Recombinant Rat Nitric Oxide Synthase, Endothelial (NOS3) Protein (His)

Name: Recombinant Rat Nitric Oxide Synthase, Endothelial (NOS3) Protein (His)
Brand: Beta LifeScience
SKU: BLC-08254P
Availability: InStock

Greater than 90% as determined by SDS-PAGE.

Collections: All products, High-quality recombinant proteins, Other recombinant proteins

Our products are highly customizable to meet your specific needs. You can choose options such as endotoxin removal, liquid or lyophilized forms, preferred tags, and the desired functional sequence range for proteins. Submitting a written inquiry expedites the quoting process.

Submit an inquiry today to inquire about all available size options and prices! Connect with us via the live chat in the bottom corner to receive immediate assistance.

Product Overview

Description	Recombinant Rat Nitric Oxide Synthase, Endothelial (NOS3) Protein (His) is produced by our E.coli expression system. This is a protein fragment.
Purity	Greater than 90% as determined by SDS-PAGE.
Uniprotkb	Q62600
Target Symbol	NOS3
Synonyms	Nos3; Nitric oxide synthase; endothelial; EC 1.14.13.39; Constitutive NOS; cNOS; EC-NOS; Endothelial NOS; eNOS; NOS type III; NOSIII
Species	Rattus norvegicus (Rat)
Expression System	E.coli
Tag	N-6His
Target Protein Sequence	ATILYGSETGRAQSYAQQLGRLFRKAFDPRVLCMDEYDVVSLEHEALVLVVTSTFGNGDPPENGESFAAALMEMSGPYNSSPRPEQHKSYKIRFNSVSCSDPLVSSWRRKRKESSNTDSAGALGTLRFCVFGLGSRAYPHFCAFARAVDTRLEELGGERLLQLGQGDELCGQ
Expression Range	519-690aa
Protein Length	Partial
Mol. Weight	22.9kDa
Research Area	Others
Form	Liquid or Lyophilized powder
Buffer	Liquid form: default storage buffer is Tris/PBS-based buffer, 5%-50% glycerol. Lyophilized powder form: the buffer before lyophilization is Tris/PBS-based buffer, 6% Trehalose, pH 8.0.
Reconstitution	Briefly centrifuged the vial prior to opening to bring the contents to the bottom. Reconstitute protein in deionized sterile water to a concentration of 0.1-1.0 mg/mL. It is recommended to add 5-50% of glycerol (final concentration) and aliquot for long-term storage at -20°C/-80°C. The default final concentration of glycerol is 50%.
Storage	1. Store at -20°C/-80°C upon receipt, aliquoting is necessary for mutiple use. 2. Avoid repeated freeze-thaw cycles. 3. Store working aliquots at 4°C for up to one week. 4. In general, protein in liquid form is stable for up to 6 months at -20°C/-80°C. Protein in lyophilized powder form is stable for up to 12 months at -20°C/-80°C.
Notes	Repeated freezing and thawing is not recommended. Store working aliquots at 4°C for up to one week.

