Journal: Cell Death & Disease

Article Title: PRMT1-mediated methylation of UBE2m promoting calcium oxalate crystal-induced kidney injury by inhibiting fatty acid metabolism

doi: 10.1038/s41419-025-07888-3

Figure Lengend Snippet: A The violin plot showing the expression level of PRMT1 in various cell clusters from the NC and the KS groups. B , C The volcano plot of different expression genes or proteins assayed using RNA- or proteome sequencing of kidney tissues. PRMT1 was significantly increased at both the RNA and protein levels. D Representative immunohistochemical staining images (100× and 400×) and quantitative analysis ( F ) of the expression of PRMT1 in the nonfunctioning kidney of patients and in kidneys with CaOx crystals injury of mice. Scale bars = 50 μm. E Representative western blot banding and quantitative analysis ( G ) of the expression levels of PRMT1 and MMA in the NC and the Gly groups. H Representative images of immunofluorescence co-staining of PRMT1 (red) and renal tubular markers LTL, PNA, and DBA (green) in kidneys of mice. Scale bars = 50 μm. I Oil Red O staining of kidney sections from the indicated groups. J GO enrichment analysis of RNA-sequencing data comparing the expression levels between NC and the Gly group. K Heat map showing differential content of acyl-CoAs between the NC and the Gly groups. L GSEA enrichment analysis of differential proteins between the Gly group and the CKO group, assayed by proteome sequencing of kidney tissues. M Relative mRNA levels of key molecules of lipogenesis, fatty acid transport, and oxidation from the indicated groups. Significance was assessed using two-way ANOVA or t-tests. Data are presented as mean ± SD.

Article Snippet: Antibodies against PRMT1 (#2449, 1:1000 for WB, 1:100 for IF or IHC, 1:50 for IP), monomethyl arginine (#8015, 1:1000 for WB), FATP2 (#78771, 1:1000 for WB), PPARγ (#2435, 1:1000 for WB, 1:30 for IP), and NEDD8 (#2745, 1:1000 for WB) were purchased from Cell Signaling Technology.

Techniques: Expressing, Sequencing, Immunohistochemical staining, Staining, Western Blot, Immunofluorescence, RNA Sequencing

Journal: Cell Death & Disease

Article Title: PRMT1-mediated methylation of UBE2m promoting calcium oxalate crystal-induced kidney injury by inhibiting fatty acid metabolism

doi: 10.1038/s41419-025-07888-3

Figure Lengend Snippet: A Representative histology images of the indicated groups: Vonkossa staining indicates the area and location of calcium oxalate crystals deposition (400×); HE staining shows the degree of renal tubular injury (200×); TUNEL staining shows the relative number of apoptotic renal cells (200×). Scale bars = 50 μm. B , C Representative TEM images demonstrate the degree of mitochondrial damage and lipid droplet accumulation. Scale bars = 500 nm. D Representative western blot banding and quantitative analysis of the expression levels of ACOX1, CPT1a, CD36, and FATP2. E Mitochondrial oxidative capacity was measured in real time after knockdown of PRMT1 or COM treatment in HK-2 cells; Quantification of basal respiration, ATP production-coupled respiration, and maximal respiration. Significance was assessed using two-way ANOVA tests. Data are shown as mean ± SD.

Article Snippet: Antibodies against PRMT1 (#2449, 1:1000 for WB, 1:100 for IF or IHC, 1:50 for IP), monomethyl arginine (#8015, 1:1000 for WB), FATP2 (#78771, 1:1000 for WB), PPARγ (#2435, 1:1000 for WB, 1:30 for IP), and NEDD8 (#2745, 1:1000 for WB) were purchased from Cell Signaling Technology.

Techniques: Staining, TUNEL Assay, Western Blot, Expressing, Knockdown

Journal: Cell Death & Disease

Article Title: PRMT1-mediated methylation of UBE2m promoting calcium oxalate crystal-induced kidney injury by inhibiting fatty acid metabolism

doi: 10.1038/s41419-025-07888-3

Figure Lengend Snippet: A Representative histology images of the indicated groups: Vonkossa staining indicates the area and location of calcium oxalate crystal deposition (1X and 200X); HE staining shows the degree of renal tubular injury (200X); TUNEL staining shows the relative number of apoptotic renal cells (200X). Scale bars = 50 μm. B , C Representative TEM images demonstrate the degree of mitochondrial damage and lipid droplet accumulation. Scale bars = 500 nm. D Representative western blot bandings show the expression levels of ACOX1 and CPT1α. E Mitochondrial oxidative capacity was measured in real time after overexpression of PRMT1 or COM treatment in HK-2 cells; basal respiration, ATP production-coupled respiration, and maximal respiration were quantified. Significance was assessed using two-way ANOVA tests. Data are shown as mean ± SD.

