Sb505124

Manufactured by Selleck Chemicals

Sourced in United States

SB505124 is a synthetic chemical compound. It functions as a selective inhibitor of the protein kinase Transforming Growth Factor-Beta Type I Receptor (TGF-beta RI). This compound is commonly used in research applications involving the study of the TGF-beta signaling pathway.

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Lab products found in correlation

Jsh 23, by Selleck Chemicals (2 mentions) Smad2 3, by Cell Signaling Technology (2 mentions) Odanacatib, by Selleck Chemicals (1 mentions) Mk 2206 2hci, by Selleck Chemicals (1 mentions) Recombinant cxcl1, by Thermo Fisher Scientific (1 mentions) Sb225002, by Selleck Chemicals (1 mentions) Recombinant tgf β1, by R&D Systems (1 mentions) Tnf α, by Thermo Fisher Scientific (1 mentions) Activin a, by Selleck Chemicals (1 mentions) Dapi d523, by Dojindo Laboratories (1 mentions) M csf, by Thermo Fisher Scientific (1 mentions) Rankl, by Thermo Fisher Scientific (1 mentions) M csf, by R&D Systems (1 mentions) Pfoxo1 3a, by Cell Signaling Technology (1 mentions) Sc 373910, by Santa Cruz Biotechnology (1 mentions) P smad2 3, by Cell Signaling Technology (1 mentions) Snail, by Cell Signaling Technology (1 mentions) Foxo3a, by Cell Signaling Technology (1 mentions) P foxo3a, by Cell Signaling Technology (1 mentions) N cadherin, by Cell Signaling Technology (1 mentions)

12 protocols using sb505124

Inhibiting TGF-β and Ctsk in Embryonic Development

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TGF-β signaling was inhibited in live embryos by introducing the indicated concentration of SB505124 (Selleckchem, solubilized in DMSO) directly into their growth media at 52 hpf. For inhibition of Ctsk, embryos were also treated with the indicated concentration of Odanacatib (Selleckchem, solubilized in DMSO) at 52 hpf. Embryos were treated for 1–2 days. In all cases, WT control embryos were treated with an equivalent amount of DMSO (0.1%). For all treatment experiments, embryos were staged and synchronized by age within the first hours after fertilization and again before 24 hpf.

Lu P.N., Moreland T., Christian C.J., Lund T.C., Steet R.A, & Flanagan-Steet H. (2020). Inappropriate cathepsin K secretion promotes its enzymatic activation driving heart and valve malformation. JCI Insight, 5(20), e133019.

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Modulating TGFβ and NF-κB Signaling in Cancer Cells

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For the treatment of KYSE30 and KYSE450 cells, recombinant TGFβ1 (R&D, Minneapolis, MN, USA) was used at a final concentration of 10 ng·mL⁻¹ unless otherwise specified. TNFα (PeproTech, Suzhou, China) was used at a final concentration of 10 ng·mL⁻¹. Treatment periods were 24 h unless otherwise specified. We used 10 μm SB505124 and 10 μm JSH‐23 (Selleck, Houston, TX, USA) to inhibit TGFβ signaling and NF‐κB signaling, respectively. These inhibitors were administered to the cells 30 min before any other treatments. In addition, 5 µm MK‐2206 2HCI (Selleck) was used to inhibit Akt phosphorylation selectively for 24 h. CAF were treated with 10 ng·mL⁻¹ recombinant CXCL1 (PeproTech) for 24 h. SB225002 (Selleck) was added 1 h prior to inhibiting CXCL1/CXCR2.

Fang L., Che Y., Zhang C., Huang J., Lei Y., Lu Z., Sun N, & He J. (2021). LAMC1 upregulation via TGFβ induces inflammatory cancer‐associated fibroblasts in esophageal squamous cell carcinoma via NF‐κB–CXCL1–STAT3. Molecular Oncology, 15(11), 3125-3146.