Target Details

Target Function	Produces nitric oxide (NO) which is implicated in vascular smooth muscle relaxation through a cGMP-mediated signal transduction pathway. NO mediates vascular endothelial growth factor (VEGF)-induced angiogenesis in coronary vessels and promotes blood clotting through the activation of platelets.
Subcellular Location	Membrane, caveola. Cytoplasm, cytoskeleton. Golgi apparatus. Cell membrane.
Protein Families	NOS family
Database References	KEGG: rno:24600 STRING: 10116.ENSRNOP00000013058 UniGene: PMID: 29471582 AM and L-NAME eliminated the CAPE-oNO2-mediated cardioprotection by restraining SIRT1 and eNOS expression, respectively. It suggested that CAPE-oNO2 ameliorated MIRI by suppressing the oxidative stress, inflammatory response, fibrosis and necrocytosis via the SIRT1/eNOS/NF-kappaB pathway PMID: 29220696 The present results indicate that Advanced glycation endproducts impairs endothelial-dependent vasodilation, and this effect is mediated via arginase overexpression and NADPH oxidase stimulation. PMID: 29627571 Activation of ACE2 had a protective role in the development of pulmonary arterial hypertension in rat model via improving the function of pulmonary arterial endothelium. This effect was potentially mediated by promoted NO release as a consequence of increased phosphorylation of eNOS at Ser1177 and dephosphorylation of eNOS at Thr495. PMID: 29146157 current studies demonstrate that PYK2 is a pivotal regulator of eNOS function in myocardial infarction and identify PYK2 as a novel therapeutic target for cardioprotection PMID: 28444132 microparticles from AMI patients decreased eNOS phosphorylation at Ser1177, increased eNOS phosphorylation at T495 and caveolin-1 expression, decreased eNOS association with Hsp90, decreased NO production but increased (O2) generation, damaged endothelial-dependent vasodilatation. PMID: 28002238 The data of the present data provide evidence that hyperhomocysteinaemia is a vascular risk factor for erectile dysfunction by impairing cavernosa endothelial nitric oxide synthase activity. PMID: 27221552 Mitochondrial dysfunction in the aging heart is accompanied by constitutive eNOS uncoupling on the background of oxidative and nitrosative stress. PMID: 29537218 Expression of eNOS protein was significantly increased in Sedimentary female when compared to Sed male rats PMID: 27562066 HIgh fat diet increases testicular eNOS expression and this was reduced by antioxidants. PMID: 29023053 Pulmonary vascular reactivity is altered in a model of murine bronchopulmonary dysplasia, the cellular mechanisms involve a decreased eNOS phosphorylation at its activating site. PMID: 28235094 these results show that coronary endothelial cells rather than cardiomyocytes play a key role in the eNOS-dependent cardioprotection of exercise. PMID: 27866931 a novel mechanism and model in which CAV1 phosphorylation facilitates CAV1 scaffolding and GRK2-CAV1 interaction, thus clustering eNOS within a complex that inhibits eNOS activity, is reported. PMID: 28162981 Intravenous delivery of rBMSCs expressing eNOS/F92A-Cav1 to PAH rats inhibits pulmonary vascular smooth muscle cell proliferation, and improves pulmonary haemodynamics, vascular remodelling and short-term survival. PMID: 27771236 Activation of endothelial NO synthase by a xanthine derivative, KMUP-1, ameliorates hypoxia-induced apoptosis in endothelial progenitor cells. PMID: 27109251 Epoetin beta pegol ameliorates flow-mediated dilation and improves endothelial nitric oxide synthase coupling state in nonobese diabetic rats. PMID: 28054454 that tempol causes hypernatremia after acute sodium overload by inhibiting the thirst mechanism and facilitating diuresis, despite increasing renal eNOS expression and natriuresis PMID: 27849390 results suggest that the AT1 receptor is involved in development of hypertension and cardiac fibrosis. Selective activating ACE2/eNOS and inhibiting CD44/HA interaction might be considered as the therapeutic targets for attenuating Ang II induced deleterious cardiovascular effects PMID: 27085217 3, 5, 7, 3', 4'-pentamethoxyflavone treatment of middle aged rats appeared to increase production of NO and H2S from the blood vessels by upregulating the expression of eNOS and cystathione-gamma-lyase.. PMID: 27468988 Antioxidant N-acetylcysteine attenuated myocardial dysfunction and myocardial I/R injury by improving Cav-3/eNOS signaling. PMID: 27733157 down-regulation of CD47 exerts a protective effect against myocardial I/R injury, which may be attributable to attenuation of oxidative stress via activation of the eNOS/nitric oxide signaling pathway. PMID: 27960187 eNOS expression at mRNA and protein levels and the number of circulating EPCs were reduced significantly in rats with monocrotaline-induced pulmonary arterial hypertension. These were reduced less in rats treated with rosuvastatin, suggesting that it ameliorates remodeling by increasing the circulating EPCs and upregulating eNOS. PMID: 27655493 hese results suggest that the protein adjustments observed in lipid raft/caveolin-1 microdomains could be visualized as a process required to protect the cells against NO overproduction and aberrant calpain activation. Alterations in eNOS, calpain-1 and HSP90 levels have been observed in aorta of Zucker Diabetic Rats (ZDR). PMID: 27956030 role in lung-protective