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Cell Signaling Technology Inc prmt1
Prmt1, supplied by Cell Signaling Technology Inc, used in various techniques. Bioz Stars score: 96/100, based on 184 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
https://www.bioz.com/product/anti+prmt1/Asymmetric+Di-Methyl+Arginine+Motif+%5Badme-R%5D+MultiMab+Rabbit+mAb+mix/pm41912914-70-6-8
Average 96 stars, based on 184 article reviews

prmt1 - by Bioz Stars, 2026-10

96/100 stars

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Western Blot:

Article Title: Protein arginine methyltransferase 1 stimulates basal cell proliferation and migration to maintain corneal epithelial homeostasis
Article Snippet: Antibodies for immunofluorescence staining include anti-K12 (ab185627, Abcam), anti-K14 (10143-1-AP, Proteintech), anti-Ki67 (ab279653, Abcam), anti-pH3 (06-570, Millipore), anti-DCS2 (13876-1-AP, Proteintech), Alexa FluorTM 568 donkey anti-mouse IgG (H + L) (A10037, Invitrogen), Alexa FluorTM 488 donkey anti-mouse IgG (H + L) (A21202, Invitrogen), Alexa FluorTM 568 donkey anti-rabbit IgG (H + L) (A10042, Invitrogen), Alexa FluorTM 488 donkey anti-rabbit IgG (H + L) (A21206, Invitrogen), and Alexa FluorTM 647 donkey anti-mouse IgG (H + L) (A31571, Invitrogen). .. Antibodies for immunoblotting include anti-PRMT1 (2449S, Cell Signaling Technology), anti-β-actin (AC026, ABclonal), anti-GFP (ab0005, Abways), anti-MAP4(11229-1-AP, Proteintech), anti-VCL (ab18058, Abcam), anti-CDK9 (11705-1-AP, Proteintech), anti-MMA (#8015, Cell Signaling Technology), anti-ADMA (#13522, Cell Signaling Technology), anti-CFL1(10960-1-AP, Proteintech), anti-MAPK2 (11257-1-AP, Proteintech), anti-RAC1 (24072-1-AP, Proteintech), and anti-RHOA (10749-1-AP, Proteintech). ..

Article Title: <scp>PRMT1</scp>‐mediated <scp>BRD4</scp> arginine methylation and phosphorylation promote partial epithelial–mesenchymal transformation and renal fibrosis
Article Snippet: Funding information Guangdong Basic and Applied Basic Research Foundation, Grant/Award Number: 2022A1515140177; Dongguan Science and Technology of Social Development Program, Grant/Award Number: 20221800905662; Talent Development Foundation of The First Dongguan Affiliated Hospital of Guangdong Medical University, Grant/Award Number: GC2022001 and PU2022001 Abstract Bromodomaincontaining protein 4 (BRD4) plays a vital role in fibrosis of various organs.. However, the underlying mechanism of BRD4 in renal fibrosis remains unclear.. To construct in vitro and in vivo models of renal fibrosis, TCMK1 cells were subjected to TGFβ1 treatment and mice were subjected to UUO surgery and adenine induction.

Article Title: Repression of PRMT activities sensitize human homologous recombination-proficient ovarian and breast cancer cells to PARP inhibitor treatment
Article Snippet: .. Western blotting was performed using the following primary antibodies: anti-PRMT1 (Cat No: 2449 S, CST); anti-PRMT5 (Cat No: 79998 S, CST); anti-aDMA (Cat No: 13522 S, CST); anti-sDMA (Cat No: 13222 S, CST); anti-ERCC1 (Cat No: 3885 S, CST); anti-phospho-H2AX (S139) (Cat No: 05–636, Clone No: JBW301, Millipore); p-TBK1 (Cat No: 5483 S, CST) and anti-β-Tubulin (Cat No: 2128, Clone No: 9F3, CST), followed by incubation with secondary antibodies conjugated with horseradish peroxidase (HRP, GE Healthcare Life Sciences). .. Western blotting was performed using the following primary antibodies: anti-PRMT1 (Cat No: 2449 S, CST); anti-PRMT5 (Cat No: 79998 S, CST); anti-aDMA (Cat No: 13522 S, CST); anti-sDMA (Cat No: 13222 S, CST); anti-ERCC1 (Cat No: 3885 S, CST); anti-phospho-H2AX (S139) (Cat No: 05–636, Clone No: JBW301, Millipore); p-TBK1 (Cat No: 5483 S, CST) and anti-β-Tubulin (Cat No: 2128, Clone No: 9F3, CST), followed by incubation with secondary antibodies conjugated with horseradish peroxidase (HRP, GE Healthcare Life Sciences).

