with furamidine and berbamine for 48 h on ( B ) the cell cycle and ( C ) apoptotic cell death in U87MG-derived GSCs. * p < 0.05, *** p < 0.001 vs. the compound alone.

Article Snippet: Furamidine (PRMT1 inhibitor), berbamine (CaMKIIγ inhibitor), and colivelin (STAT3 activator) were purchased from Tocris (Bristol, UK), Sigma-Aldrich (St. Louis, MO, USA), and MedChemExpress (Monmouth Junction, NJ, USA), respectively.

Techniques: Derivative Assay

Effect of combined treatment of furamidine and berbamine on ( A ) PRMT1, CaMKIIγ, STAT3, and ( B ) stemness markers in U87MG-derived GSCs. ( A , B ) U87MG-derived GSCs were treated with the indicated concentrations of furamidine and berbamine for 48 h. Protein levels were detected by Western blotting and quantified by densitometry. β-Actin levels were used as a loading control. * p < 0.05 vs. the compound alone.

Journal: International Journal of Molecular Sciences

Article Title: Inhibition of PRMT1 Suppresses the Growth of U87MG-Derived Glioblastoma Stem Cells by Blocking the STAT3 Signaling Pathway

doi: 10.3390/ijms25052950

Figure Lengend Snippet: Effect of combined treatment of furamidine and berbamine on ( A ) PRMT1, CaMKIIγ, STAT3, and ( B ) stemness markers in U87MG-derived GSCs. ( A , B ) U87MG-derived GSCs were treated with the indicated concentrations of furamidine and berbamine for 48 h. Protein levels were detected by Western blotting and quantified by densitometry. β-Actin levels were used as a loading control. * p < 0.05 vs. the compound alone.

Article Snippet: Furamidine (PRMT1 inhibitor), berbamine (CaMKIIγ inhibitor), and colivelin (STAT3 activator) were purchased from Tocris (Bristol, UK), Sigma-Aldrich (St. Louis, MO, USA), and MedChemExpress (Monmouth Junction, NJ, USA), respectively.

Techniques: Derivative Assay, Western Blot, Control

Proposed functional role of PRMT1 in GSC growth. Inhibition of PRMT1 suppresses the growth of GSCs by blocking the STAT3 signaling pathway.

Journal: International Journal of Molecular Sciences

Article Title: Inhibition of PRMT1 Suppresses the Growth of U87MG-Derived Glioblastoma Stem Cells by Blocking the STAT3 Signaling Pathway

doi: 10.3390/ijms25052950

Figure Lengend Snippet: Proposed functional role of PRMT1 in GSC growth. Inhibition of PRMT1 suppresses the growth of GSCs by blocking the STAT3 signaling pathway.

Article Snippet: Furamidine (PRMT1 inhibitor), berbamine (CaMKIIγ inhibitor), and colivelin (STAT3 activator) were purchased from Tocris (Bristol, UK), Sigma-Aldrich (St. Louis, MO, USA), and MedChemExpress (Monmouth Junction, NJ, USA), respectively.

Techniques: Functional Assay, Inhibition, Blocking Assay

Upon TPO stimulation, human umbilical cord blood CD34+ cells differentiate into mature megakaryocytes. (A) FACS analysis of CD41 and CD42 double-positive cells cultured in medium containing high TPO on days 7, 10, 13 and 18. (B) Changes to RBM15 and PRMT1 expression at 12, 24, 48 and 72 h of TPO treatment. The mRNA levels were calculated as the mean ± standard deviation from three independent experiments. (C) Intracellular immunostaining with anti-PRMT1 and anti-RBM15 antibodies (magnification, ×400). (D) PRMT1 and RBM15 protein levels were detected by FACS analysis in the course of megakaryocyte differentiation. Results are displayed as histogram overlays. **P<0.01 vs. 0 h. CD, cluster of differentiation; FACS, fluorescence-activated cell sorting; RBM15, RNA binding motif protein 15; PRMT1, protein arginine methyltransferase 1; PRMT1V2, PRMT1 V2 isoform; DAPI, 4,6-diamidino-2-phenylindole; TPO, thrombopoitin.

