Log In Sign up
The largest database of trusted experimental protocols

S nitroso n acetyl dl penicillamine snap

Manufactured by Merck Group
Visit Supplier
Sourced in United States

SNAP (S-Nitroso-N-acetyl-DL-penicillamine) is a chemical compound used as a laboratory reagent. It functions as a nitric oxide (NO) donor, providing a controlled release of NO in experimental settings.

Automatically generated - may contain errors

Lab products found in correlation

Adenosine, by Merck Group (3 mentions) Bradykinin, by Merck Group (3 mentions) Acetylcholine, by Merck Group (3 mentions) A23187, by Merck Group (3 mentions) S nitrosoglutathione gsno, by Merck Group (2 mentions) Interleukin 4 (il 4), by Thermo Fisher Scientific (2 mentions) Il 13, by Thermo Fisher Scientific (2 mentions) L name, by Merck Group (2 mentions) Nω nitro l arginine methyl ester hydrochloride, by Merck Group (2 mentions) Dmfo dl α difluoromethylornithine, by Merck Group (2 mentions) L sepiapterin, by Merck Group (2 mentions) Inos inhibitor 1400 w, by Cayman Chemical (2 mentions) Phorbol 12 myristate 13 acetate pma, by InvivoGen (2 mentions) Media 199, by Thermo Fisher Scientific (1 mentions) Collagenase type 1, by Worthington (1 mentions) 4 2 hydroxyethyl piperazine 1 ethanesulfonic acid hepes, by Merck Group (1 mentions) Streptomycin, by Thermo Fisher Scientific (1 mentions) Penicillin, by Thermo Fisher Scientific (1 mentions) High performance liquid chromatography (hplc), by Merck Group (1 mentions) Affi gel blue agarose beads, by Bio-Rad (1 mentions)

Spelling variants of this product

S-nitroso-N-acetyl-DL-penicillamine (15 citations) Penicillamine (11 citations) N-Acetyl-DL-penicillamine (3 citations)

12 protocols using s nitroso n acetyl dl penicillamine snap

1

Modulation of Nitric Oxide and Polyamine Pathways

Cited 1 time
Check if the same lab product or an alternative is used in the 5 most similar protocols
For inhibition of NO production, cells were treated with 2.5 mM L-NAME (Nω-Nitro-L-arginine methyl ester hydrochloride, Sigma-Aldrich, St. Louis, MO, USA); for induction of NO production, 2.5 μM SNAP (S-Nitroso-N-acetyl-DL-penicillamine, Sigma-Aldrich) or 2.5 μM GSNO (S-nitrosoglutathione, Sigma-Aldrich) was used. To inhibit ODC1, the rate-limiting enzyme of polyamine synthesis, DMFO (DL-α-Difluoromethylornithine, Sigma-Aldrich) was used at 5 mM. To compensate for the reduced BH4 level in cancer cells and M2-type macrophages, 20 or 100 μM L-sepiapterin (BH4 precursor, Sigma-Aldrich or Santa Cruz Biotech. (Santa Cruz, CA, USA)) was used. For iNOS inhibition, iNOS inhibitor (1400 W) was obtained from Cayman Chemical (Ann Arbor, MI, USA) and used at 50 and 100 μM for 2 days [40 (link)]. For inhibition of STAT3, 2.5 μM Stattic (Tocris Biosci., Minneapolis, MN, USA) was used. For inhibition of SMAD3, 25 μM SIS3 (Sigma-Aldrich) was used. For macrophage differentiation/polarization, 100 ng/ml phorbol 12-myristate 13-acetate (PMA, Invivogen, San Diego, CA, USA), 5 ng/ml lipopolysaccharide (LPS, Sigma-Aldrich), 20 ng/ml Interferon-γ (IFN-γ, PeproTech, Rocky Hill, NJ, USA), 20 ng/ml interleukin-4 (IL-4, PeproTech) and 20 ng/ml interleukin-13 (IL-13, Pepro-Tech) were used.
Zheng X., Fernando V., Sharma V., Walia Y., Letson J, & Furuta S. (2020). Correction of arginine metabolism with sepiapterin—the precursor of nitric oxide synthase cofactor BH4—induces immunostimulatory-shift of breast cancer. Biochemical pharmacology, 176, 113887.
+ Open protocol
+ Expand
2

Modulation of Nitric Oxide and Polyamine Pathways

Cited 1 time
Check if the same lab product or an alternative is used in the 5 most similar protocols
For inhibition of NO production, cells were treated with 2.5 mM L-NAME (Nω-Nitro-L-arginine methyl ester hydrochloride, Sigma-Aldrich, St. Louis, MO, USA); for induction of NO production, 2.5 μM SNAP (S-Nitroso-N-acetyl-DL-penicillamine, Sigma-Aldrich) or 2.5 μM GSNO (S-nitrosoglutathione, Sigma-Aldrich) was used. To inhibit ODC1, the rate-limiting enzyme of polyamine synthesis, DMFO (DL-α-Difluoromethylornithine, Sigma-Aldrich) was used at 5 mM. To compensate for the reduced BH4 level in cancer cells and M2-type macrophages, 20 or 100 μM L-sepiapterin (BH4 precursor, Sigma-Aldrich or Santa Cruz Biotech. (Santa Cruz, CA, USA)) was used. For iNOS inhibition, iNOS inhibitor (1400 W) was obtained from Cayman Chemical (Ann Arbor, MI, USA) and used at 50 and 100 μM for 2 days [40 (link)]. For inhibition of STAT3, 2.5 μM Stattic (Tocris Biosci., Minneapolis, MN, USA) was used. For inhibition of SMAD3, 25 μM SIS3 (Sigma-Aldrich) was used. For macrophage differentiation/polarization, 100 ng/ml phorbol 12-myristate 13-acetate (PMA, Invivogen, San Diego, CA, USA), 5 ng/ml lipopolysaccharide (LPS, Sigma-Aldrich), 20 ng/ml Interferon-γ (IFN-γ, PeproTech, Rocky Hill, NJ, USA), 20 ng/ml interleukin-4 (IL-4, PeproTech) and 20 ng/ml interleukin-13 (IL-13, Pepro-Tech) were used.
Zheng X., Fernando V., Sharma V., Walia Y., Letson J, & Furuta S. (2020). Correction of arginine metabolism with sepiapterin—the precursor of nitric oxide synthase cofactor BH4—induces immunostimulatory-shift of breast cancer. Biochemical pharmacology, 176, 113887.
+ Open protocol
+ Expand
3

Reagents and Materials for Cardiovascular Research

Check if the same lab product or an alternative is used in the 5 most similar protocols
Analytical grade solvents for Tyrode buffer, HPLC, and RIA analysis were purchased from Merck (Darmstadt, Germany). Adenosine 5′-triphosphate disodium salt hydrate (ATP); uridine 5′-triphosphate trisodium salt dehydrate (UTP); 2-(methylthio) adenosine 5′-diphosphate trisodium salt hydrate (2-MeSADP); 2′(3′)-O-(4-benzoylbenzoyl) adenosine 5′-triphosphate triethylammonium salt (BzATP); 3,4-dihydroxybenzylamine; (-)-norepinephrine (NA); streptozotocin (STZ): bovine serum albumin (BSA); Endothelial Cell Growth Supplement (ECGS); 4-(2-hydroxyethyl)piperazine-1-ethanesulfonic acid (HEPES); S-nitroso-N-acetyl-D,L-penicillamine (SNAP); sodium nitroprusside (SNP); saponin, were purchased from Sigma-Aldrich. NPY was obtained from Bachem. Media 199; penicillin; streptomycin plus amphotericin-B (Antibiotic-Antimycotic, 100×); fetal bovine serum (FBS), were obtained from Gibco. Collagenase type I, Worthington Biochemical Corporation.
Donoso M.V., Mascayano M.J., Poblete I.M, & Huidobro-Toro J.P. (2018). Increased ATP and ADO Overflow From Sympathetic Nerve Endings and Mesentery Endothelial Cells Plus Reduced Nitric Oxide Are Involved in Diabetic Neurovascular Dysfunction. Frontiers in Pharmacology, 9, 546.
+ Open protocol
+ Expand
4

Xenopus Craniofacial Development Assays

Check if the same lab product or an alternative is used in the 5 most similar protocols
Peptides (Thermo Scientific) were designed according to predicted sequences including 9 amino acid (AA) Xenopus Bradykinin (xBdk) (SYKGLSPFR) and 8AA Des-Arg xBdk (SYKGLSPF), and diluted to 0.1 mg/ml or 0.2mg/ml. Affi-gel blue agarose beads (50–100 mesh, Bio-Rad) loaded with peptides were prepared according to Carmona-Fontaine, Thesis, 2011 . For rescues, beads resuspended in 0.1mg/ml peptide solution were implanted in the presumptive mouth region at stage 22 and scored at stage 40. For NC assays, beads resuspended in 0.2mg/ml peptide solution were implanted in side of head or presumptive mouth at stage 20–22. Embryos were fixed at tailbud (st. 26) for in situ hybridization analysis. For peptide-rescue assays, partial LOF morphants were employed to maximize viability.
NO donor, S-Nitroso-N-acetyl-DL-penicillamine (SNAP) (Sigma) was diluted to 100 mM in a 50% DMSO solution. For early rescues, 1nl of SNAP was coinjected with 17ng of morpholino into one-cell stage embryos. For late rescues (st. 20), 2–3nl of SNAP was injected into the presumptive mouth region. The nNOS inhibitor, TRIM (Sigma- T7313), was diluted to 1M concentration in DMSO, and applied to late neurula (st. 20) embryos. Embryos were collected at tailbud (st. 26) for sox9 in situ hybridization and at swimming tadpole (st. 40) for craniofacial morphology.
Jacox L., Sindelka R., Chen J., Rothman A., Dickinson A, & Sive H. (2014). The Extreme Anterior Domain Is an Essential Craniofacial Organizer Acting through Kinin-Kallikrein Signaling. Cell reports, 8(2), 596-609.
+ Open protocol
+ Expand
5

Vasopressin-Induced Ca2+ Signaling Regulation

Check if the same lab product or an alternative is used in the 5 most similar protocols
Physiological saline of the following composition was used (mM): NaCl 120.4, KCl 5.9, MgSO4 1.2, CaCl2 2, glucose 11.5, and HEPES 11. The Ca2+-free solutions contained 2 mM EGTA. [Arg8]-Vasopressin acetate salt (AVP), Carbachol (CCh), Caffeine, Zaprinast (ZAP), 1H-[1,2,4]Oxadiazolo[4,3-a]quinoxalin-1-one (ODQ), Rp-8-pCPT-cGMPS sodium salt, 8pCPT-cGMP, S-nitroso-N-acetyl-DL-penicillamine (SNAP) were from Sigma. Fluo-4 acetoxymethyl ester was from Molecular Probes, Life Technologies, UK.
[Arg8]-Vasopressin acetate salt, Carbachol, Caffeine, Rp-8-pCPT-cGMPS sodium salt, 8pCPT-cGMP were dissolved in water; S-nitroso-N-acetyl-DL-penicillamine (SNAP), 1H-[1,2,4]Oxadiazolo[4,3-a]quinoxalin-1-one (ODQ), Zaprinast in DMSO.
Borysova L, & Burdyga T. (2015). Evidence that NO/cGMP/PKG signalling cascade mediates endothelium dependent inhibition of IP3R mediated Ca2+ oscillations in myocytes and pericytes of ureteric microvascular network in situ. Cell Calcium, 58(6), 535-540.
+ Open protocol
+ Expand
6

Cerebral Blood Flow Modulation

Cited 2 times
Check if the same lab product or an alternative is used in the 5 most similar protocols
CBF recordings were started after arterial pressure and blood gases were stable. To test functional hyperemia, the CBF response evoked by gently stroking the whiskers with a cotton-tipped applicator for 60 s was recorded. To test endothelium-dependent vasodilatation, acetylcholine (10 µM, Sigma), the Ca2+ ionophore A23187 (3 µM; Sigma) or bradykinin (50 µM; Sigma) was topically superfused for 3–5 min and the evoked CBF increases recorded. To test smooth muscle function, the CBF responses to adenosine (400 µM, Sigma) or to the NO donor S-Nitroso-N-acetyl-DL-penicillamine (SNAP; 50 µM, Sigma) were examined [25 (link), 31 (link), 37 (link)]. All pharmacological agents were dissolved in a modified Ringer’s solution [36 (link)]. The increase in CBF produced by hypercapnia was tested by introducing 5% CO2 in the ventilator to increase arterial pCO2 up to 50–60 mmHg. Once a stable increase in CBF was obtained for 3–5 min, pCO2 was returned to normocapnia.
Uekawa K., Hattori Y., Ahn S.J., Seo J., Casey N., Anfray A., Zhou P., Luo W., Anrather J., Park L, & Iadecola C. (2023). Border-associated macrophages promote cerebral amyloid angiopathy and cognitive impairment through vascular oxidative stress. Molecular Neurodegeneration, 18, 73.
+ Open protocol
+ Expand
7

Investigating ROS and RIPK1 in Hepatocytes

Check if the same lab product or an alternative is used in the 5 most similar protocols
To evaluate the effects of ROS on RIPK1-inhibited hepatocytes, the medium was replaced with serum-free Williams’ medium E, including the vehicle (0.05% DMSO), or each of the tested Nec-1 concentrations. After 1 h, H2O2 (30% v/v; Wako Pure Chemical Industries, Osaka, Japan) or the nitric oxide (NO) donor S-nitroso-N-acetyl-dl-penicillamine (SNAP; Sigma–Aldrich), which was diluted to a final concentration of 250 μM and 2 mM in serum-free Williams’ medium E, was added, and the cells were incubated for 6 h. Thereafter, cell death assays were performed.
Takemoto K., Hatano E., Iwaisako K., Takeiri M., Noma N., Ohmae S., Toriguchi K., Tanabe K., Tanaka H., Seo S., Taura K., Machida K., Takeda N., Saji S., Uemoto S, & Asagiri M. (2014). Necrostatin-1 protects against reactive oxygen species (ROS)-induced hepatotoxicity in acetaminophen-induced acute liver failure. FEBS Open Bio, 4, 777-787.
+ Open protocol
+ Expand
8

Utilization of S-Nitrosothiol Compounds in Cardiomyocyte and Single-Channel Studies

Cited 1 time
Check if the same lab product or an alternative is used in the 5 most similar protocols
S-Nitroso-N-acetyl-DL-penicillamine (SNAP; Sigma, n3398) was used as NO donor in the cardiomyocyte experiments. SNAP was solved in DMSO; the drug-free control bath solutions contained the same amount of DMSO as the experimental solutions. Another S-nitrosothiol compound the S-nitroso-l-glutathione (GSNO, Cayman Chemical, 82,240) was used in the single-channel experiments [27 (link)]. Stock solution was made by using DMSO. Since many studies have suggested important role for cell enzymes in GSNO metabolism/NO liberation (γ-glutamyltranspeptidase, superoxide dismutase, glutathione peroxidase, reviewed in [4 (link)]) for our cell-free experimental system, sodium nitroprusside dihydrate (SNP, Sigma 71,778) was used as NO donor.
Ebner J., Cagalinec M., Kubista H., Todt H., Szabo P.L., Kiss A., Podesser B.K., Cserne Szappanos H., Hool L.C., Hilber K, & Koenig X. (2019). Neuronal nitric oxide synthase regulation of calcium cycling in ventricular cardiomyocytes is independent of Cav1.2 channel modulation under basal conditions. Pflugers Archiv, 472(1), 61-74.
+ Open protocol
+ Expand
9

Cerebral Blood Flow Regulation Mechanisms

Check if the same lab product or an alternative is used in the 5 most similar protocols
CBF recordings were started after arterial pressure and blood gases were in a steady state. CBF responses to whisker stimulation were recorded while gently stroking the whiskers with a cotton-tipped applicator for 60 sec. All pharmacological agents were dissolved in a modified Ringer’s solution. To test endothelium-dependent responses, the endothelial nitric oxide (eNOS)-dependent vasodilator acetylcholine (10 μM, Sigma), the Ca2+ ionophore A23187 (3 μM; Sigma) or bradykinin (50 μM; Sigma) was topically superfused for 3–5 min and the evoked CBF increases recorded. To test smooth muscle reactivity, CBF response to adenosine (400 μM, Sigma) or the NO donor S-Nitroso-N-acetyl-DL-penicillamine (SNAP; 50 μM, Sigma) were examined24 (link), 25 (link), 42 . The increase in CBF produced by hypercapnia was tested by introducing 5% CO2 in the ventilator to increase arterial pCO2 up to 50–60 mmHg. Once a stable increase in CBF was obtained for 3–5 min, pCO2 was returned to normocapnia.
Park L., Uekawa K., Bonilla L.G., Koizumi K., Murphy M., Pistik R., Younkin L., Younkin S., Zhou P., Carlson G., Anrather J, & Iadecola C. (2017). Brain Perivascular Macrophages Initiate the Neurovascular Dysfunction of Alzheimer Aβ Peptides. Circulation research, 121(3), 258-269.
+ Open protocol
+ Expand
10

Cerebral Blood Flow Regulation Assays

Cited 2 times
Check if the same lab product or an alternative is used in the 5 most similar protocols
CBF recordings were started after arterial pressure and blood gases were stable. To test functional hyperemia, the CBF response evoked by gently stroking the whiskers with a cotton-tipped applicator for 60 sec was recorded. To test endothelium-dependent vasodilatation, acetylcholine (10 µM, Sigma), the Ca2+ ionophore A23187 (3 µM; Sigma) or bradykinin (50 µM; Sigma) was topically superfused for 3–5 min and the evoked CBF increases recorded. To test smooth muscle function, the CBF responses to adenosine (400 µM, Sigma) or to the NO donor S-Nitroso-N-acetyl-DL-penicillamine (SNAP; 50 µM, Sigma) were examined [25 (link), 30 (link), 36 (link)]. All pharmacological agents were dissolved in a modified Ringer’s solution [35 (link)]. The increase in CBF produced by hypercapnia was tested by introducing 5% CO2 in the ventilator to increase arterial pCO2 up to 50–60 mmHg. Once a stable increase in CBF was obtained for 3–5 min, pCO2 was returned to normocapnia.
Uekawa K., Hattori Y., Ahn S.J., Seo J., Casey N., Anfray A., Zhou P., Luo W., Anrather J., Park L, & Iadecola C. (2023). Border-associated macrophages promote cerebral amyloid angiopathy and cognitive impairment through vascular oxidative stress. Research Square.
+ Open protocol
+ Expand

About PubCompare

Our mission is to provide scientists with the largest repository of trustworthy protocols and intelligent analytical tools, thereby offering them extensive information to design robust protocols aimed at minimizing the risk of failures.

We believe that the most crucial aspect is to grant scientists access to a wide range of reliable sources and new useful tools that surpass human capabilities.

However, we trust in allowing scientists to determine how to construct their own protocols based on this information, as they are the experts in their field.

Ready to get started?

Sign up for free.
Registration takes 20 seconds.
Available from any computer
No download required

Sign up now

Revolutionizing how scientists
search and build protocols!