Article Title: Repression of PRMT activities sensitize human homologous recombination-proficient ovarian and breast cancer cells to PARP inhibitor treatment
Article Snippet: Cell line ( Homo sapiens ) , HEK293T , ATCC , Cat: #CRL-3216; RRID: CVCL_0063 , . .. Antibody , Anti-PRMT1 (Rabbit polyclonal) , Cell Signaling Technology , Cat: #2449 S; RRID: AB_2237696 , WB (1:1000). .. Antibody , Anti-PRMT5 (Rabbit monoclonal) , Cell Signaling Technology , Clone:D5P2T; Cat: #79998 S; RRID: AB_2799945 , WB (1:1000).

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Article Title: Energy Deficiency-Induced ATG4B Nuclear Translocation Inhibits PRMT1-Mediated DNA Repair and Promotes Leukemia Progression.
Article Snippet: Cells stably expressing mCherry-LC3B were created by transient transfection followed by selection with G418 (500 μg mL−1) (Gibco, 11811031).

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10-week combined exercise preconditioning prevented 1-week hindlimb immobilization-induced muscle atrophy in mice. (A–C) Body weight, gross weight gain and food intake data during 10-week exercise preconditioning. ∗ p < 0.05 vs. C; # p < 0.05 vs. E. Two-way ANOVA was used and data are shown as means ± standard error of the mean ( SEM ) (C, n = 16, E, n = 8, E+5003, n = 8). (D) Food intake data during 1-week immobilization. ∗ p < 0.05 vs. C. Two-way ANOVA was used and data are shown as means ± SEM . (E–F) aDMA level indicated for Prmt1 enzymatic activity after 10-week TC-E−5003 administration via subcutaneous injection at a dose of 2 mg/kg body weight, once daily, 5 days a week. (G–J) Skeletal muscle functions tests, G, grip strength, H, suspension time of hang test, I, time of the latency to fall in rotarod test, J, maximum voluntary climbing capacity (MVCC) test. (K–P) Total hindlimb mass and specific muscle mass of various parts of hindlimb, GAS, gastrocnemius, SOL, soleus, QUA, quadriceps femoris, lateralis, TA, tibialis anterior, EDL, extensor digitorum longus. H-S, ∗ p < 0.05 vs. C; ∗∗ p < 0.01 vs. C; # p < 0.05 vs. Im; ## p < 0.01 vs. Im; $ p < 0.05 vs. E + Im; $$ p < 0.01 vs. E + Im. Two-way ANOVA was used and data are shown as means ± SEM (C, n = 8, Im, n = 8, E + Im, n = 8, E+5003+Im, n = 8).

Journal: Sports Medicine and Health Science

Article Title: Exercise preconditioning prevents immobilization-induced skeletal muscle atrophy by activating Prmt1-p38/ATF2-Sesn1 signaling axis in C57BL/6J mice

doi: 10.1016/j.smhs.2025.04.001

Figure Lengend Snippet: 10-week combined exercise preconditioning prevented 1-week hindlimb immobilization-induced muscle atrophy in mice. (A–C) Body weight, gross weight gain and food intake data during 10-week exercise preconditioning. ∗ p < 0.05 vs. C; # p < 0.05 vs. E. Two-way ANOVA was used and data are shown as means ± standard error of the mean ( SEM ) (C, n = 16, E, n = 8, E+5003, n = 8). (D) Food intake data during 1-week immobilization. ∗ p < 0.05 vs. C. Two-way ANOVA was used and data are shown as means ± SEM . (E–F) aDMA level indicated for Prmt1 enzymatic activity after 10-week TC-E−5003 administration via subcutaneous injection at a dose of 2 mg/kg body weight, once daily, 5 days a week. (G–J) Skeletal muscle functions tests, G, grip strength, H, suspension time of hang test, I, time of the latency to fall in rotarod test, J, maximum voluntary climbing capacity (MVCC) test. (K–P) Total hindlimb mass and specific muscle mass of various parts of hindlimb, GAS, gastrocnemius, SOL, soleus, QUA, quadriceps femoris, lateralis, TA, tibialis anterior, EDL, extensor digitorum longus. H-S, ∗ p < 0.05 vs. C; ∗∗ p < 0.01 vs. C; # p < 0.05 vs. Im; ## p < 0.01 vs. Im; $ p < 0.05 vs. E + Im; $$ p < 0.01 vs. E + Im. Two-way ANOVA was used and data are shown as means ± SEM (C, n = 8, Im, n = 8, E + Im, n = 8, E+5003+Im, n = 8).