Journal: Experimental and Therapeutic Medicine

Article Title: PRMT1-RBM15 axis regulates megakaryocytic differentiation of human umbilical cord blood CD34 + cells

doi: 10.3892/etm.2018.5693

Figure Lengend Snippet: Upon TPO stimulation, human umbilical cord blood CD34+ cells differentiate into mature megakaryocytes. (A) FACS analysis of CD41 and CD42 double-positive cells cultured in medium containing high TPO on days 7, 10, 13 and 18. (B) Changes to RBM15 and PRMT1 expression at 12, 24, 48 and 72 h of TPO treatment. The mRNA levels were calculated as the mean ± standard deviation from three independent experiments. (C) Intracellular immunostaining with anti-PRMT1 and anti-RBM15 antibodies (magnification, ×400). (D) PRMT1 and RBM15 protein levels were detected by FACS analysis in the course of megakaryocyte differentiation. Results are displayed as histogram overlays. **P<0.01 vs. 0 h. CD, cluster of differentiation; FACS, fluorescence-activated cell sorting; RBM15, RNA binding motif protein 15; PRMT1, protein arginine methyltransferase 1; PRMT1V2, PRMT1 V2 isoform; DAPI, 4,6-diamidino-2-phenylindole; TPO, thrombopoitin.

Article Snippet: To further investigate the function of PRMT1 in megakaryocytic differentiation, a PRMT1 inhibitor DB75 (Sigma-Aldrich; Merck KGaA) was used to treat the cells overexpressing PRMT1 protein and cultured in the MK differentiation medium.

Techniques: Cell Culture, Expressing, Standard Deviation, Immunostaining, Fluorescence, FACS, RNA Binding Assay

PRMT1 blocks the differentiation of human umbilical cord blood CD34+ cells into mature megakaryocytes. (A) FACS analysis of CD41 and CD42 double-positive cells cultured in high TPO-containing medium on day 10. (B) PRMT1 and (C) RBM15 mRNA expression levels in CD34+ cells overexpressing PRMT1. **P<0.01 vs. Vector. Three independent experiments were performed. (D) FACS analysis of the RBM15 protein expression level in cells with or without PRMT1 overexpression. (E) Intracellular immunostaining with anti-RBM15 antibody (magnification, ×400). PRMT1, protein arginine methyltransferase 1; CD, cluster of differentiation; FACS, fluorescence-activated cell sorting; RBM15, RNA binding motif protein 15; DAPI, 4,6-diamidino-2-phenylindole; TPO, thrombopoitin.

Journal: Experimental and Therapeutic Medicine

Article Title: PRMT1-RBM15 axis regulates megakaryocytic differentiation of human umbilical cord blood CD34 + cells

doi: 10.3892/etm.2018.5693

Figure Lengend Snippet: PRMT1 blocks the differentiation of human umbilical cord blood CD34+ cells into mature megakaryocytes. (A) FACS analysis of CD41 and CD42 double-positive cells cultured in high TPO-containing medium on day 10. (B) PRMT1 and (C) RBM15 mRNA expression levels in CD34+ cells overexpressing PRMT1. **P<0.01 vs. Vector. Three independent experiments were performed. (D) FACS analysis of the RBM15 protein expression level in cells with or without PRMT1 overexpression. (E) Intracellular immunostaining with anti-RBM15 antibody (magnification, ×400). PRMT1, protein arginine methyltransferase 1; CD, cluster of differentiation; FACS, fluorescence-activated cell sorting; RBM15, RNA binding motif protein 15; DAPI, 4,6-diamidino-2-phenylindole; TPO, thrombopoitin.

Article Snippet: To further investigate the function of PRMT1 in megakaryocytic differentiation, a PRMT1 inhibitor DB75 (Sigma-Aldrich; Merck KGaA) was used to treat the cells overexpressing PRMT1 protein and cultured in the MK differentiation medium.