Article Snippet: Antibodies against PRMT1 (#2449, 1:1000 for WB, 1:100 for IF or IHC, 1:50 for IP), monomethyl arginine (#8015, 1:1000 for WB), FATP2 (#78771, 1:1000 for WB), PPARγ (#2435, 1:1000 for WB, 1:30 for IP), and NEDD8 (#2745, 1:1000 for WB) were purchased from Cell Signaling Technology.

Techniques: Staining, TUNEL Assay, Western Blot, Expressing, Over Expression

Journal: Cell Death & Disease

Article Title: PRMT1-mediated methylation of UBE2m promoting calcium oxalate crystal-induced kidney injury by inhibiting fatty acid metabolism

doi: 10.1038/s41419-025-07888-3

Figure Lengend Snippet: A Silver-stained SDS-PAGE gel of the immunoprecipitation product. B MS/MS spectra of the peptide “FSPSGIFGAFQR-COOH.” Peaks in color are the detected b (green) and y (red) ions. C The volcano plot indicating potential target proteins of PRMT1. D Molecular docking pattern diagram of PRMT1 and UBE2m. E Representative images of immunofluorescence staining of UBE2m (green) and PRMT1 (red) in HK-2 cells treated with COM. Scale bars = 50 μm. F Reciprocal co-IP analysis of PRMT1 and UBE2m in HK-2 cells with COM treatment. IgG was used as a negative control. G Recombinant GST-PRMT1 was incubated with recombinant His-UBE2m, followed by GST-pulldown and immunoblotting analysis with GST and His antibodies. H Endogenous UBE2m was immunoprecipitated in cells from the indicated groups. The mono-methylation (me1) level of UBE2m was determined using immunoblotting. I PLA detection of PRMT1 and UBE2m interaction in HK-2 cells from the indicated groups. Scale bars = 50 μm. J The me1 level of UBE2m was determined using immunoblotting after UBE2m was immunoprecipitated in HK-2 cells with PRMT1 knockdown or overexpression.

Article Snippet: Antibodies against PRMT1 (#2449, 1:1000 for WB, 1:100 for IF or IHC, 1:50 for IP), monomethyl arginine (#8015, 1:1000 for WB), FATP2 (#78771, 1:1000 for WB), PPARγ (#2435, 1:1000 for WB, 1:30 for IP), and NEDD8 (#2745, 1:1000 for WB) were purchased from Cell Signaling Technology.

Techniques: Staining, SDS Page, Immunoprecipitation, Tandem Mass Spectroscopy, Immunofluorescence, Co-Immunoprecipitation Assay, Negative Control, Recombinant, Incubation, Western Blot, Methylation, Knockdown, Over Expression

Journal: Cell Death & Disease

Article Title: PRMT1-mediated methylation of UBE2m promoting calcium oxalate crystal-induced kidney injury by inhibiting fatty acid metabolism

doi: 10.1038/s41419-025-07888-3

Figure Lengend Snippet: A The scores of potential methylation sites of UBE2m predicted using the GPS-MSP tool. B MS identification of R169 mono-methylation of HA-UBE2m immunopurified by HA beads. C Sequence alignment of UBE2m protein from indicated species. D HA-UBE2m WT or different point mutants were co-transfected with FLAG-PRMT in HEK293T cells. The me1 level of UBE2m was measured by immunoblotting following immunopurification. E The me1 of immunopurified HA-UBE2m was measured using a site-specific antibody against R169 mono-methylation (meUBE2m (R169me1)). Antibody efficacy and specificity were examined by pre-incubating with the R169me1 peptide or the unmodified peptide prior to application. F Dot blot analysis of different amounts of R169me1 peptide or unmodified peptide by a site-specific antibody against meUBE2m (R169me1). G Endogenous UBE2m was immunoprecipitated in cells from the indicated groups. The R169me1 level of UBE2m was determined using immunoblotting. H The R169me1 level of UBE2m was determined using immunoblotting after UBE2m was immunoprecipitated in HK-2 cells with PRMT1 knockdown or overexpression. I Recombinant GST-PRMT1 and His-UBE2m proteins were incubated with or without SAM to detect the methylation of UBE2m mediated by PRMT1 in vitro. The reaction mixture was then subjected to CBB staining and immunoblotting with meUBE2m (R169me1) antibody. J Mitochondrial oxidative capacity was measured in real time after reintroduced UBE2m WT or RK treatment in UBE2m KO HK-2 cells; basal respiration, ATP production-coupled respiration, and maximal respiration were quantified. Significance was assessed using two-way ANOVA tests. Data are shown as mean ± SD.