Article Snippet: ChIP grade antibodies to Prmt1 (1:100, Proteintech, USA) were used to perform immunoprecipitation.

Techniques: Activity Assay, Injection, Suspension

10-week combined exercise preconditioning ameliorated 1-week hindlimb immobilization-induced imbalance between synthesis and degradation of protein in skeletal muscle. (A) Representative images of hematoxylin and eosin staining (H&E) of GAS muscle cross-sections. Scale bar = 50 μm. (B) The average CSA of GAS muscle was quantified. (C–D) Real-time PCR results of TIRM63 (MuRF1), FBXO32 (Atrogin-1), Prmt1, and Sesn1 in GAS muscle. (E–N) Western blot results of Prmt1, Sesn1, p-FoxO3a, FoxO3a, Atrogin-1, MuRF1, IGF-1, pAkt-S473, Akt, mTOR, Raptor in GAS muscle. B-N, ∗ p < 0.05 vs. C; ∗∗ p < 0.01 vs. C; # p < 0.05 vs. Im; ## p < 0.01 vs. Im; $ p < 0.05 vs. E + Im; $$ p < 0.01 vs. E + Im. Two-way ANOVA was used and data are shown as means ± standard error of the mean (C, n = 8, Im, n = 8, E + Im, n = 8, E+5003+Im, n = 8).

Journal: Sports Medicine and Health Science

Article Title: Exercise preconditioning prevents immobilization-induced skeletal muscle atrophy by activating Prmt1-p38/ATF2-Sesn1 signaling axis in C57BL/6J mice

doi: 10.1016/j.smhs.2025.04.001

Figure Lengend Snippet: 10-week combined exercise preconditioning ameliorated 1-week hindlimb immobilization-induced imbalance between synthesis and degradation of protein in skeletal muscle. (A) Representative images of hematoxylin and eosin staining (H&E) of GAS muscle cross-sections. Scale bar = 50 μm. (B) The average CSA of GAS muscle was quantified. (C–D) Real-time PCR results of TIRM63 (MuRF1), FBXO32 (Atrogin-1), Prmt1, and Sesn1 in GAS muscle. (E–N) Western blot results of Prmt1, Sesn1, p-FoxO3a, FoxO3a, Atrogin-1, MuRF1, IGF-1, pAkt-S473, Akt, mTOR, Raptor in GAS muscle. B-N, ∗ p < 0.05 vs. C; ∗∗ p < 0.01 vs. C; # p < 0.05 vs. Im; ## p < 0.01 vs. Im; $ p < 0.05 vs. E + Im; $$ p < 0.01 vs. E + Im. Two-way ANOVA was used and data are shown as means ± standard error of the mean (C, n = 8, Im, n = 8, E + Im, n = 8, E+5003+Im, n = 8).

Article Snippet: ChIP grade antibodies to Prmt1 (1:100, Proteintech, USA) were used to perform immunoprecipitation.

Techniques: Staining, Real-time Polymerase Chain Reaction, Western Blot

Exercise preconditioning increased Sestrin1 (Sesn1) expression by activating protein arginine methyltransferase 1 (Prmt1)-p38/activating transcription factor 2 (ATF2) signaling in mice. (A) ChIP analysis of Prmt1 binding to the ATF2 sequence of mouse Sesn1 promoter in GAS muscle. (B–D) Western blot results of p-p38-T180/182, p38, and ATF2 in GAS muscle. (E–F) Co-IP results, IP: Prmt1, GAS muscle was used. (G–H) Co-IP results, IP: ATF2, GAS muscle was used. (I–J) Co-IP results, IP: p38, GAS muscle was used. A-J, ∗ p < 0.05 vs. C; ∗∗ p < 0.01 vs. C; # p < 0.05 vs. Im; ## p < 0.01 vs. Im; $ p < 0.05 vs. E + Im; $$ p < 0.01 vs. E + Im. Two-way ANOVA was used and data are shown as means ± standard error of the mean (C, n = 8, Im, n = 8, E + Im, n = 8, E+5003+Im, n = 8).

