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MedChemExpress enos inhibitor ng nitroarginine methyl ester hydrochloride
Glutamine increased vasodilation ex vivo but did not impact <t>eNOS</t> phosphorylation or nitric oxide in vitro. (a) Mouse carotid artery vasodilation in response to acetylcholine with an intact endothelium. Isolated mouse carotid arteries were incubated at 4°C overnight in physiological saline containing either 0 or 2 mM glutamine. Vasodilation was measured the following day by pressure myography. n = 4–5 arteries per condition. (b) representative Western blot with quantification of eNOS and p‐eNOS in HCAEC cultured in 0 and 2 mM glutamine. n = 10–11 samples per condition. (c) HCAECs were treated with 0, 0.5, and 2 mM glutamine in 5.5 and 15 mM glucose. L‐glucose at 2 mM and 11.5 mM was included as positive control for glutamine and glucose respectively. After 24 h cells were treated with 20 μM of yoda1 and then the nitrites in the culture media was measured using a Griess assay. n = 9 samples. Data shown as mean ± standard deviation. Statistical significance determined by repeated measures ANOVA (a), Mann–Whitney nonparametric test (b), and two‐way ANOVA followed by Tukey's post hoc test.
Enos Inhibitor Ng Nitroarginine Methyl Ester Hydrochloride, supplied by MedChemExpress, used in various techniques. Bioz Stars score: 95/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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Glutamine increased vasodilation ex vivo but did not impact <t>eNOS</t> phosphorylation or nitric oxide in vitro. (a) Mouse carotid artery vasodilation in response to acetylcholine with an intact endothelium. Isolated mouse carotid arteries were incubated at 4°C overnight in physiological saline containing either 0 or 2 mM glutamine. Vasodilation was measured the following day by pressure myography. n = 4–5 arteries per condition. (b) representative Western blot with quantification of eNOS and p‐eNOS in HCAEC cultured in 0 and 2 mM glutamine. n = 10–11 samples per condition. (c) HCAECs were treated with 0, 0.5, and 2 mM glutamine in 5.5 and 15 mM glucose. L‐glucose at 2 mM and 11.5 mM was included as positive control for glutamine and glucose respectively. After 24 h cells were treated with 20 μM of yoda1 and then the nitrites in the culture media was measured using a Griess assay. n = 9 samples. Data shown as mean ± standard deviation. Statistical significance determined by repeated measures ANOVA (a), Mann–Whitney nonparametric test (b), and two‐way ANOVA followed by Tukey's post hoc test.
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Thermo Fisher snp nos3 c 15903863 10
10-year overall survival (OS) by Kaplan-Meier and log-rank test for CC patients, according to <t>NOS3</t> rs2070744 ( N = 379): (a) In the entire cohort, while only marginally significant, women with the CC genotype presented a lower OS compared to T allele carriers (10-year OS of 82.0 ± 5.7 months and 92.3 ± 2.6 months, respectively; log-rank test, p = 0.057). (b) The negative effect of the SNP CC genotype was verified when focusing on younger women (≤ 49 years) (10-year OS of 75.2 ± 7.9 months and 92.3 ± 3.6 months, respectively; log-rank test, p = 0.028). (c) In contrast, no significant impact of the SNP was observed in the subgroup of older women (10-year OS of 89.5 ± 8.1 months and 92.2 ± 3.8 months, respectively; log-rank test, p = 0.068)
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Thermo Fisher snp nos3 c 3219460 20
10-year overall survival (OS) by Kaplan-Meier and log-rank test for CC patients, according to <t>NOS3</t> rs2070744 ( N = 379): (a) In the entire cohort, while only marginally significant, women with the CC genotype presented a lower OS compared to T allele carriers (10-year OS of 82.0 ± 5.7 months and 92.3 ± 2.6 months, respectively; log-rank test, p = 0.057). (b) The negative effect of the SNP CC genotype was verified when focusing on younger women (≤ 49 years) (10-year OS of 75.2 ± 7.9 months and 92.3 ± 3.6 months, respectively; log-rank test, p = 0.028). (c) In contrast, no significant impact of the SNP was observed in the subgroup of older women (10-year OS of 89.5 ± 8.1 months and 92.2 ± 3.8 months, respectively; log-rank test, p = 0.068)
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Thermo Fisher gene exp nos3 mm00435217 m1
RT-PCR analysis. Selected mRNA expression in sorted LECs from db/db and control mice hearts. Some mRNA levels significantly increase in db/db mice compared to controls. Statistically significant differences ( p -value < 0.05) are marked (*). Abbreviations: Acta2—Actin 2/smooth muscle actin; Bax—BCL2 Associated X; Bcl2—B-cell CLL/lymphoma 2; CCL21—Chemokine (C-C motif) ligand 21; CEACAM1—Carcinoembryonic antigen-related cell adhesion molecule 1; CPT1A—Carnitine Palmitoyltransferase 1A; CX3CL1—chemokine (C-X3-C motif) ligand 1; <t>eNOS—endothelial</t> nitric oxide synthase;Fbn1—fibrillin-1; FOXO1—Forkhead Box O1; GATA2—GATA-binding factor 2; ICAM-1—intercellular adhesion molecule 1; KLF2—Krüppel-like Factor 2; MMP2—Metalloproteinase 2; PDPN—podoplanin; PTEN—phosphatase and tensin homolog deleted on chromosome ten; Reln—reelin; Sdc4—syndecan 4; Snail1—Snail family transcriptional repressor-1; Snail2—Snail family transcriptional repressor-2; VCAM-1—vascular cell adhesion molecule 1; VE-cadherin—Vascular Endothelial Cadherin.
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Glutamine increased vasodilation ex vivo but did not impact eNOS phosphorylation or nitric oxide in vitro. (a) Mouse carotid artery vasodilation in response to acetylcholine with an intact endothelium. Isolated mouse carotid arteries were incubated at 4°C overnight in physiological saline containing either 0 or 2 mM glutamine. Vasodilation was measured the following day by pressure myography. n = 4–5 arteries per condition. (b) representative Western blot with quantification of eNOS and p‐eNOS in HCAEC cultured in 0 and 2 mM glutamine. n = 10–11 samples per condition. (c) HCAECs were treated with 0, 0.5, and 2 mM glutamine in 5.5 and 15 mM glucose. L‐glucose at 2 mM and 11.5 mM was included as positive control for glutamine and glucose respectively. After 24 h cells were treated with 20 μM of yoda1 and then the nitrites in the culture media was measured using a Griess assay. n = 9 samples. Data shown as mean ± standard deviation. Statistical significance determined by repeated measures ANOVA (a), Mann–Whitney nonparametric test (b), and two‐way ANOVA followed by Tukey's post hoc test.