Article Snippet: Antibodies against PRMT1 (#2449, 1:1000 for WB, 1:100 for IF or IHC, 1:50 for IP), monomethyl arginine (#8015, 1:1000 for WB), FATP2 (#78771, 1:1000 for WB), PPARγ (#2435, 1:1000 for WB, 1:30 for IP), and NEDD8 (#2745, 1:1000 for WB) were purchased from Cell Signaling Technology.

Techniques: Methylation, Sequencing, Transfection, Western Blot, Immu-Puri, Dot Blot, Immunoprecipitation, Knockdown, Over Expression, Recombinant, Incubation, In Vitro, Staining

Journal: Cell Death & Disease

Article Title: PRMT1-mediated methylation of UBE2m promoting calcium oxalate crystal-induced kidney injury by inhibiting fatty acid metabolism

doi: 10.1038/s41419-025-07888-3

Figure Lengend Snippet: A RT-PCR was used to detect the RNA levels of PPARγ from the indicated groups. Representative western blot banding and quantitative analysis show the expression levels of PPARγ from the indicated groups in mice ( B ) or in HK-2 cells ( C ). D Detection of endogenous ubiquitination levels of PPARγ in HK-2 cells with COM-treatment. E Detection of endogenous ubiquitination levels of PPARγ in CaOx crystals kidney injury in mice. F , G Detection of exogenous ubiquitination levels of PPARγ in HEK193T cells with PRMT1 knockdown or overexpression. H Detection of exogenous ubiquitination levels of PPARγ in HEK193T cells from the indicated groups. Representative western blot banding and quantitative analysis of the expression levels of NEDD4 from the indicated groups in mice ( I ) or HK-2 cells ( J ). K HK-2 cells were treated with MG132. Representative western blot banding and quantitative analysis showed the expression levels of PPARγ from the indicated groups. L PLA detection of NEDD4 and PPARγ interaction in HK-2 cells from the indicated groups. Scale bars = 50 μm. M Detection of exogenous ubiquitination levels of PPARγ in HEK193T cells with knockdown of NEDD4. N Detection of exogenous ubiquitination levels of PPARγ in HEK193T cells from the indicated groups. Significance was assessed using two-way ANOVA tests. Data are shown as mean ± SD.

Article Snippet: Antibodies against PRMT1 (#2449, 1:1000 for WB, 1:100 for IF or IHC, 1:50 for IP), monomethyl arginine (#8015, 1:1000 for WB), FATP2 (#78771, 1:1000 for WB), PPARγ (#2435, 1:1000 for WB, 1:30 for IP), and NEDD8 (#2745, 1:1000 for WB) were purchased from Cell Signaling Technology.

Techniques: Reverse Transcription Polymerase Chain Reaction, Western Blot, Expressing, Ubiquitin Proteomics, Knockdown, Over Expression

Journal: Cell Death & Disease

Article Title: PRMT1-mediated methylation of UBE2m promoting calcium oxalate crystal-induced kidney injury by inhibiting fatty acid metabolism

doi: 10.1038/s41419-025-07888-3

Figure Lengend Snippet: A Representative immunohistochemical staining images (400X) and quantitative analysis of the expression of M-UBE2m in the nonfunctioning kidney of patients with stones or the control. Scale bars = 50 μm. B Pearson correlation analysis of the expression of PRMT1 and M-UBE2m. C Representative immunohistochemical staining images (400X) and quantitative analysis of the expression of KIM-1 in the nonfunctioning kidney of patients with stones or the control. Scale bars = 50 μm. D – G Pearson correlation analysis of the expression of PRMT1 and eGFR ( D ), PRMT1 and KIM-1 ( E ), M-UBE2m and eGFR ( F ), M-UBE2m and KIM-1 ( G ). Significance was assessed using t-tests. Data are presented as mean ± SD.