Journal: Sports Medicine and Health Science

Article Title: Exercise preconditioning prevents immobilization-induced skeletal muscle atrophy by activating Prmt1-p38/ATF2-Sesn1 signaling axis in C57BL/6J mice

doi: 10.1016/j.smhs.2025.04.001

Figure Lengend Snippet: Exercise preconditioning increased Sestrin1 (Sesn1) expression by activating protein arginine methyltransferase 1 (Prmt1)-p38/activating transcription factor 2 (ATF2) signaling in mice. (A) ChIP analysis of Prmt1 binding to the ATF2 sequence of mouse Sesn1 promoter in GAS muscle. (B–D) Western blot results of p-p38-T180/182, p38, and ATF2 in GAS muscle. (E–F) Co-IP results, IP: Prmt1, GAS muscle was used. (G–H) Co-IP results, IP: ATF2, GAS muscle was used. (I–J) Co-IP results, IP: p38, GAS muscle was used. A-J, ∗ p < 0.05 vs. C; ∗∗ p < 0.01 vs. C; # p < 0.05 vs. Im; ## p < 0.01 vs. Im; $ p < 0.05 vs. E + Im; $$ p < 0.01 vs. E + Im. Two-way ANOVA was used and data are shown as means ± standard error of the mean (C, n = 8, Im, n = 8, E + Im, n = 8, E+5003+Im, n = 8).

Article Snippet: ChIP grade antibodies to Prmt1 (1:100, Proteintech, USA) were used to perform immunoprecipitation.

Techniques: Expressing, Binding Assay, Sequencing, Western Blot, Co-Immunoprecipitation Assay

Protein arginine methyltransferase 1 (Prmt1)-Sestrin1 (Sesn1) coordinated the differentiation of C2C12 myoblasts into mature myotubes. (A–B) H&E staining of C2C12 myotubes at the 7 th day of differentiation with si-Sesn, and Ad-Sesn1 treatment. Scale bar = 100 μm. (C–D) Western blot results of Sesn1, FoxO3a, Atrogin-1 and MuRF1 in C2C12. A-D, C, control, si-Sesn1, si-RNA of Sesn1, Ad-Sesn1, Adenoviruses overexpressing Sesn1, ∗ p < 0.05 vs. C; ∗∗ p < 0.01 vs. C; # p < 0.05 vs. si-Sesn1; ## p < 0.01 vs. Si-Sesn1. Two-way ANOVA was used and data are shown as means ± standard error of the mean ( SEM ) ( n = 6 in each group). (E–F) H&E staining of C2C12 myotubes at the 7 th day of differentiation with si-Prmt1, and Ad-Prmt1. Scale bar = 100 μm. (G–N) Western blot results of Prmt1, p-p38-T180/182, p38, ATF2, Sesn1, FoxO3a, Atrogin-1 and MuRF1 in C2C12. E-N, C, control, si-Prmt1, si-RNA of Prmt1, Ad-Prmt1, Adenoviruses overexpressing Prmt1, ∗ p < 0.05 vs. C; ∗∗ p < 0.01 vs. C; # p < 0.05 vs. si-Prmt1; ## p < 0.01 vs. si-Prmt1. Two-way ANOVA was used and data are shown as means ± SEM ( n = 3 in each group). (O–R) Western blot results of Prmt1, ATF2 and Sesn1 in C2C12 myoblasts, ∗ p < 0.05; ∗∗ p < 0.01, unpaired Student's t -test was used and data are shown as means ± SEM ( n = 6 in each group). (S–W) Western blot results of Prmt1, FoxO3a, Atrogin-1 and MuRF1 in C2C12 myoblasts, ∗ p < 0.05; ∗∗ p < 0.01, unpaired Student's t -test was used and data are shown as means ± SEM ( n = 6 in each group).