Journal: Physiological Reports

Article Title: Glutamine enhances endothelial cell survival and vasodilation by increasing glutathione to reduce oxidative stress

doi: 10.14814/phy2.70737

Figure Lengend Snippet: Glutamine increased vasodilation ex vivo but did not impact eNOS phosphorylation or nitric oxide in vitro. (a) Mouse carotid artery vasodilation in response to acetylcholine with an intact endothelium. Isolated mouse carotid arteries were incubated at 4°C overnight in physiological saline containing either 0 or 2 mM glutamine. Vasodilation was measured the following day by pressure myography. n = 4–5 arteries per condition. (b) representative Western blot with quantification of eNOS and p‐eNOS in HCAEC cultured in 0 and 2 mM glutamine. n = 10–11 samples per condition. (c) HCAECs were treated with 0, 0.5, and 2 mM glutamine in 5.5 and 15 mM glucose. L‐glucose at 2 mM and 11.5 mM was included as positive control for glutamine and glucose respectively. After 24 h cells were treated with 20 μM of yoda1 and then the nitrites in the culture media was measured using a Griess assay. n = 9 samples. Data shown as mean ± standard deviation. Statistical significance determined by repeated measures ANOVA (a), Mann–Whitney nonparametric test (b), and two‐way ANOVA followed by Tukey's post hoc test.

