PA1-037

antibody from Invitrogen Antibodies

Targeting: NOS3 ECNOS, eNOS

Provider product page for PA1-037

Western blot

Immunohistochemistry

Other assay

Antibody data

Antibody Data
Antigen structure
References [77]
Comments [0]
Validations
Immunohistochemistry [1]
Other assay [16]

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Product number: PA1-037 - Provider product page
Provider: Invitrogen Antibodies
Product name: eNOS Polyclonal Antibody
Antibody type: Polyclonal
Antigen: Synthetic peptide
Description: PA1-037 detects endothelial nitric oxide synthase (eNOS) from bovine, canine, human, mouse, porcine and rat tissues as well as recombinant protein. This antibody does not detect human iNOS or rat nNOS. PA1-037 has been successfully used in Western blot and immunohistochemistry (paraffin and frozen) procedures. By Western blot, this antibody detects an ~140 kDa protein representing eNOS from human endothelial cells. By Western blot PA1-037 also detects eNOS in rat lung, brain, and canine cardiac microsomes. Immunohistochemical staining of eNOS in human vascular endothelial cells with PA1-037 results in prominent staining of the epithelial cells. The PA1-037 immunogen is a synthetic peptide corresponding to residues S(1179) L Q E R Q L R G A V P W A F D(1194) of human eNOS.
Reactivity: Human, Mouse, Rat, Bovine, Canine, Porcine
Host: Rabbit
Isotype: IgG
Vial size: 100 µL
Concentration: 0.2 mg/mL
Storage: -20° C, Avoid Freeze/Thaw Cycles

NOS3 protein structure - PA1-037 shown in red.

Supportive validation

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Experimental details: NULL

Supportive validation

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Experimental details: NULL

Supportive validation

Submitted by: Invitrogen Antibodies (provider)
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Experimental details: NULL

Supportive validation

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Experimental details: NULL

Supportive validation

Submitted by: Invitrogen Antibodies (provider)
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Experimental details: NULL

Supportive validation

Submitted by: Invitrogen Antibodies (provider)
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Experimental details: NULL

Supportive validation

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Experimental details: NULL

Supportive validation

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Experimental details: NULL

Supportive validation

Submitted by: Invitrogen Antibodies (provider)
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Experimental details: Figure 2 IRF2BP2 increases the expression of KLF2 and improves endothelial function. (A) The expression levels of ICAM-1 and VCAM-1 were determined using reverse transcription-quantitative PCR analysis. (B) The protein expression levels of KLF2, p-eNOS, total eNOS and GAPDH were measured using western blot analysis. (C) A Nitrate/Nitrite assay kit was utilized to estimate the release of NO. (D) The expression of KLF2 was evaluated by immunofluorescence analysis (magnification, x200). Scale bar, 50 um. ** P

Supportive validation

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Experimental details: Figure 4 KLF2 is required for IRF2BP2-regulated endothelial function. (A) The mRNA expression levels of ICAM-1 and VCAM-1 were measured by reverse transcription-quantitative PCR analysis. (B) The protein expression levels of total eNOS, p-eNOS and GAPDH were evaluated using western blot analysis. (C) A Nitrate/Nitrite assay kit was used to estimate the release of NO. *** P

Supportive validation

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Experimental details: 1 (A) Western blot analysis of hepatic eNOS in representative photographs of rat livers obtained from the control and OLP groups before EHx. The relative eNOS levels were quantified by densitometry. The data are expressed as means and standard deviations (n = 4, * P < 0.05). (B,C) Immunohistochemistry of hepatic eNOS in representative photographs (x400) obtained from the control and OLP groups, respectively. eNOS was expressed in endothelial cells in the control group. In the OLP group, it was expressed in hepatocytes, other nonendothelial hepatic cells, and endothelial cells. Arrows indicate sinusoidal endothelial cells, and arrowheads indicate nonendothelial hepatic cells.