Journal: Sports Medicine and Health Science

Article Title: Exercise preconditioning prevents immobilization-induced skeletal muscle atrophy by activating Prmt1-p38/ATF2-Sesn1 signaling axis in C57BL/6J mice

doi: 10.1016/j.smhs.2025.04.001

Figure Lengend Snippet: Protein arginine methyltransferase 1 (Prmt1)-Sestrin1 (Sesn1) coordinated the differentiation of C2C12 myoblasts into mature myotubes. (A–B) H&E staining of C2C12 myotubes at the 7 th day of differentiation with si-Sesn, and Ad-Sesn1 treatment. Scale bar = 100 μm. (C–D) Western blot results of Sesn1, FoxO3a, Atrogin-1 and MuRF1 in C2C12. A-D, C, control, si-Sesn1, si-RNA of Sesn1, Ad-Sesn1, Adenoviruses overexpressing Sesn1, ∗ p < 0.05 vs. C; ∗∗ p < 0.01 vs. C; # p < 0.05 vs. si-Sesn1; ## p < 0.01 vs. Si-Sesn1. Two-way ANOVA was used and data are shown as means ± standard error of the mean ( SEM ) ( n = 6 in each group). (E–F) H&E staining of C2C12 myotubes at the 7 th day of differentiation with si-Prmt1, and Ad-Prmt1. Scale bar = 100 μm. (G–N) Western blot results of Prmt1, p-p38-T180/182, p38, ATF2, Sesn1, FoxO3a, Atrogin-1 and MuRF1 in C2C12. E-N, C, control, si-Prmt1, si-RNA of Prmt1, Ad-Prmt1, Adenoviruses overexpressing Prmt1, ∗ p < 0.05 vs. C; ∗∗ p < 0.01 vs. C; # p < 0.05 vs. si-Prmt1; ## p < 0.01 vs. si-Prmt1. Two-way ANOVA was used and data are shown as means ± SEM ( n = 3 in each group). (O–R) Western blot results of Prmt1, ATF2 and Sesn1 in C2C12 myoblasts, ∗ p < 0.05; ∗∗ p < 0.01, unpaired Student's t -test was used and data are shown as means ± SEM ( n = 6 in each group). (S–W) Western blot results of Prmt1, FoxO3a, Atrogin-1 and MuRF1 in C2C12 myoblasts, ∗ p < 0.05; ∗∗ p < 0.01, unpaired Student's t -test was used and data are shown as means ± SEM ( n = 6 in each group).

Article Snippet: ChIP grade antibodies to Prmt1 (1:100, Proteintech, USA) were used to perform immunoprecipitation.

Techniques: Staining, Western Blot, Control

Exercise preconditioning activated AMP-Activated protein kinase α2 (AMPKα2)-transcriptional co-activator PPAR-γ co-activator-1 α (PGC-1α) through protein arginine methyltransferase 1 (Prmt1)-Sestrin1 (Sesn1) in immobilized mice. (A–C) Western blot results of p-AMPKα2, AMPKα2, and PGC-1α in GAS muscle. (D–E) Co-IP results, IP: Prmt1, GAS muscle was used. (F–G) Co-IP results, IP: PGC-1α, GAS muscle was used. (H–I) Co-IP results, IP: Sesn1, GAS muscle was used. (J–K) Co-IP results, IP: PGC-1α, GAS muscle was used. (L–M) Co-IP results, IP: AMPKα2, GAS muscle was used. A-M, ∗ p < 0.05 vs. C; ∗∗ p < 0.01 vs. C; # p < 0.05 vs. Im; ## p < 0.01 vs. Im; $ p < 0.05 vs. E + Im; $$ p < 0.01 vs. E + Im. Two-way ANOVA was used and data are shown as means ± standard error of the mean (C, n = 8, Im, n = 8, E + Im, n = 8, E+5003+Im, n = 8).