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Osteoclast Differentiation from Mouse Bone Marrow

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Bone marrow cells derived from WT mice or CX₃CR1-EGFP/TRAP-tdTomato mice were cultured with 10 ng/mL M-CSF (R&D Systems) in α-MEM containing 10% fetal calf serum for 3 days. Then bone marrow macrophages were cultured for 3 days in the presence of 50 ng/mL RANKL (PeproTech) and 10 ng/mL M-CSF to induce differentiation into osteoclasts^{58 (link)}. Human/mouse recombinant activin A (R&D Systems), mouse recombinant SFRP2 (R&D Systems), and mouse recombinant IGF2 (R&D Systems) were added at the concentrations indicated in Figure legends. Nuclei were stained with DAPI (D523; Dojindo Molecular Technologies, Kumamoto, Japan). To evaluate the inhibition of activin A-mediated osteoclast differentiation, the ALK4 inhibitor SB505124 (#S2186; Selleck Chemicals, Houston, TX, USA) was added at a concentration of 10 μM; 0.005% DMSO was used as vehicle control.

Shimizu K., Kikuta J., Ohta Y., Uchida Y., Miyamoto Y., Morimoto A., Yari S., Sato T., Kamakura T., Oshima K., Imai R., Liu Y.C., Okuzaki D., Hara T., Motooka D., Emoto N., Inohara H, & Ishii M. (2023). Single-cell transcriptomics of human cholesteatoma identifies an activin A-producing osteoclastogenic fibroblast subset inducing bone destruction. Nature Communications, 14, 4417.

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Akt1 Knockdown Effects on EMT Markers

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Human PC3 and DU145 cell lines were purchased from ATCC (Manassas, VA), cultured in DMEM high glucose medium (Hyclone, Logan, UT) with 10% Fetal bovine serum (FBS, Atlanta Biologicals, Atlanta, GA), 100 U/ml penicillin, and 100 mg/ml streptomycin in a humidified incubator at 37°C and 5% CO2. Cells were routinely passaged and when they were 80–90% confluent, transfection was carried out using SMARTvector 2.0 Lentivirus ShControl (non-targeting) and ShAkt1 (ACGCTTAACCTTTCCGCTG) from Dharmacon (Lafayette, CO), followed by selection with puromycin (0.6 ng/ml, Sigma Millipore, St. Louis, MO). Primary antibodies against Akt1 (Cat #2938), p^Ser473Akt (Cat #4060), p^Thr308Akt (Cat #2965), pFoxO1/3a (Cat #9464), p FoxO3a (Cat #9465), FoxO3a (Cat #2497), FoxO1 (Cat #2880), p Smad2/3 (Cat #8828), Smad2/3 (Cat #8685), Snail (Cat #3879), E-cadherin (Cat #3195), and N-cadherin (Cat #4061) were purchased from Cell Signaling (Danvers, MA). Nodal antibodies (Cat # SC-28913 and SC-373910) were purchased from Santa Cruz Biotechnology (Santa Cruz, CA). β-actin antibody (Cat #A5441) was purchased from Sigma (St. Louis, MO). Triciribine (TCBN) and SB505124 were purchased from Selleckchem (Houston, TX), and FoxO1/3a inhibitor (AS1842856) was purchased from Calbiochem (San Diego, CA). All other reagents were purchased from Fisher Scientific (Hanover Park, IL).

Alwhaibi A., Verma A., Artham S., Adil M.S, & Somanath P.R. (2019). Nodal pathway activation due to Akt1 suppression is a molecular switch for prostate cancer cell epithelial-to-mesenchymal transition and metastasis. Biochemical pharmacology, 168, 1-13.