Article Snippet: Antibodies against PRMT1 (#2449, 1:1000 for WB, 1:100 for IF or IHC, 1:50 for IP), monomethyl arginine (#8015, 1:1000 for WB), FATP2 (#78771, 1:1000 for WB), PPARγ (#2435, 1:1000 for WB, 1:30 for IP), and NEDD8 (#2745, 1:1000 for WB) were purchased from Cell Signaling Technology.

Techniques: Immunohistochemical staining, Staining, Expressing, Control

Journal: Hepatology communications

Article Title: Hepatocellular Protein Arginine Methyltransferase 1 Suppresses Alcohol-Induced Hepatocellular Carcinoma Formation by Inhibition of Inducible Nitric Oxide Synthase.

doi: 10.1002/hep4.1488

Figure Lengend Snippet: FIG. 1. PRMT1 regulates tumor cell proliferation. (A) 2,3-bis-(2-methoxy-4-nitro-5-sulfophenyl)-2H-tetrazolium-5-carboxanilide assay of Huh7 or HepG2 cells untreated or treated with PRMT1 inhibitor AMI-1 or expressing PRMT1 wild type or DN mutant (V82L83D84 mutated to AAA, DN) at 24, 48, and 72 hours posttranfection. Data presented as average ± SD, n = 4; *P < 0.05, **P < 0.01. (B) Relative mRNA in isolated mouse hepatocytes expressing PRMT1 wild type or DN mutant (VLD-> AAA, DN) were untreated or treated with 40 mM LiCl to induce WNT/β-catenin signaling. Data presented as average ± SD, n = 4; **P < 0.01. (C) Male PRMT1 flox/ flox mice received a single injection of 10 mg/kg DEN at 2 weeks of age. At 6 months of age, mice received either AAV.TBG.control (WT) or AAV.TBG.CRE (HepKO) vector 1011 gc/mouse. Mice were killed at 8 months of age. (D,E) Relative mRNA levels in livers and tumors of mice as in C, n = 6 animals per group, n = 3-5 for tumor samples; mRNA was isolated from largest tumor per mouse; *P < 0.05, **P < 0.01. Abbreviations: AMI-1, arginine methyltransferase inhibitor 1; d, day; fl, flox; h, hour; ns, not significant.

Article Snippet: Mice received weekly injections of 10 mg/kg of the iNOS inhibitor 1400 W or saline control. antiBoDies useD Anti-PRMT1 (F339) and anti-β-catenin (N terminal, cat. #9581) antibodies were from Cell Signaling.

Techniques: Expressing, Mutagenesis, Isolation, Injection, Control, Plasmid Preparation

Journal: Hepatology communications

Article Title: Hepatocellular Protein Arginine Methyltransferase 1 Suppresses Alcohol-Induced Hepatocellular Carcinoma Formation by Inhibition of Inducible Nitric Oxide Synthase.

doi: 10.1002/hep4.1488

Figure Lengend Snippet: FIG. 2. PRMT1 protects from alcohol-associated HCC in mice. (A) PRMT1 flox/flox mice received a single injection of 10 mg/kg DEN at 2 weeks of age. At 6 months of age, mice were separated into groups and fed Lieber-DeCarli alcohol liquid diet (4.8% alcohol) or control liquid diet (pair) or left on chow diet for 7 weeks. On the first day of alcohol, mice received either AAV.TBG.control (WT) or AAV.TBG. CRE (HepKO) vector 1011 gc/mouse (arrows indicate visible tumors). (B) Representative liver images of mice from eight groups. (C,D) Liver to body weight ratios (C) and surface tumor number (D) in these animals, n = 6-10 animals per group; *P < 0.05, **P < 0.01. Data show interquartile range (box), median (vertical line), and outliers (whiskers). Groups with significant difference in surface tumors is in red. Abbreviations: fl, flox; ns, not significant.

Article Snippet: Mice received weekly injections of 10 mg/kg of the iNOS inhibitor 1400 W or saline control. antiBoDies useD Anti-PRMT1 (F339) and anti-β-catenin (N terminal, cat. #9581) antibodies were from Cell Signaling.

