Dorsomorphin

Manufactured by Selleck Chemicals

Sourced in United States

Dorsomorphin is a small molecule compound used as a laboratory reagent. It functions as an inhibitor of bone morphogenetic protein (BMP) signaling pathways.

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Lab products found in correlation

Sb431542, by Selleck Chemicals (10 mentions) Glutamax, by Thermo Fisher Scientific (6 mentions) Heparin, by Merck Group (4 mentions) Neurobasal, by Thermo Fisher Scientific (4 mentions) Non essential amino acids (neaa), by Thermo Fisher Scientific (4 mentions) Ruxolitinib, by Selleck Chemicals (3 mentions) Sb431542, by Merck Group (3 mentions) Dmem f12, by Thermo Fisher Scientific (3 mentions) Chir99021, by Selleck Chemicals (3 mentions) Flavopiridol, by Selleck Chemicals (2 mentions) 1 azakenpaullone, by Selleck Chemicals (2 mentions) U0126, by Cell Signaling Technology (2 mentions) Actinomycin d, by Merck Group (2 mentions) Sqstm1 p62, by Cell Signaling Technology (2 mentions) Insulin, by Thermo Fisher Scientific (2 mentions) Glutamax, by Merck Group (2 mentions) Penicillin streptomycin, by Merck Group (2 mentions) Neurocult sm1 without vitamin a, by STEMCELL (2 mentions) Fibroblast growth factor 2 (fgf2), by Thermo Fisher Scientific (2 mentions) Accutase, by Thermo Fisher Scientific (2 mentions)

40 protocols using dorsomorphin

Transcriptional Inhibition Assay in Halocynthia Embryos

Cited 3 times

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Actinomycin D (50-76-0; A1410; Sigma) was diluted into DMSO at 10 mg/mL stock. The stock solution was diluted into ASW to a final concentration of 40 μg/mL. This concentration was reported to block transcription in Halocynthia embryos (Miyaoku et al, 2018 (link)). Flavopiridol (146426-40-6; S1230; Selleck chemicals) was diluted into water to 10 mM stock. The stock solution was diluted into ASW to final concentration 1 and 10 μM. The transcriptional inhibitor-treated embryos were fixed by MEM-PFA (4% PFA, 0.1 M MOPS, 0.5 M NaCl, 1 mM EGTA, 2 mM MgSO₄) after 1 h inhibitor treatment, and used for in situ hybridization.
1-Azakenpaullone (S7193; Selleckchem; Feinberg et al, 2019 (link)), Ruxolitinib (INCB018424; S1378; Selleckchem), Vismodegib (GDC-0449; S1082; Selleckchem), DAPT (208255-80-5; D5942; Millipore Sigma), SB431542 (S1067; Selleckchem; Ohta and Satou, 2013 (link)), U0126 (9903; Cell Signaling Technology; (Hudson et al, 2003 (link))) and Dorsomorphin (1219168-18-9; S7306; Selleckchem; (Ohta and Satou, 2013 (link); Feinberg et al, 2019 (link))) were used to perturb define signaling pathways as described in corresponding references. These treatments were done in a final concentration of 10 μM for 2 or 4 h. The inhibitor-treated embryos were fixed by MEM-PFA after 2 h inhibitor treatment, and used for in situ hybridization.

Ohta N, & Christiaen L. (2024). Cellular remodeling and JAK inhibition promote zygotic gene expression in the Ciona germline. EMBO Reports, 25(5), 2188-2201.

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Differentiating Human hESCs into Neurons

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Human neurons were derived by differentiating human hESCs using a small-molecule cocktail as described before, with minor adjustments [42 ]. N2B27 medium (N2B27 basal medium; 50% DMEM/F12 and 50% Neurobasal medium supplemented with 0.5 × N2 and 0.5 × B27, 1 mM GlutaMAX, and 1 × Penicillin–Streptomycin) was used throughout the differentiation protocol. Before induction, hESCs were passaged in mTeSR™ Plus and replated to form a uniform monolayer of cells. When the cells had reached around 95% confluence, medium was replaced with dual SMAD inhibition medium: N2B27 supplemented with 2 µM dorsomorphin (Selleckchem S7306) and 10 µM SB431542 (Sigma S4317). On day 10, the cells were replated in 1:2 ratio using 200 U/mL Collagenase IV (Gibco) onto Matrigel-coated dishes in N2B27 supplemented with 10 µM Y-27632 (Selleckchem S1049). From day 11 to day 20, N2B27 was supplemented with 100 ng/mL of FGF8 (PeproTech AF-100–25). On day 20, cells were detached using 0.5 mM EDTA and replated in N2B27 at 1:8 ratio. The next day following the split, N2B27 was supplemented with 20 µM DAPT (Selleckchem S2215) and the medium was replaced every 2 days.

Li S., Wang Y., van der Stoel M., Zhou X., Madhusudan S., Kanerva K., Nguyen V.D., Eskici N., Olkkonen V.M., Zhou Y., Raivio T, & Ikonen E. (2024). HiHo-AID2: boosting homozygous knock-in efficiency enables robust generation of human auxin-inducible degron cells. Genome Biology, 25, 58.