Techniques: Cell Culture, Expressing, Plasmid Preparation, Over Expression, Immunostaining, Fluorescence, FACS, RNA Binding Assay

Knockdown of RBM15 blocks megakaryocytic differentiation. (A) Percentages of CD41+CD42+ double-positive cells cultured in high TPO-containing medium on day 10 following RBM15 knock down. mRNA expression levels of (B) RBM15 and (C) PRMT1 in CD34+ cells with RBM15 knockdown. Three independent experiments were performed. (D) FACS analysis of the RBM15 protein level in cells with or without RBM15 knockdown. (E) Intracellular immunostaining with anti-PRMT1 antibody. **P<0.01 vs. the vector group. RBM15, RNA binding motif protein 15; CD, cluster of differentiation; FACS, fluorescence-activated cell sorting; PRMT1, protein arginine methyltransferase 1; sh, short hairpin; TPO, thrombopoitin.

Journal: Experimental and Therapeutic Medicine

Article Title: PRMT1-RBM15 axis regulates megakaryocytic differentiation of human umbilical cord blood CD34 + cells

doi: 10.3892/etm.2018.5693

Figure Lengend Snippet: Knockdown of RBM15 blocks megakaryocytic differentiation. (A) Percentages of CD41+CD42+ double-positive cells cultured in high TPO-containing medium on day 10 following RBM15 knock down. mRNA expression levels of (B) RBM15 and (C) PRMT1 in CD34+ cells with RBM15 knockdown. Three independent experiments were performed. (D) FACS analysis of the RBM15 protein level in cells with or without RBM15 knockdown. (E) Intracellular immunostaining with anti-PRMT1 antibody. **P<0.01 vs. the vector group. RBM15, RNA binding motif protein 15; CD, cluster of differentiation; FACS, fluorescence-activated cell sorting; PRMT1, protein arginine methyltransferase 1; sh, short hairpin; TPO, thrombopoitin.

Article Snippet: To further investigate the function of PRMT1 in megakaryocytic differentiation, a PRMT1 inhibitor DB75 (Sigma-Aldrich; Merck KGaA) was used to treat the cells overexpressing PRMT1 protein and cultured in the MK differentiation medium.

Techniques: Cell Culture, Expressing, Immunostaining, Plasmid Preparation, RNA Binding Assay, Fluorescence, FACS

Treatment with PRMT1 inhibitor rescues PRMT1-blocked megakaryocytic differentiation. (A) FACS analysis of CD41 and CD42 expression following treatment with DB75. (B) FACS analysis of the RBM15 protein expression level in cells ectopically expressing PRMT1 with or without treatment with DB75. PRMT1, protein arginine methyltransferase 1; FACS, fluorescence-activated cell sorting; CD, cluster of differentiation; DB75, PRMT1 inhibitor; DMSO, dimethyl sulfoxide.

Journal: Experimental and Therapeutic Medicine

Article Title: PRMT1-RBM15 axis regulates megakaryocytic differentiation of human umbilical cord blood CD34 + cells

doi: 10.3892/etm.2018.5693

Figure Lengend Snippet: Treatment with PRMT1 inhibitor rescues PRMT1-blocked megakaryocytic differentiation. (A) FACS analysis of CD41 and CD42 expression following treatment with DB75. (B) FACS analysis of the RBM15 protein expression level in cells ectopically expressing PRMT1 with or without treatment with DB75. PRMT1, protein arginine methyltransferase 1; FACS, fluorescence-activated cell sorting; CD, cluster of differentiation; DB75, PRMT1 inhibitor; DMSO, dimethyl sulfoxide.

Article Snippet: To further investigate the function of PRMT1 in megakaryocytic differentiation, a PRMT1 inhibitor DB75 (Sigma-Aldrich; Merck KGaA) was used to treat the cells overexpressing PRMT1 protein and cultured in the MK differentiation medium.

Techniques: Expressing, Fluorescence, FACS