Techniques: Injection, Control, Plasmid Preparation

Journal: Hepatology communications

Article Title: Hepatocellular Protein Arginine Methyltransferase 1 Suppresses Alcohol-Induced Hepatocellular Carcinoma Formation by Inhibition of Inducible Nitric Oxide Synthase.

doi: 10.1002/hep4.1488

Figure Lengend Snippet: FIG. 4. Hepatic PRMT1 protects from inflammation in the liver of alcohol-fed mice. (A,B) Relative mRNA levels in livers and tumors of mice, n = 6-10 animals per group, n = 3-6 for tumor samples; *P < 0.05, **P < 0.01. (C) Representative images of F4/80 and cd11b immunostaining in liver sections from alcohol-fed male mice. Magnification is 10×. (D) Relative mRNA levels in tumors of mice, n = 3-6 for tumor samples; *P < 0.05, **P < 0.01. (E) Correlation between liver F4/80 mRNA and surface tumor number in mice fed a chow or alcohol diet, n = 27. Abbreviations: N, normal; T, tumor. Data show interquartile range (box), median (vertical line), and outliers (whiskers).

Article Snippet: Mice received weekly injections of 10 mg/kg of the iNOS inhibitor 1400 W or saline control. antiBoDies useD Anti-PRMT1 (F339) and anti-β-catenin (N terminal, cat. #9581) antibodies were from Cell Signaling.

Techniques: Immunostaining

Journal: Hepatology communications

Article Title: Hepatocellular Protein Arginine Methyltransferase 1 Suppresses Alcohol-Induced Hepatocellular Carcinoma Formation by Inhibition of Inducible Nitric Oxide Synthase.

doi: 10.1002/hep4.1488

Figure Lengend Snippet: FIG. 5. PRMT1 deficiency results in an increase in oxidative stress in the livers of alcohol-fed mice. Data show interquartile range (box), median (vertical line), and outliers (whiskers). Magnification is 10×. (A) Representative images of TUNEL staining in male wild-type mice (AAV-control) and hepatocyte-specific PRMT1-knockout mice (AAV-CRE) fed alcohol. (B) Serum ALT levels in mice fed either alcohol or control liquid diet, n = 6-10 animals per group; **P < 0.01. (C) Relative mRNA levels in livers, n = 6-10 animals per group; *P < 0.05. (D) Representative images of 4-HNE staining in male wild-type mice (AAV-control) and hepatocyte-specific PRMT1- knockout-mice (AAV-CRE) fed alcohol or chow.

Article Snippet: Mice received weekly injections of 10 mg/kg of the iNOS inhibitor 1400 W or saline control. antiBoDies useD Anti-PRMT1 (F339) and anti-β-catenin (N terminal, cat. #9581) antibodies were from Cell Signaling.

Techniques: TUNEL Assay, Staining, Control, Knock-Out

Journal: Hepatology communications

Article Title: Hepatocellular Protein Arginine Methyltransferase 1 Suppresses Alcohol-Induced Hepatocellular Carcinoma Formation by Inhibition of Inducible Nitric Oxide Synthase.

doi: 10.1002/hep4.1488

Figure Lengend Snippet: FIG. 8. Inhibition of iNOS protects alcohol-fed PRMT1-knockout mice from liver inflammation. (A) Relative mRNA levels in livers of mice as in Fig. 5C, n = 4-5 animals per group; *P < 0.05. Data show interquartile range (box), median (vertical line), and outliers (whiskers). (B) Representative images of β-catenin staining from male wild-type mice (AAV-control) and hepatocyte-specific PRMT1-knockout mice (AAV-CRE). Magnification is 10×. (Right panel) Relative staining intensity. Data presented as average ± SD, n = 4 animals per group; *P < 0.05, **P < 0.01. (C,D) Relative mRNA levels in livers of mice as in Fig. 5C, n = 4-10 animals per group; *P < 0.05. Data show interquartile range (box), median (vertical line), and outliers (whiskers). (E) (Left and middle panels). Liver to body weight ratios in male mice of indicated age, n = 4 animals per group; **P < 0.01, paired. (Right panel) Surface tumor number in male mice, n = 8 animals per group; **P < 0.01. (F) Model of protumor and antitumor PRMT1-dependent pathways. Abbreviation: IL, interleukin.