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Ferroptosis Inducers and Inhibitors Screening

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erastin (Bio-techne, 5449); SAS (MedchemExpress, HY-14655); RSL3 (Cayman, 19288); FIN56 (Cayman, 25180); FINO2 (MedchemExpress, HY-129457); PANKi (Cayman, 31002); BSO (Sigma, B2515); DEM (Sigma, D97703); etomoxir sodium salt (Selleckchem, S8244); lovastatin (Selleckchem, S2061); TOFA (Selleckchem, S6690); dorsomorphin (Selleckchem, S7306); alisertib (Selleckchem, S1133); verdinexor (Cayman, 26171); leptomycin B (Cayman, 10004976); tipifarnib (MedchemExpress, HY-10502); methotrexate (Selleckchem, S1210); pitstop2 (Sigma, SML1169); EML425 (Selleckchem, S2977); C646 (Selleckchem, S7152); brequinar (Selleckchem, S3565); elamipretide (Selleckchem, S9803)

Chen S.Y., Lin C.C., Wu J., Chen Y., Wang Y.E., Setayeshpour Y., Mestre A, & Chi J.T. (2024). NINJ1 regulates ferroptosis via xCT antiporter interaction and CoA modulation. bioRxiv.

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Fluorescent Reporter Assay Conditions

Cited 2 times

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β–estradiol (E2758, MilliporeSigma) was dissolved in H₂O and added at a final concentration of 1 μM. CuSO₄ (C1297, MilliporeSigma) was dissolved in H₂O and added at a final concentration of 0.5 mM. D-luciferin potassium salt (LUCK, GoldBio) was freshly dissolved in appropriate yeast media at a final concentration of 0.5 mM. Dorsomorphin (S7840, Selleck Chemicals; 11967, Cayman Chemical) dissolved in DMSO was added to RPE-1 cells at the final concentration of 10 μM for 24 hours (66 (link)). AICAR was dissolved in DMSO (S1802, Selleck Chemicals) and added at the final concentration of 2 mM for 48 hours in the FlucDM experiment, or dissolved directly in media at the concentration of 2 mM (10010241, Cayman Chemical) for the FUS^P525L experiment (67 (link)). MG132 (C2211, MilliporeSigma) was dissolved in DMSO and added to YEP-based medium at a final concentration of 80 μM.

Wang Y., Ruan L., Zhu J., Zhang X., Chih-Chieh Chang A., Tomaszewski A, & Li R. (2023). Metabolic regulation of misfolded protein import into mitochondria. bioRxiv.

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AMPK Inhibitor Blocks Norepinephrine

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For blocking experiments, LX2 cells were pre-incubated with Dorsomorphin (200 nM, 1 μM or 5 μM) (α-AMPK inhibitor, Selleck Chemicals, China) for 2 h prior to exposure to NE (10 μM) for another 4 h or 24 h.

Lin X.H., Liu H.H., Hsu S.J., Zhang R., Chen J., Chen J., Gao D.M., Cui J.F., Ren Z.G, & Chen R.X. (2020). Norepinephrine-stimulated HSCs secrete sFRP1 to promote HCC progression following chronic stress via augmentation of a Wnt16B/β-catenin positive feedback loop. Journal of Experimental & Clinical Cancer Research : CR, 39, 64.

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Modulation of Autophagy and AMPK in OGD/R

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The cells were treated with 3-MA (5 mM; Selleck, Houston, TX, USA) for 1 hour, which inhibits autophagy. The cells were treated for 0, 3, 12 or 24 hours with 1 × 10^–5–1 × 10^–9 M LIG. The 5′-adenosine monophosphate-activated protein kinase (AMPK) inhibitor dorsomorphin (10 μM; Selleck; treated for 30 minutes) was added to inhibit the AMPK pathway (Rao et al., 2016). In the LIG + 3-MA + OGD/R group, the cells were pretreated with 3-MA (5 mM) for 1 hour, followed by a 3-hour treatment with LIG (1 × 10^–6 M), and then subjected to OGD/R. For cells used for apoptosis detection, we added dorsomorphin to assess the role of the AMPK pathway. In the 3-MA + dorsomorphin + LIG + OGD/R group, the cells were pretreated with 3-MA (5 mM) for 1 hour, followed by LIG (1 × 10^–6 M) for 3 hours, and then dorsomorphin (10 μM) for 30 minutes. These cells were thereafter subjected to OGD/R.

Zhao D.Y., Yu D.D., Ren L, & Bi G.R. (2019). Ligustilide protects PC12 cells from oxygen-glucose deprivation/reoxygenation-induced apoptosis via the LKB1-AMPK-mTOR signaling pathway. Neural Regeneration Research, 15(3), 473-481.