Journal: Sports Medicine and Health Science

Article Title: Exercise preconditioning prevents immobilization-induced skeletal muscle atrophy by activating Prmt1-p38/ATF2-Sesn1 signaling axis in C57BL/6J mice

doi: 10.1016/j.smhs.2025.04.001

Figure Lengend Snippet: Exercise preconditioning activated AMP-Activated protein kinase α2 (AMPKα2)-transcriptional co-activator PPAR-γ co-activator-1 α (PGC-1α) through protein arginine methyltransferase 1 (Prmt1)-Sestrin1 (Sesn1) in immobilized mice. (A–C) Western blot results of p-AMPKα2, AMPKα2, and PGC-1α in GAS muscle. (D–E) Co-IP results, IP: Prmt1, GAS muscle was used. (F–G) Co-IP results, IP: PGC-1α, GAS muscle was used. (H–I) Co-IP results, IP: Sesn1, GAS muscle was used. (J–K) Co-IP results, IP: PGC-1α, GAS muscle was used. (L–M) Co-IP results, IP: AMPKα2, GAS muscle was used. A-M, ∗ p < 0.05 vs. C; ∗∗ p < 0.01 vs. C; # p < 0.05 vs. Im; ## p < 0.01 vs. Im; $ p < 0.05 vs. E + Im; $$ p < 0.01 vs. E + Im. Two-way ANOVA was used and data are shown as means ± standard error of the mean (C, n = 8, Im, n = 8, E + Im, n = 8, E+5003+Im, n = 8).

Article Snippet: ChIP grade antibodies to Prmt1 (1:100, Proteintech, USA) were used to perform immunoprecipitation.

Techniques: Western Blot, Co-Immunoprecipitation Assay

Exercise preconditioning prevented muscle atrophy through protein arginine methyltransferase 1 (Prmt1)-Sestrin1 (Sesn1)-transcriptional co-activator PPAR-γ co-activator-1 α (PGC-1α)-mediated skeletal muscle regeneration. (A–B) Western blot results of MyoD, Myf5, MEF2 and MyoG in GAS muscle. (C–D) Co-IP results, IP: MyoD, GAS muscle was used. A-B, ∗ p < 0.05 vs. C; ∗∗ p < 0.01 vs. C; ## p < 0.01 vs. Im; $ p < 0.05 vs. E + Im; $$ p < 0.01 vs. E + Im. Two-way ANOVA was used, and data are shown as means ± standard error of the mean ( SEM ) (C, n = 8, Im, n = 8, E + Im, n = 8, E+5003+Im, n = 8). (E–F) H&E staining of myotubes at each differentiation time points of C2C12 myoblasts overexpressing Sesn1. Scale bar = 100 μm ∗ p < 0.05 vs. Ad-Sesn1-, unpaired Student's t-test was used and data are shown as means ± SEM ( n = 3 in each group). (G–H) Western blot results of Sesn1, Prmt1, PGC-1α, MyoD, MEF2, Myf5, and MyoG in C2C12 myoblasts at each time points of differentiation. ∗ p < 0.05 vs. D0, unpaired Student's t -test was used and data are shown as means ± SEM ( n = 6 in each group). (I–J) Western blot results of PGC-1α in nucleus of C2C12 myoblasts overexpressing Sesn1 at each time points of differentiation. ∗∗ p < 0.01 vs. Ad-Sesn1, unpaired Student's t -test was used and data are shown as means ± SEM ( n = 6 in each group). (K–L) Western blot results of PGC-1α in cytoplasm of C2C12 myoblasts overexpressing Sesn1 at each time points of differentiation. ∗∗ p < 0.01 vs. Ad-Sesn1-, unpaired Student's t -test was used and data are shown as means ± SEM ( n = 6 in each group).

Journal: Sports Medicine and Health Science

Article Title: Exercise preconditioning prevents immobilization-induced skeletal muscle atrophy by activating Prmt1-p38/ATF2-Sesn1 signaling axis in C57BL/6J mice