effects of bubble continuous positive airway pressure after extubation PMID: 26800273 Combined therapy with Carthamus tinctorius L. extract and captopril in L-NAME-induced hypertensive rats normalized eNOS levels. PMID: 26938552 The enhanced expression of eNOS in L-arginine treated LVH rats resulted in the amelioration of oxidative and haemodynamic parameters. PMID: 27010893 This study demonstrated that enos increases in male rat with aneurysmal subarachnoid hemorrhage. PMID: 26923576 Exercise managed to prevent most of the disturbances in insulin signaling caused by fructose diet (except phosphorylation of IRS1 at Tyr 632 and phosphorylation and protein expression of ERK1/2) and consequently restored function of eNOS. PMID: 26644274 Combined stress decreased eNOS expression in the endothelium of microvessels and almost complete disappearance of eNOS expression in endothelial cells of the majority of capillaries. PMID: 26608376 Data suggest that mild hyperglycemia in type 2 diabetes (as seen in GK rats) preserves eNOS expression in vascular endothelium and thus enhances endothelium-dependent relaxation after acute myocardial infarction preventing myocardial reperfusion injury. PMID: 26219999 ZFP580 promotes not only the differentiation of EPCs into ECs by increasing the expression of eNOS and the availability of nitric oxide, but also the vessel formation in vitro and in vivo PMID: 26268592 These results suggest that administration of ghrelin ameliorates impaired angiogenesis in diabetic MI rats. And these beneficial effects derive from regulating GHSR1a-mediated AMPK/eNOS signal pathway PMID: 26364514 This result confirmed that Arctigenin might exert dural effects in preventing SAH-induced vasospasm through upregulating eNOS expression via the PI3K/Akt signaling pathway and attenuate endothelins after subarachnoid hemorrhage PMID: 26539501 Jujuboside B increased extracellular Ca2+ influx through endothelial transient receptor potential cation (TRPC) channels, phosphorylated eNOS and promoted NO generation in vascular endothelial cells. PMID: 26901291 PAR2 stimulation of NO production via an additional pathway that targets phosphorylation of Ser1177-eNOS suggests a regulatory mechanism for sustaining agonist-mediated vasodilation in metabolic syndrome. PMID: 26760532 Perivascular adipose tissue in Dahl SS rats buffers vasoconstriction by activating endothelial NOS via mechanisms that may include the involvement of leptin. PMID: 26608658 There was a significant reduction in eNOS expression in Metabolic Syndrome thoracic ducts suggesting that diminished NO production is partially responsible for impaired flow response. PMID: 26637560 Results suggest that eNOS-mediated endoplasmic reticulum stress may participate in status epilepticus-induced vasogenic edema formation PMID: 26115585 These findings provide direct evidence that in vivo I/R induces eNOS dysfunction secondary to BH4 depletion, and that pre-ischemic liposomal BH4 administration preserves eNOS function conferring cardioprotection with reduced oxidative stress PMID: 26116866 Results suggest that status epilepticus-induced ETB receptor/eNOS-mediated MMP-9 activation may lead to impairments of endothelial cell function via tight junctions protein degradation PMID: 26232046 Suggest that telmisartan reduced susceptibility to atrial arrhythmia to a greater extent than valsartan, ameliorated atrial remodeling, and reversed imbalances in the RAS-ERK and PI3K-Akt-eNOS pathways. PMID: 26158699 miR-22 down-regulated Cav3, leading to restored eNOS activity/NO production, which inhibited cardiac myocyte apoptosis and promoted cardiac function after myocardial ischemia and reperfusion. PMID: 26191152 Data suggest that activity of Nos3 in aorta endothelium can be regulated by dietary factors; here, activity of aorta Nos3 is up-regulated by high-fructose diet and further up-regulated by an antioxidant dietary supplement, epicatechin. PMID: 25943039 Vasculoprotective effect of insulin after arterial injury is mediated by an eNOS-dependent mechanism. PMID: 25974101 Study showed that the mRNA expression of eNOS did not increase on day 3 after the experimental spinal cord injury, with a consistent result as compared with the sham-operated and healthy control groups PMID: 25644387 Data suggest that, in polycystic ovary syndrome, heart exhibits down-regulation of both eNOS (nitric oxide synthase 3) and Na+/K+-ATPase (Na+/K+ transporting ATPase alpha 1) activities, but up-regulation of iNOS (nitric oxide synthase 2) activity. PMID: 25988879 Data show that resveratrol (Res) reversed caveolin-1 (Cav-1)/endothelial nitric oxide synthase (eNOS) expressions in high-fat/sucrose diet (HFS) rats. PMID: 25419974 Data from in vitro studies suggest that genistein and magnesium (sometimes used as dietary supplements) enhance vasodilation of vascular smooth muscle via mechanisms involving eNOS and BK(Ca) [KCa1.1 calcium-activated potassium channel]. PMID: 25494655 In response to CI-1044, activation of eNOS produces excessive levels of Nitric Oxide and vascular injury, and modulation of upstream activators of eNOS leads to regulation of eNOS activity. PMID: 24705881 Suggest a potential role for ILK, the cytoskeleton and ILK signalling partners including Rho in regulating intrahepatic sinusoidal endothelial cell eNOS expression and function. PMID: 24906011