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Gallbladder Epithelial Inflammatory Cell Model

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In vitro gallbladder mucosal epithelial inflammatory cell injury model was established as follows: 200 µg/mL LPS (L2630, Sigma-Aldrich, St. Louis, MO, USA) was added to the gallbladder mucosal epithelial cells in a logarithmic growth phase in each group and stimulated for 24 h (Lali et al. 2000 (link); Zhao et al. 2015 (link)). The in vitro cell experiments were divided into the following groups: Control group (primary gallbladder mucosal epithelial cells), LPS group (primary gallbladder mucosal epithelial cells treated with LPS for 24 h), LPS + oe-NC group (primary gallbladder mucosal epithelial cells stably transfected with overexpression negative control plasmid and treated with LPS for 24 h), LPS + oe-AQP3 group (primary gallbladder mucosal epithelial cells stably transfected with AQP3 overexpression plasmid and treated with LPS for 24 h), and LPS + oe-AQP3 + AMPK inhibitor group (primary gallbladder mucosal epithelial cells stably transfected with AQP3 overexpression plasmid, and treated with LPS and AMPK inhibitor for 24 h). The AMPK inhibitor was Dorsomorphin (at a concentration of 10 µM, S7840, Selleck) (Mattos et al. 2022 (link)). oe: overexpression; NC: negative control.

Wang G., Zhang H., Zhou Z., Jin W., Zhang X., Ma Z, & Wang X. (2023). AQP3-mediated activation of the AMPK/SIRT1 signaling pathway curtails gallstone formation in mice by inhibiting inflammatory injury of gallbladder mucosal epithelial cells. Molecular Medicine, 29, 116.

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Modulation of Autophagy Flux in IPC

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PC12 cells or cortical neurons were pretreated with dibromo-1,2-bis(aminophenoxy) ethane N,N,N9,N9- tetraacetic acid (BAPTA, Invitrogen B1205) 0.125 μM, 0.5 μM, 2 μM or compound C (Dorsomorphin, Selleck S7306) 5 μM 60 min before IPC. The cells continued to be incubated with these agents during the reperfusion episode after IPC. To access autophagy flux, ammonium chloride (NH₄Cl), an inhibitor of lysosome acidification, was used to inhibit lysosome degradation. PC12 cells were treated with or without NH₄Cl (Greagent G17391B) 20 mM for 12 h during the reperfusion episode after IPC.

Zhang X.Y., Zhang T.T., Song D.D., Zhou J.H., Han R., Qin Z.H, & Sheng R. (2015). Endoplasmic reticulum chaperone GRP78 is involved in autophagy activation induced by ischemic preconditioning in neural cells. Molecular Brain, 8, 20.

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Stem Cell Self-Renewal Pathway Modulation

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The cells were incubated with 10 μM FGFR inhibitor AZD4547 (Selleck, S2801), 5 μM BMP signaling pathway inhibitor Dorsomorphin (Selleck, P5499) or 10 μM JAK inhibitor Ruxolitinib (Selleck, S1378) for 3 days, then passaged once. The same number of cells (1×10⁴ cells per well) was seeded into 6-well plate. Inhibitors were added to the cells and allowed to incubate for 3 days. AP staining was performed and pictures were captured. DMSO was a negative control group. Medium was changed daily

Zhang W., Pei Y., Zhong L., Wen B., Cao S, & Han J. (2015). Pluripotent and Metabolic Features of Two Types of Porcine iPSCs Derived from Defined Mouse and Human ES Cell Culture Conditions. PLoS ONE, 10(4), e0124562.

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Investigating Autophagy-Apoptosis Interplay

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BA was supplied by MedChemExpress, USA. CCK-8 kit, dorsomorphin, AICAR, CQ, and Rapamycin (Rap) were provided by Selleck Chemicals, USA. Hoechst 33342 was procured from Sigma, USA. RiboBio Co., China, supplied ATG7 siRNA (SIGS0005319-1). NAC (N-acetyl-L-cysteine) was provided by Beyotime Biotechnology, China. Z-VAD-FMK powder was provided by Feifan Wang. The apoptosis detection kit (Cat. 556547) was purchased from BD Biosciences, USA. Antibodies against Bmi-1 (ab126783), Bcl-2 (ab182858), mTOR (ab2732), p-mTOR (Ser 2448), Bax (ab32503), AMPKα (ab32047), and LC3B (ab192890) were purchased from Abcam, UK. Anti-β-actin antibody (20536-1-AP) was supplied by Proteintech, USA. Antibodies against p-ULK1 (Ser555; Cat. 5869), cleaved poly (ADP-ribose) polymerase (PARP) (Cat. 9541), p-AMPKα (Cat. 2535), SQSTM1/p62 (Cat. 8025), and cleaved caspase 3 (Cat. 9664) were procured from Cell Signaling Technology, USA.

Zhang Y., He N., Zhou X., Wang F., Cai H., Huang S.H., Chen X., Hu Z, & Jin X. (2021). Betulinic acid induces autophagy-dependent apoptosis via Bmi-1/ROS/AMPK-mTOR-ULK1 axis in human bladder cancer cells. Aging (Albany NY), 13(17), 21251-21267.

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