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Gw501516

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GW501516 is a synthetic compound that acts as a selective agonist for the peroxisome proliferator-activated receptor delta (PPARδ). It is commonly used in research applications to study the biological functions of PPARδ.

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Lab products found in correlation

Clone 29f 1a12, by BioXCell (2 mentions) Gw0742, by Cayman Chemical (2 mentions) Doxycycline, by Merck Group (2 mentions) Celltiter glo luminescent cell viability assay reagent, by Promega (2 mentions) Gw1929, by Merck Group (1 mentions) Luciferase assay reagent, by Promega (1 mentions) Gw9662, by Cayman Chemical (1 mentions) Rosiglitazone, by Cayman Chemical (1 mentions) Dna ligase, by Promega (1 mentions) Xhoi, by Promega (1 mentions) Trizol reagent, by Thermo Fisher Scientific (1 mentions) Lipofectamine 2000, by Thermo Fisher Scientific (1 mentions) M mlv reverse transcriptase, by Promega (1 mentions) Taq polymerase, by Promega (1 mentions) Cystamine dihydrochloride, by Thermo Fisher Scientific (1 mentions) Fenofibrate, by Cayman Chemical (1 mentions) Gw4064, by Cayman Chemical (1 mentions) Uvi3003, by Bio-Techne (1 mentions) Bms189453, by Merck Group (1 mentions) Bms453, by Merck Group (1 mentions)

8 protocols using gw501516

1

Tumor Induction, Engraftment, and Treatment Protocols

Cited 2 times
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For tumor induction, 3-week-old Braf/Pten mice were treated with 4-hydroxytamoxifen on the skin surface as described before to induce tumor formation49 (link). For tumor engraftment, 5 × 104 cells YUMM1.7, B16-OVA, or one million1 × 106 MC38 tumor cells were injected subcutaneously in 50 μl PBS. Tumors were measured every 2-3 days post tumor engraftment or indicated treatments and calculated. Tumor volume was calculated by volume = (length × width2)/2 for engrafted tumor or volume = (length × width × height) for inducible tumor. For in vivo treatment, Yumm1.7-bearing mice were administrated every 3 days with either DMSO or PPAR-β agonist (GW 501516) (1 mg per kg of body weight, Cayman Chemical) by intraperitoneal injection. For antibody-based treatment, tumor-bearing mice were treated with anti-PD-1 antibody (200 μg per injection, BioXcell, clone 29F.1A12) and anti-CD36 antibody (200 μg per injection, clone CRF D-2712 50 (link), provided by R. Silverstein at Medical College of Wisconsin) according to indicated combination by intraperitoneal injection. For antibody treatment in the Braf/Pten mouse model, four weeks after tumor induction, tumor-bearing Braf/Pten mice were treated with anti-CD36 antibody and/or anti-PD-1 antibody as indicated above for a period of 10 days. All experiments were conducted according to Swiss federal regulations.
Wang H., Franco F., Tsui Y.C., Xie X., Trefny M.P., Zappasodi R., Mohmood S.R., Fernández-García J., Tsai C.H., Schulze I., Picard F., Meylan E., Silverstein R., Goldberg I., Fendt S.M., Wolchok J.D., Merghoub T., Jandus C., Zippelius A, & Ho P.C. (2020). CD36-mediated metabolic adaptation supports regulatory T cell survival and function in tumors. Nature immunology, 21(3), 298-308.
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2

Macrophage Inflammasome Activation by Palmitic Acid

Cited 1 time
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Recombinant mouse Il-4 (rIl-4, 10 ng/ml, Peprotech, Rocky Hill, NJ, USA), GW501516, GW0742 (0.1 μM for both, Cayman Chemical, Ann Arbor, MI, USA), GW1929 (1 μM, Sigma, St. Louis, MO, USA), or vehicle (DMSO for Ppar agonists) were incubated with macrophages overnight in 10% FBS, DMEM. PA (Sigma) was prepared as previously described [26] (link) and added to cells at final concentrations of 300 μM in 0.45% BSA, 2% double stripped FBS, DMEM for 16 h. For PA-induced inflammasome activation, lipopolysaccharide (LPS, 10 ng/ml, Sigma) was pre-incubated with macrophages for 3 h in 10% FBS, DMEM before the addition of PA.
Dai L., Bhargava P., Stanya K.J., Alexander R.K., Liou Y.H., Jacobi D., Knudsen N.H., Hyde A., Gangl M.R., Liu S, & Lee C.H. (2017). Macrophage alternative activation confers protection against lipotoxicity-induced cell death. Molecular Metabolism, 6(10), 1186-1197.
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3