Article Snippet: Mice received weekly injections of 10 mg/kg of the iNOS inhibitor 1400 W or saline control. antiBoDies useD Anti-PRMT1 (F339) and anti-β-catenin (N terminal, cat. #9581) antibodies were from Cell Signaling.

Techniques: Inhibition, Knock-Out, Staining, Control

Journal: Cancers

Article Title: L-Arginine/Nitric Oxide Pathway Is Altered in Colorectal Cancer and Can Be Modulated by Novel Derivatives from Oxicam Class of Non-Steroidal Anti-Inflammatory Drugs

doi: 10.3390/cancers12092594

Figure Lengend Snippet: Comparison of arginine/nitric oxide pathway enzymes’ expression in normal colonic tissue and tumor and non-cancerous tumor-adjacent tissue: ( a ) ARG1 ; ( b ) DDAH1 ; ( c ) DDAH2 ; ( d ) NOS2 ; ( e ) PRMT1 ; ( f ) PRMT2 . Data analyzed using a Kruskal–Wallis H test. Numeric data present medians of normalized relative quantities (NRQ), accompanied by 95% confidence interval (CI). Boxes indicate median with interquartile range; whiskers—95% CI; grey dots ‒ outlying observations. *, significant between-group differences ( p < 0.05); ARG2 , arginase 2; DDAH , dimethylarginine dimethylaminohydrolase; NOS2 , inducible nitric oxide synthase; PRMT , protein methyltransferase.

Article Snippet: The following dilutions were applied: arginase-2 (1:1000; cat. no. CSB-PA002006GA01HU), DDAH1 (1:1000; cat. no. CSB-PA877002), DDAH2 (1:5000; cat. no. CSB-PA006580LA01HU), PRMT5 (1:1000; cat. no. CSB-PA018734GA01HU), and PRMT1 (1:80; R&D Systems, Minneapolis, MN, USA; cat. No. AF6016).

Techniques: Comparison, Expressing

Journal: Cancers

Article Title: L-Arginine/Nitric Oxide Pathway Is Altered in Colorectal Cancer and Can Be Modulated by Novel Derivatives from Oxicam Class of Non-Steroidal Anti-Inflammatory Drugs

doi: 10.3390/cancers12092594

Figure Lengend Snippet: Effect of novel oxicam analogues on arginine/nitric oxide pathway enzymes.

Article Snippet: The following dilutions were applied: arginase-2 (1:1000; cat. no. CSB-PA002006GA01HU), DDAH1 (1:1000; cat. no. CSB-PA877002), DDAH2 (1:5000; cat. no. CSB-PA006580LA01HU), PRMT5 (1:1000; cat. no. CSB-PA018734GA01HU), and PRMT1 (1:80; R&D Systems, Minneapolis, MN, USA; cat. No. AF6016).

Techniques: Analogues

Journal: Cancers

Article Title: L-Arginine/Nitric Oxide Pathway Is Altered in Colorectal Cancer and Can Be Modulated by Novel Derivatives from Oxicam Class of Non-Steroidal Anti-Inflammatory Drugs

doi: 10.3390/cancers12092594

Figure Lengend Snippet: Dose-dependent effect of oxicams on enzyme gene expression in Caco-2 cells stimulated with 5, 50 and 200 µM drug concentrations for 24 h: ( a ) Arginase-2 ( ARG2 ); ( b ) Dimethylarginine dimethylaminohydrolase-1 ( DDAH1 ); ( c ) Dimethylarginine dimethylaminohydrolase-2 ( DDAH2 ); ( d ) Nitric oxide synthase-2 ( NOS2 ); ( e ) Protein methyltransferase-1 ( PRMT1 ); ( f ) Protein methyltransferase-5 ( PRMT5 ). Bars represent mean ( n = 3) concentration ratios treated-to-untreated cells (t/u) with standard deviation (whiskers). No effect is marked by horizontal blue reference line. Data were analyzed using one-way analysis of variance. *, significant between-group differences; #1–5, oxicam analogues; M, meloxicam; P, piroxicam.

Article Snippet: The following dilutions were applied: arginase-2 (1:1000; cat. no. CSB-PA002006GA01HU), DDAH1 (1:1000; cat. no. CSB-PA877002), DDAH2 (1:5000; cat. no. CSB-PA006580LA01HU), PRMT5 (1:1000; cat. no. CSB-PA018734GA01HU), and PRMT1 (1:80; R&D Systems, Minneapolis, MN, USA; cat. No. AF6016).