FAQs

Please fill out the Online Inquiry form located on the product page. Key product information has been pre-populated. You may also email your questions and inquiry requests to sales1@betalifesci.com. We will do our best to get back to you within 4 business hours.

Feel free to use the Chat function to initiate a live chat. Our customer representative can provide you with a quote immediately.

Proteins are sensitive to heat, and freeze-drying can preserve the activity of the majority of proteins. It improves protein stability, extends storage time, and reduces shipping costs. However, freeze-drying can also lead to the loss of the active portion of the protein and cause aggregation and denaturation issues. Nonetheless, these adverse effects can be minimized by incorporating protective agents such as stabilizers, additives, and excipients, and by carefully controlling various lyophilization conditions.

Commonly used protectant include saccharides, polyols, polymers, surfactants, some proteins and amino acids etc. We usually add 8% (mass ratio by volume) of trehalose and mannitol as lyoprotectant. Trehalose can significantly prevent the alter of the protein secondary structure, the extension and aggregation of proteins during freeze-drying process; mannitol is also a universal applied protectant and fillers, which can reduce the aggregation of certain proteins after lyophilization.

Our protein products do not contain carrier protein or other additives (such as bovine serum albumin (BSA), human serum albumin (HSA) and sucrose, etc., and when lyophilized with the solution with the lowest salt content, they often cannot form A white grid structure, but a small amount of protein is deposited in the tube during the freeze-drying process, forming a thin or invisible transparent protein layer.

Reminder: Before opening the tube cap, we recommend that you quickly centrifuge for 20-30 seconds in a small centrifuge, so that the protein attached to the tube cap or the tube wall can be aggregated at the bottom of the tube. Our quality control procedures ensure that each tube contains the correct amount of protein, and although sometimes you can't see the protein powder, the amount of protein in the tube is still very precise.

To learn more about how to properly dissolve the lyophilized recombinant protein, please visit Lyophilization FAQs.