PDAC Cell Viability Assay

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PDAC cells were seeded into 96-well plates at 2 × 103 cells per well in DMEM containing 10% FBS. Cells were treated as indicated in the text with 100 nmol/L GW501516 (Cayman Chemical 10004272) at the time of cell seeding or 5 mg/mL doxycycline (Sigma-Aldrich D9891) 48 hours prior to cell seeding. GW501516 and doxycycline treatments were both replenished every 48 hours for extended time points. After 72 hours or at the time points indicated in the text, cells were lysed with the CellTiter-Glo Luminescent Cell Viability Assay reagent (Promega), and luminescence was read using a GloMax plate reader.
Abrego J., Sanford-Crane H., Oon C., Xiao X., Betts C.B., Sun D., Nagarajan S., Diaz L., Sandborg H., Bhattacharyya S., Xia Z., Coussens L.M., Tontonoz P, & Sherman M.H. (2022). A Cancer Cell–Intrinsic GOT2–PPARδ Axis Suppresses Antitumor Immunity. Cancer Discovery, 12(10), 2414-2433.
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4

Cell Viability Assay for PDAC Cells

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PDAC cells were seeded into 96-well plates at 2 x 103 cells per well in DMEM containing 10% FBS. Cells were treated as indicated in the manuscript text with 100 nM GW501516 (Cayman Chemical 10004272) at the time of cell seeding or 5mg/mL doxycycline (Sigma-Aldrich D9891) 48 hours prior to cell seeding. GW501516 and doxycycline treatments were both replenished every 48 hours for extended time points. After 72 hours or at the time points indicated in the manuscript, cells were lysed with CellTiter-Glo Luminescent Cell Viability Assay reagent (Promega) and luminescence was read using a GloMax plate reader.
Abrego J., Sanford-Crane H., Oon C., Xiao X., Betts C.B., Sun D., Nagarajan S., Diaz L., Sandborg H., Bhattacharyya S., Xia Z., Coussens L.M., Tontonoz P, & Sherman M.H. (2022). A Cancer Cell–Intrinsic GOT2–PPARδ Axis Suppresses Antitumor Immunity. Cancer Discovery, 12(10), 2414-2433.
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5

Tumor Induction, Engraftment, and Treatment Protocols

Cited 2 times
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For tumor induction, 3-week-old Braf/Pten mice were treated with 4-hydroxytamoxifen on the skin surface as described before to induce tumor formation49 (link). For tumor engraftment, 5 × 104 cells YUMM1.7, B16-OVA, or one million1 × 106 MC38 tumor cells were injected subcutaneously in 50 μl PBS. Tumors were measured every 2-3 days post tumor engraftment or indicated treatments and calculated. Tumor volume was calculated by volume = (length × width2)/2 for engrafted tumor or volume = (length × width × height) for inducible tumor. For in vivo treatment, Yumm1.7-bearing mice were administrated every 3 days with either DMSO or PPAR-β agonist (GW 501516) (1 mg per kg of body weight, Cayman Chemical) by intraperitoneal injection. For antibody-based treatment, tumor-bearing mice were treated with anti-PD-1 antibody (200 μg per injection, BioXcell, clone 29F.1A12) and anti-CD36 antibody (200 μg per injection, clone CRF D-2712 50 (link), provided by R. Silverstein at Medical College of Wisconsin) according to indicated combination by intraperitoneal injection. For antibody treatment in the Braf/Pten mouse model, four weeks after tumor induction, tumor-bearing Braf/Pten mice were treated with anti-CD36 antibody and/or anti-PD-1 antibody as indicated above for a period of 10 days. All experiments were conducted according to Swiss federal regulations.
Wang H., Franco F., Tsui Y.C., Xie X., Trefny M.P., Zappasodi R., Mohmood S.R., Fernández-García J., Tsai C.H., Schulze I., Picard F., Meylan E., Silverstein R., Goldberg I., Fendt S.M., Wolchok J.D., Merghoub T., Jandus C., Zippelius A, & Ho P.C. (2020). CD36-mediated metabolic adaptation supports regulatory T cell survival and function in tumors. Nature immunology, 21(3), 298-308.
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6