Techniques: Gene Expression, Concentration Assay, Standard Deviation, Analogues

Journal: Cancers

Article Title: L-Arginine/Nitric Oxide Pathway Is Altered in Colorectal Cancer and Can Be Modulated by Novel Derivatives from Oxicam Class of Non-Steroidal Anti-Inflammatory Drugs

doi: 10.3390/cancers12092594

Figure Lengend Snippet: Dose-dependent effect of oxicams on enzyme gene expression in HCT 116 cells stimulated with 5, 50 and 200 µM drug concentrations for 24 h: ( a ) Arginase-2 ( ARG2 ); ( b ) Dimethylarginine dimethylaminohydrolase-1 ( DDAH1 ); ( c ) Dimethylarginine dimethylaminohydrolase-2 ( DDAH2 ); ( d ) Protein methyltransferase-1 ( PRMT1 ); ( e ) Protein methyltransferase-5 ( PRMT5 ). Bars represent mean ( n = 3) concentration ratios treated-to-untreated cells (t/u) with standard deviation (whiskers). No effect is marked by horizontal blue reference line. Data were analyzed using one-way analysis of variance. *, significant between-group differences; #1–5, oxicam analogues; M, meloxicam; P, piroxicam.

Article Snippet: The following dilutions were applied: arginase-2 (1:1000; cat. no. CSB-PA002006GA01HU), DDAH1 (1:1000; cat. no. CSB-PA877002), DDAH2 (1:5000; cat. no. CSB-PA006580LA01HU), PRMT5 (1:1000; cat. no. CSB-PA018734GA01HU), and PRMT1 (1:80; R&D Systems, Minneapolis, MN, USA; cat. No. AF6016).

Techniques: Gene Expression, Concentration Assay, Standard Deviation, Analogues

Journal: Cancers

Article Title: L-Arginine/Nitric Oxide Pathway Is Altered in Colorectal Cancer and Can Be Modulated by Novel Derivatives from Oxicam Class of Non-Steroidal Anti-Inflammatory Drugs

doi: 10.3390/cancers12092594

Figure Lengend Snippet: Dose-dependent effect of oxicams on enzyme gene expression in HT-29 cells stimulated with 5, 50 and 200 µM drug concentrations for 24 h: ( a ) Arginase-2 ( ARG2 ); ( b ) Dimethylarginine dimethylaminohydrolase-1 ( DDAH1 ); ( c ) Dimethylarginine dimethylaminohydrolase-2 ( DDAH2 ); ( d ) Protein methyltransferase-1 ( PRMT1 ); ( e ) Protein methyltransferase-5 ( PRMT5 ). Bars represent mean ( n = 3) concentration ratios treated-to-untreated cells (t/u) with standard deviation (whiskers). No effect is marked by horizontal blue reference line. Data were analyzed using one-way analysis of variance. * significant between-group differences; #1–5, oxicam analogues; M, meloxicam; P, piroxicam.

Article Snippet: The following dilutions were applied: arginase-2 (1:1000; cat. no. CSB-PA002006GA01HU), DDAH1 (1:1000; cat. no. CSB-PA877002), DDAH2 (1:5000; cat. no. CSB-PA006580LA01HU), PRMT5 (1:1000; cat. no. CSB-PA018734GA01HU), and PRMT1 (1:80; R&D Systems, Minneapolis, MN, USA; cat. No. AF6016).

Techniques: Gene Expression, Concentration Assay, Standard Deviation, Analogues

Journal: Cancers

Article Title: L-Arginine/Nitric Oxide Pathway Is Altered in Colorectal Cancer and Can Be Modulated by Novel Derivatives from Oxicam Class of Non-Steroidal Anti-Inflammatory Drugs

doi: 10.3390/cancers12092594

Figure Lengend Snippet: Characteristics of applied primers.

Article Snippet: The following dilutions were applied: arginase-2 (1:1000; cat. no. CSB-PA002006GA01HU), DDAH1 (1:1000; cat. no. CSB-PA877002), DDAH2 (1:5000; cat. no. CSB-PA006580LA01HU), PRMT5 (1:1000; cat. no. CSB-PA018734GA01HU), and PRMT1 (1:80; R&D Systems, Minneapolis, MN, USA; cat. No. AF6016).

Techniques: Sequencing