Article Snippet: Endothelial‐independent vasodilation was measured by preincubating carotid arteries with eNOS inhibitor NG‐Nitroarginine methyl ester hydrochloride (L‐NAME, 10 −5 M; HY‐18729A; Med Chem Express) for 1 h. Vasodilation to acetylcholine was then measured as previously described.

Techniques: Ex Vivo, Phospho-proteomics, In Vitro, Isolation, Incubation, Saline, Western Blot, Cell Culture, Positive Control, Griess Assay, Standard Deviation, MANN-WHITNEY

10-year overall survival (OS) by Kaplan-Meier and log-rank test for CC patients, according to NOS3 rs2070744 ( N = 379): (a) In the entire cohort, while only marginally significant, women with the CC genotype presented a lower OS compared to T allele carriers (10-year OS of 82.0 ± 5.7 months and 92.3 ± 2.6 months, respectively; log-rank test, p = 0.057). (b) The negative effect of the SNP CC genotype was verified when focusing on younger women (≤ 49 years) (10-year OS of 75.2 ± 7.9 months and 92.3 ± 3.6 months, respectively; log-rank test, p = 0.028). (c) In contrast, no significant impact of the SNP was observed in the subgroup of older women (10-year OS of 89.5 ± 8.1 months and 92.2 ± 3.8 months, respectively; log-rank test, p = 0.068)

Journal: Molecular Biology Reports

Article Title: Endothelial dysfunction markers in cervical cancer and their influence on patient outcome

doi: 10.1007/s11033-026-11448-z

Figure Lengend Snippet: 10-year overall survival (OS) by Kaplan-Meier and log-rank test for CC patients, according to NOS3 rs2070744 ( N = 379): (a) In the entire cohort, while only marginally significant, women with the CC genotype presented a lower OS compared to T allele carriers (10-year OS of 82.0 ± 5.7 months and 92.3 ± 2.6 months, respectively; log-rank test, p = 0.057). (b) The negative effect of the SNP CC genotype was verified when focusing on younger women (≤ 49 years) (10-year OS of 75.2 ± 7.9 months and 92.3 ± 3.6 months, respectively; log-rank test, p = 0.028). (c) In contrast, no significant impact of the SNP was observed in the subgroup of older women (10-year OS of 89.5 ± 8.1 months and 92.2 ± 3.8 months, respectively; log-rank test, p = 0.068)

Article Snippet: Each reaction comprised a mixture of 6.0 μL, including 2.5 μL of TaqPathTM ProAmpTM Master Mix (1×), 2.375 μL of sterile water, 0.125 μL of TaqMan ® Genotyping Assay Mix (C___3219460_20 for NOS3 rs1799983, C__15903863_10 for NOS3 rs2070744, C___3288406_30 for VWF rs1063856 and C__11975277_20 for SELP rs6136), and 1.0 μL of genomic DNA.

Techniques:

RT-PCR analysis. Selected mRNA expression in sorted LECs from db/db and control mice hearts. Some mRNA levels significantly increase in db/db mice compared to controls. Statistically significant differences ( p -value < 0.05) are marked (*). Abbreviations: Acta2—Actin 2/smooth muscle actin; Bax—BCL2 Associated X; Bcl2—B-cell CLL/lymphoma 2; CCL21—Chemokine (C-C motif) ligand 21; CEACAM1—Carcinoembryonic antigen-related cell adhesion molecule 1; CPT1A—Carnitine Palmitoyltransferase 1A; CX3CL1—chemokine (C-X3-C motif) ligand 1; eNOS—endothelial nitric oxide synthase;Fbn1—fibrillin-1; FOXO1—Forkhead Box O1; GATA2—GATA-binding factor 2; ICAM-1—intercellular adhesion molecule 1; KLF2—Krüppel-like Factor 2; MMP2—Metalloproteinase 2; PDPN—podoplanin; PTEN—phosphatase and tensin homolog deleted on chromosome ten; Reln—reelin; Sdc4—syndecan 4; Snail1—Snail family transcriptional repressor-1; Snail2—Snail family transcriptional repressor-2; VCAM-1—vascular cell adhesion molecule 1; VE-cadherin—Vascular Endothelial Cadherin.