Supportive validation

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Experimental details: Figure 5 The Autonomic Nervous System Regulates Lymphatic Contractility In Vivo (A) Schematic overview of in vivo imaging of flank collector contractility. (B) Representative example of measured NIR-dye intensity in the flank collector over time; topical treatment was done at time point 2 min. (C-E) Effects of topical treatment with neural agonists and antagonists on lymphatic contraction frequency (C), amplitude (D), and pumping score (E). Shown are the post-treatment values as a percentage of pretreatment values for mice under injection anesthesia (ketamine, xylazine, and acepromazine). (G-I) Same is shown for mice under isoflurane: changes in frequency (G), amplitude (H) and pumping score (I). (F and J) Quantification of the tonic contraction of the flank collector upon treatment with neural agonists and antagonists under injection anesthesia (F; ketamine, xylazine, acepromazine) and isoflurane (J). (K and L) Isoproterenol-mediated phosphorylation of eNOS, as assessed (K) and quantified (L) by western blot. VEGF-A was used as positive control. The western blot shown is a representative example of at least three independent experiments. * p < 0.05, ** p

Supportive validation

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Experimental details: Figure 4 Overexpression of STEAP4 ameliorated HG-induced endothelial dysfunction. The expression of VEGF, KLF2, eNOS and ICAM-1 was detected by Western blot. n=3, ***p

Supportive validation

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Experimental details: FIGURE 5 Knocking down p38 MAPK protects against endothelial destruction induced by OGD/R. (A) Western blot of phospho-p38 MAPK, p38 MAPK, AQP1, ICAM-1, ZO-1, and VE-cadherin in rPMVECs. (B-F) Quantification of proteins from western blots in panel A. (G) Western blot of eNOS and ET-1 in rPMVECs. (H,I) Quantification of proteins from western blots in panel G. Each experiment was performed independently at least three times. ns, not significant, * p < 0.05.

Supportive validation

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Experimental details: FIGURE 8 RAP Accelerated Angiogenesis of the Sciatic Nerve through activation of the AKT/eNOS signaling pathway (A-C) Representative images of immunofluorescence staining for CD31 (red), VEGFR (orange), CD34 (green) of sciatic nerve transverse sections in each group 28 days after PNI. Nuclei are stained with DAPI (blue) (100x amplification, scale bar = 100 mum), arrows show neovascularization; (D) Representative images of double immunofluorescence co-localization staining for AKT (red) and eNOS (green) of sciatic nerve longitudinal sections in each group 28 days after PNI. Nuclei are stained with DAPI (blue) (400x amplification, scale bar = 50 mum); (E) Representative images of double immunofluorescence staining for p-AKT (red) and p-eNOS (green) of sciatic nerve longitudinal sections in each group 28 days after PNI. Nuclei are stained with DAPI (blue) (400x amplification, scale bar = 50 mum) (F) Statistical analysis of Microvessel area (G) Statistical analysis of fluorescence integrated density of AKT, eNOS, p-AKT, and p-eNOS. Data are presented as means +- SD. * p < 0.05**, p < 0.001,*** p < 0.0005.

Supportive validation

Submitted by: Invitrogen Antibodies (provider)
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Experimental details: Figure 4. A, eNOS protein expression (red) in ears of rats given tap water (LSD) or 1.0% saline (HSD), with or without additional MPS cell depletion by Clod treatment, with or without additional DOCA treatment. HSD and DOCA HSD increased eNOS protein expression, and additional Clod treatment reversed this effect back to the control level. B, Colocalization of eNOS protein expression (red) and podoplanin staining (green) in the same rats. The increase of eNOS expression observed in HSD and DOCA HSD rats did not colocalize with the lymphatic endothelium of a lymph capillary (LC). C, Summary of changes in eNOS protein expression in skin (rat ear). eNOS expression in skin in response to HSD and/or DOCA HSD treatment was dependent on MPS activity. &ast P