doi: 10.1016/j.smhs.2025.04.001

Figure Lengend Snippet: Exercise preconditioning prevented muscle atrophy through protein arginine methyltransferase 1 (Prmt1)-Sestrin1 (Sesn1)-transcriptional co-activator PPAR-γ co-activator-1 α (PGC-1α)-mediated skeletal muscle regeneration. (A–B) Western blot results of MyoD, Myf5, MEF2 and MyoG in GAS muscle. (C–D) Co-IP results, IP: MyoD, GAS muscle was used. A-B, ∗ p < 0.05 vs. C; ∗∗ p < 0.01 vs. C; ## p < 0.01 vs. Im; $ p < 0.05 vs. E + Im; $$ p < 0.01 vs. E + Im. Two-way ANOVA was used, and data are shown as means ± standard error of the mean ( SEM ) (C, n = 8, Im, n = 8, E + Im, n = 8, E+5003+Im, n = 8). (E–F) H&E staining of myotubes at each differentiation time points of C2C12 myoblasts overexpressing Sesn1. Scale bar = 100 μm ∗ p < 0.05 vs. Ad-Sesn1-, unpaired Student's t-test was used and data are shown as means ± SEM ( n = 3 in each group). (G–H) Western blot results of Sesn1, Prmt1, PGC-1α, MyoD, MEF2, Myf5, and MyoG in C2C12 myoblasts at each time points of differentiation. ∗ p < 0.05 vs. D0, unpaired Student's t -test was used and data are shown as means ± SEM ( n = 6 in each group). (I–J) Western blot results of PGC-1α in nucleus of C2C12 myoblasts overexpressing Sesn1 at each time points of differentiation. ∗∗ p < 0.01 vs. Ad-Sesn1, unpaired Student's t -test was used and data are shown as means ± SEM ( n = 6 in each group). (K–L) Western blot results of PGC-1α in cytoplasm of C2C12 myoblasts overexpressing Sesn1 at each time points of differentiation. ∗∗ p < 0.01 vs. Ad-Sesn1-, unpaired Student's t -test was used and data are shown as means ± SEM ( n = 6 in each group).

Article Snippet: ChIP grade antibodies to Prmt1 (1:100, Proteintech, USA) were used to perform immunoprecipitation.

Techniques: Western Blot, Co-Immunoprecipitation Assay, Staining

Associations between PRMT1 and Hallmark Pathways across Pan-Cancer. Colors represent the normalized enrichment score (NES) for each pathway, and “Nonsense” indicates P > 0.05.

Journal: International Journal of Medical Sciences

Article Title: Multi-Omics and Clinical Data Analyses of Protein Arginine Methyltransferases in Pan-Cancer and Colorectal Cancer

doi: 10.7150/ijms.129345

Figure Lengend Snippet: Associations between PRMT1 and Hallmark Pathways across Pan-Cancer. Colors represent the normalized enrichment score (NES) for each pathway, and “Nonsense” indicates P > 0.05.

Article Snippet: After blocking with 5% non-fat milk for 1 h at room temperature, the membranes were probed overnight at 4 °C with primary antibodies against PRMT1 (1:1000, A1055, Abclonal, China) and GAPDH (1:2000, UM4002, Utibody, China).

Techniques:

PRMT1 is overexpressed in CRC and required for tumor cell growth. (A) Representative IHC staining of PRMT1 in CRC tissues (C1-C3) and adjacent normal mucosa (N1-N3). (B) Quantification of PRMT1 expression in the clinical cohort, shown as positivity rates. (C, D) Basal expression levels of PRMT1 in CRC cell lines detected by qRT-PCR (C) and Western blotting (D). (E, F) Validation of PRMT1 knockdown efficiency in HCT8 cells at the mRNA level (E) and protein level (F). (G-I) Effects of PRMT1 knockdown on HCT8 cell proliferation, assessed by CCK-8 assay (G), colony formation assay (H), and EdU proliferation assay (I).

Journal: International Journal of Medical Sciences

Article Title: Multi-Omics and Clinical Data Analyses of Protein Arginine Methyltransferases in Pan-Cancer and Colorectal Cancer

doi: 10.7150/ijms.129345

Figure Lengend Snippet: PRMT1 is overexpressed in CRC and required for tumor cell growth. (A) Representative IHC staining of PRMT1 in CRC tissues (C1-C3) and adjacent normal mucosa (N1-N3). (B) Quantification of PRMT1 expression in the clinical cohort, shown as positivity rates. (C, D) Basal expression levels of PRMT1 in CRC cell lines detected by qRT-PCR (C) and Western blotting (D). (E, F) Validation of PRMT1 knockdown efficiency in HCT8 cells at the mRNA level (E) and protein level (F). (G-I) Effects of PRMT1 knockdown on HCT8 cell proliferation, assessed by CCK-8 assay (G), colony formation assay (H), and EdU proliferation assay (I).

Techniques: Immunohistochemistry, Expressing, Quantitative RT-PCR, Western Blot, Biomarker Discovery, Knockdown, CCK-8 Assay, Colony Assay, Proliferation Assay

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