Endothelial Cell Culture Protocol

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Human umbilical vein endothelial cells (HUVECs) were cultured as previously described [20 (link)]. Bovine aortic endothelial cells (BAECs) were harvested from bovine aorta and maintained in DMEM with 10% FBS [21 ]. Rosiglitazone, GW501516, and GW9662 were obtained from Cayman Chemical. Polyclonal rabbit anti-PPARγ and rabbit IgG were from Santa Cruz Biotechnology. Luciferase assay reagent, MMLV reverse transcriptase, Taq polymerase, restriction enzymes (XhoI, NheI), and DNA ligase were from Promega Corporation. Lipofectamine 2000 and Trizol reagent were obtained from Invitrogen. The QuikChange site-directed mutagenesis kit was from Stratagene Corporation.
Huang Y., Zhao B., Liu Y, & Wang N. (2014). Peroxisome Proliferator-Activated Receptor γ Regulates the Expression of Lipid Phosphate Phosphohydrolase 1 in Human Vascular Endothelial Cells. PPAR Research, 2014, 740121.
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7

Molecular Regulation of Phagocytosis

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Transcriptional activation of RAR‐reporter constructs by tRA was found to be maximal between 0.1 and 10 μM (Allenby et al. 1993), and experiments with glial cultures showed strong effects with 0.01–1 μM (van Neerven, Regen, et al., 2010). To test the molecular regulation of phagocytosis we therefore tested 10 nM, 0.1 μM, and 0.5 μM of the pan‐RAR agonist all‐tRA (R2625; Sigma); 0.1 and 0.5 μM pan‐RXR agonist bexarotene (153559‐49‐0; LC Laboratories); 1 μM pan‐RXR antagonist UVI3003 (3303; Tocris); 1 μM RARβ agonist‐RARα/γ antagonist BMS189453 (SML1149; identical to BMS453; Sigma); 1 and 10 μM pan LXR agonist T0901317 (Cay71810‐10; Cayman); 9 and 18 μM PPARα agonist fenofibrate (Cay10005368‐1; Cayman); 50 nM and 0.1 μM PPARγ antagonist rosiglitazone (LKT‐R5773.100; LKT Laboratories); 0.2 and 0.5 μM PPARβ/δ agonist GW501516 (Cay10004272‐1; Cayman); 1 and 2 μM FXR agonist GW4064 (Cay10006611‐5; Cayman); 0.5 and 1 μM TGM2 inhibitor cystamine dihydrochloride (B22873.14; Alfa Aesar); 15, 25, 50, and 100 μM TGM2 inhibitor ERW1041E (5095220001; Merck); and 1, 5, and 25 μM blocker of scavenger receptor CD36 sulfo‐N‐succinimidyl oleate (SSO; SML2148; Merck).
Wu S., Romero‐Ramírez L, & Mey J. (2020). Retinoic acid increases phagocytosis of myelin by macrophages. Journal of Cellular Physiology, 236(5), 3929-3945.
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8

PPARδ Antagonist-Mediated Oxidative Stress

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PT-S58 (PPARδ antagonist), catalase, thapsigargin and β-actin antibodies were from Sigma-Aldrich (St Louis, MO, USA). DCFH was from Life-Tech (Carlsbad, CA, USA) while 7-aminoactinomycin D was from Biolegend (San Diego, CA, USA). GW0742 and GW501516 (PPARδ agonists) were from Cayman Chemical (Ann Arbor, MI, USA). Dexamethasone (Omega, Montreal, QC, Canada), insulin (Eli Lilly, Toronto, ON, Canada) and interferon-α2b (Schering Canada Inc., Pointe-Claire, QC, Canada) were purchased from the hospital pharmacy. AKT inhibitor IV was from Calbiochem (San Diego, CA, USA). DG172 (PPARδ antagonist) has been previously described.28 (link) NXT1511 (PPARδ antagonist) was provided by Peppi Prasit (Inception, San Diego, CA, USA).
Antibodies to PERK, PDPK1, p-AKT(T308), AKT, p-SAPK/JNK (T183/Y185), CHOP, anti-Rabbit IgG and anti-Mouse IgG were from Cell Signaling Technology (Danvers, MA, USA). The PPARδ antibody (101720) was from Cayman.
Wang X., Wang G., Shi Y., Sun L., Gorczynski R., Li Y.J., Xu Z, & Spaner D.E. (2016). PPAR-delta promotes survival of breast cancer cells in harsh metabolic conditions. Oncogenesis, 5(6), e232-.
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