Journal: Pathophysiology

Article Title: Metabolic Syndrome-Driven Changes in Cardiac Lymphatic Endothelium: mRNA Expression and Emerging Questions

doi: 10.3390/pathophysiology33010004

Figure Lengend Snippet: RT-PCR analysis. Selected mRNA expression in sorted LECs from db/db and control mice hearts. Some mRNA levels significantly increase in db/db mice compared to controls. Statistically significant differences ( p -value < 0.05) are marked (*). Abbreviations: Acta2—Actin 2/smooth muscle actin; Bax—BCL2 Associated X; Bcl2—B-cell CLL/lymphoma 2; CCL21—Chemokine (C-C motif) ligand 21; CEACAM1—Carcinoembryonic antigen-related cell adhesion molecule 1; CPT1A—Carnitine Palmitoyltransferase 1A; CX3CL1—chemokine (C-X3-C motif) ligand 1; eNOS—endothelial nitric oxide synthase;Fbn1—fibrillin-1; FOXO1—Forkhead Box O1; GATA2—GATA-binding factor 2; ICAM-1—intercellular adhesion molecule 1; KLF2—Krüppel-like Factor 2; MMP2—Metalloproteinase 2; PDPN—podoplanin; PTEN—phosphatase and tensin homolog deleted on chromosome ten; Reln—reelin; Sdc4—syndecan 4; Snail1—Snail family transcriptional repressor-1; Snail2—Snail family transcriptional repressor-2; VCAM-1—vascular cell adhesion molecule 1; VE-cadherin—Vascular Endothelial Cadherin.

Article Snippet: To detect mRNA levels of selected genes, the following TaqMan Gene Expression Assays were used: CD36: Mm00432403_m1; Pten: Mm00477208_m1; Foxo1: Mm00490671_m1; Klf2: Mm00500486_g1; Bax: Mm00432051_m1; Bcl2: Mm00477631_m1; Cpt1a: Mm01231183_m1; Ccl21a: Mm03646971_gH; Cx3cl1: Mm00436454_m1; Icam1: Mm00516023_m1; Vcam1: Mm01320970_m1; Emilin1: Mm00467244_m1; Mmp2: Mm00439498_m1; Reln: Mm00465200_m1; Snai1: Mm00441533_g1; Snai2: Mm00441531_m1; Acta2: Mm00725412_s1; Cdh5: Mm00546194_s1; Gata2: Mm00492301_m1; Cldn5: Mm00727012_s1; Ceacam1: Mm04204476_m1; Pdpn: Mm01348912_g1; Fbn1: Mm00435217_m1; Nos3: Mm00435217_m1; Sdc4: Mm00488527_m1.

Techniques: Reverse Transcription Polymerase Chain Reaction, Expressing, Control, Binding Assay

Journal: bioRxiv

Article Title: Structural basis for the inhibition of Trypanosoma brucei enolase by a camelid single-domain antibody

doi: 10.64898/2025.12.17.694860

Figure Lengend Snippet:

Article Snippet: The crystal plates were incubated at 20 ° C. Diffraction-quality crystals of Tbr ENO - sdAbR1-10 were obtained in JBScreen Classic 3 (Jena Bioscience) condition no. A3 (10% (w/v) PEG 4000, 10% (w/v) 2-propanol, 100 mM tri-sodium citrate, pH 5.6) and the crystals grew after approximately 7 days.

Techniques: