Gts 21

Manufactured by Merck Group

Sourced in United States

The GTS-21 is a laboratory equipment product manufactured by Merck Group. It is designed for general laboratory use. The core function of the GTS-21 is to perform specific laboratory tasks, though detailed specifications are not available.

Automatically generated - may contain errors

Lab products found in correlation

Lipopolysaccharides (lps), by Merck Group (2 mentions) Exendin 4 ex4, by Bachem (1 mentions) Pyrrolidine dithiocarbamate, by Merck Group (1 mentions) Methyllycaconitine citrate, by Merck Group (1 mentions) Iodogen, by Thermo Fisher Scientific (1 mentions) Gts 21, by Abcam (1 mentions) Clone cd28, by BD (1 mentions) α bungarotoxin α bgt, by Merck Group (1 mentions) Clone hit3a, by BD (1 mentions) Nicotine hydrogen bitartrate, by Merck Group (1 mentions) Dihydro β erythroidine hydrobromide dhβe, by Bio-Techne (1 mentions) Anti cd4, by BioXCell (1 mentions) L2630, by Merck Group (1 mentions)

8 protocols using gts 21

GTS-21 Dose-Response Effects on Diet-Induced Obesity

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Rats had access to either chow (n=14; 346.0 ±16.5g at start of testing) or 60% HFD (n=15; 513.4 ±39.6g at start of testing) and were given an IP injection of GTS-21 (Sigma-Aldrich) at either a high (10 mg/kg), medium (5 mg/kg), or low (2.5 mg/kg) dose, the GLP-1 receptor agonist, exendin-4 (Ex4; Bachem; 3 μg/kg) as a positive control [27 (link)], or vehicle only (1 ml/kg sterile 0.9% NaCl). GTS-21 doses were selected based on previous work in mice [17 (link)]. Food intake and body weight were measured as described above. Two rats were excluded as statistical outliers (defined below) resulting in a final n=12 for the chow diet condition. For the HFD experiment, four rats were excluded as statistical outliers resulting in a final n=11.

DiBrog A.M., Kern K.A., Mukherjee A., Przybysz J.T, & Mietlicki-Baase E.G. (2022). The alpha-7 nicotinic acetylcholine receptor agonist GTS-21 does not affect food intake in rats. Pharmacology, biochemistry, and behavior, 219, 173444.

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Effects of Intracerebral GTS-21 on Feeding

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Rats were maintained on rodent chow (n=11; 443.8 ± 24.1g at start of testing) and given an ICV injection of GTS-21 (Sigma-Aldrich) at either a high (0.5mg), medium (0.25mg), low dose (0.1mg), or Veh (2μL aCSF). As ICV GTS-21 has not been well-studied in the literature for effects on food intake, doses were chosen based on outcomes of our systemic GTS-21 feeding studies. Chow intake and body weight were measured as detailed above. Two rats were excluded as statistical outliers resulting in a final n=9 for this experiment.

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Quantification of Cellular Signaling Pathways

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α-Bungarotoxin (αBGT) was obtained from Biotoxins Inc., St Cloud, FL, and radioiodinated using iodogen (Pierce Chemical, Rockford, IL) as previously described [32 (link)]. Rat TNF (catalog# CYT-393) was purchased from ProSpecbio, East Brunswick, NJ. GTS-21 (# SML0326), Pyrrolidine dithiocarbamate (PDTC, # P8765), methyllycaconitine citrate (MLA, # M168), and LPS (# L6529) were purchased from Sigma Aldrich, St. Louis, MO. Rabbit polyclonal anti-GAPDH (# PA1-988) and monoclonal anti-phospho-IκBα pSer32 (#PIMA515087) were obtained from Thermo-Fisher Scientific, Waltham, MA. Alexa Fluor 488 anti-mouse/human CD11b #101219 and Alexa Fluor 647 anti-mouse F4/80 Antibody #123121 were purchased from BioLegend, San Diego, CA. Secondary HRP-conjugated anti-rabbit (# 7074) antibody was purchased from Cell Signaling Technology and used at 1:1000 dilution.

Garg B.K, & Loring R.H. (2019). GTS-21 has cell-specific anti-inflammatory effects independent of α7 nicotinic acetylcholine receptors. PLoS ONE, 14(4), e0214942.

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Modulation of T-cell activation by GTS-21

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Cells were suspended in RPMI-1640 medium supplemented with 10% fetal calf serum (FCS), 100 U/ml penicillin and 100 g/ml streptomycin at 37°C in a 5% CO₂ atmosphere. The PBMCs (1×10⁶ cells/ml) were cultured for 72 h in 24-well plates and subsequently stimulated with anti-CD3 (3 μg/ml, clone HIT3a; BD Biosciences, Franklin Lakes, NJ, USA) and anti-CD28 (3 μg/ml, clone CD28.2; BD Biosciences) antibodies in the presence or absence of different concentrations (0.01, 0.1 or 1 μmol/l) of GTS-21 (Abcam, Cambridge, MA, USA). Purified CD4⁺ T cells (1×10⁶ cells/ml) were stimulated using anti-CD3-coated 96-well plates (BioCoat™ anti-human CD3 T-cell activation plates; BD Biosciences) plus anti-CD28 antibodies (3 μg/ml), in the presence of IL-12 (15 ng/ml, Peprotech, Inc., Rocky Hill, NJ, USA) and anti-IL-4 antibodies (4 μg/ml, Peprotech, Inc.) for Th1 differentiation for 72 h with GTS-21 (1 μmol/l) alone or combined with α-bungarotoxin (αBgt, 1 μmol/l; Sigma, St. Louis, MO, USA).

WU S., ZHAO H., LUO H., XIAO X., ZHANG H., LI T, & ZUO X. (2014). GTS-21, an α7-nicotinic acetylcholine receptor agonist, modulates Th1 differentiation in CD4+ T cells from patients with rheumatoid arthritis. Experimental and Therapeutic Medicine, 8(2), 557-562.

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Nicotine and Nicotinic Receptor Ligands

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Nicotine hydrogen bitartrate (Sigma-Aldrich, St. Louis, MO, USA) and dissolved in 0.9% normal saline (vehicle). pH was adjusted to 7.0 ± 0.5 with 1M sodium hydroxide (J.T. Baker, Center Valley, PA, USA), and solutions were prepared fresh daily and kept in the dark with aluminum foil. Nicotine doses are expressed as free-base [17 (link)] and were injected intraperitoneally (i.p.) 10 minutes prior to testing. Dihydro-β-erythroidine (DHβE) hydrobromide (Tocris, Ellisville, MO, USA) and methyllycaconitine (MLA) citrate salt (Sigma-Aldrich) were dissolved in 0.9% normal saline vehicle, and for pretreatment experiments were injected i.p. 15 minutes prior to nicotine or vehicle i.p. injection, with behavioral testing commencing 10 minutes after last injection. DHβE and MLA doses are expressed as their salts. GTS-21 (Sigma-Aldrich) was dissolved in 0.9% normal saline vehicle and injected i.p. 10 minutes prior to resident-intruder testing. Volumes for i.p. injections were 10 mL/kg for B6 and BALB/c mice, and 5 mL/kg for CD1 mice due to increased body mass.

Lewis A.S., Mineur Y.S., Smith P.H., Cahuzac E.L, & Picciotto M.R. (2015). Modulation of aggressive behavior in mice by nicotinic receptor subtypes. Biochemical pharmacology, 97(4), 488-497.

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Treating Wasting Phenotype in Animals

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Animals were dosed with intraperitoneal injections of the indicated treatments at P10 and P12 except as noted and monitored daily for improvement of the wasting phenotype. Anti-TNF (100 μg/animal) was from Thermo Fisher Scientific (Carlsbad, CA). Anti-CD4 (100 μg/animal) was from Bio X Cell (West Lebanon, NH). TNFR Fc (75 μg/animal) was produced as previously described (15 (link)). Clodronate liposome solution (50 μl/animal) was from Encapsula Nanosciences (Brentwood, TN). Dexamethasone was injected daily from P9 (100 μg/animal) was a gift from Jesus Rivera-Nieves. GTS-21 (40 μg/animal) was from Sigma-Aldrich (Saint Louis, MO).

Veny M., Grases D., Kucharova K., Lin W.W., Nguyen J., Huang S., Ware C.F., Ranscht B, & Šedý J.R. (2020). Contactin-1 Is Required for Peripheral Innervation and Immune Homeostasis Within the Intestinal Mucosa. Frontiers in Immunology, 11, 1268.

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Septic AKI Mouse Model via LPS

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Septic AKI mouse models were created through intraperitoneal injection of lipopolysaccharides (LPS) from Escherichia coli O111:B4 and purified using phenol extraction (Sigma-Aldrich, Cat#L2630, LPS; 5 mg kg⁻¹). As in our previous study, GTS-21 (20 mg kg⁻¹, Sigma-Aldrich, Cat#SML0326) was injected intraperitoneally 15 min before LPS administration. The vehicle control received an equal volume of normal saline. Four hours after the LPS injection, the mice were euthanized.

Nakamura Y., Matsumoto H., Wu C.H., Fukaya D., Uni R., Hirakawa Y., Katagiri M., Yamada S., Ko T., Nomura S., Wada Y., Komuro I., Nangaku M., Inagi R, & Inoue T. (2023). Alpha 7 nicotinic acetylcholine receptors signaling boosts cell-cell interactions in macrophages effecting anti-inflammatory and organ protection. Communications Biology, 6, 666.

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Astrocyte Cytokine Modulation Assay

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Astrocytes were plated in 24 well plates at the density of 100,000 cells/well in DMEM with 20% FBS medium for 24 h. Cells were serum starved before adding compounds. Cells were then stimulated with or without 60 ng/ml LPS (Sigma, L6529) in the presence or absence of different doses of GTS21 (Sigma) to measure cytokine levels.

Patel H., McIntire J., Ryan S., Dunah A, & Loring R. (2017). Anti-inflammatory effects of astroglial α7 nicotinic acetylcholine receptors are mediated by inhibition of the NF-κB pathway and activation of the Nrf2 pathway. Journal of Neuroinflammation, 14, 192.

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