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Melanoma cell lines and fibroblasts

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The 1205Lu, WM9, WM793, WM164, WM983A and 451Lu melanoma cells lines and FF2504, FF2507 and FF2447 human primary skin fibroblasts were a gift from Dr. Meenhard Herlyn (The Wistar Institute, Philadelphia, PA). WM9-GFP was from Dr. Peter Forsyth (Moffitt Cancer Center, Tampa, FL). The identities of all cell lines were confirmed by Biosynthesis Inc (Lewisville, Tx) through STR validation analysis. Cell lines were maintained in 5% FBS/RPMI-1640. Conditioned media was prepared by adding fresh media to 1205Lu cells for 48 hrs in the presence of vehicle or 3 μM vemurafenib. Then the media was collected and diluted 1:1 with fresh media, matching the concentrations of drugs/vehicle. SB505124 was obtained from Selleck Chemicals (Houston, TX).

Fedorenko I.V., Wargo J.A., Flaherty K.T., Messina J.L, & Smalley K.S. (2015). BRAF inhibition generates a host/tumor niche that mediates therapeutic escape. The Journal of investigative dermatology, 135(12), 3115-3124.

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ESCC Cell Line Characterization and Manipulation

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A total of seven cell lines, including six ESCC cell lines (KYSE30, KYSE70, KYSE150, KYSE180, KYSE450, and KYSE510) and the immortalized normal human esophageal epithelial cell line Het-1a, were used in this study. The cell lines were cultured as described previously [17 (link)]. We confirmed cell line identities by matching the short-tandem repeat (STR) profile of each line to the registered information in the DSMZ online STR database. TNF-α and IL-1β were purchased from Peprotech (USA) and used at a concentration of 10 ng/ml, and TGF-β1 was purchased from R&D (USA) and used at a concentration of 5 ng/ml. The treatment time was 24 h unless otherwise specified. To inhibit TGF-β and NF-κB signaling, we added 10 μM JSH-23 (Selleck, USA) or 5 μM SB505124 (Selleck, USA) to the cell culture media 30 min prior to the specified treatments.
Full-length NKILA cDNA was compounded by Generay (Shanghai, China) and ligated into a pCDH-CMV-MCS-EF1-GFP + Puro (CD513B-1) vector. Non-targeting control shRNA and two shRNAs against NKILA (sh1 and sh2, respectively) were obtained from OBiO (Shanghai, China). The transfection and lentivirus packaging were performed as described previously [17 (link)].

Lu Z., Chen Z., Li Y., Wang J., Zhang Z., Che Y., Huang J., Sun S., Mao S., Lei Y., Gao Y, & He J. (2018). TGF-β-induced NKILA inhibits ESCC cell migration and invasion through NF-κB/MMP14 signaling. Journal of Molecular Medicine (Berlin, Germany), 96(3), 301-313.

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Immunoblotting and Flow Cytometry Protocol

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FAM83D antibody (Santa Cruz Biotechnology, CA, USA), Goat anti-Mouse HRP (ABCAM, Cambridge, MA, USA), β-actin antibody, CD44 antibody, Smad2/3 antibody, Smad2/3-P antibody, YAP/TAZ antibody, YAP-P antibody, ERK1/2 antibody and ERK1/2-P antibody, Goat anti-Rabbit HRP (Cell Signaling Technology, Beverly, MA, USA). Anti-CD44-PE, Anti-CD44-FITC (BD Pharmingen, NJ, USA). SCH772984, SB505124 and Verteporfin (Selleck Chemicals, TX, USA).

Lin B., Chen T., Zhang Q., Lu X., Zheng Z., Ding J., Liu J., Yang Z., Geng L., Wu L., Zhou L, & Zheng S. (2016). FAM83D associates with high tumor recurrence after liver transplantation involving expansion of CD44+ carcinoma stem cells. Oncotarget, 7(47), 77495-77507.

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Inhibitors of TGF-β and Tak1 Signaling

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Dorsomorphin (compound C) was purchased from Sigma Aldrich (St. Louis, MO) and DMH1, and LDN-193189 (LDN) were purchased from Selleckchem (Houston, TX.) DMH2 was synthesized at Rutgers- New Jersey Medical School (Dave Augeri). TGFβ inhibitors LY2109761 and SB-505124 were purchased from Selleckchem and Sigma Aldrich (St. Louis, MO) respectively. The Tak1 inhibitor 5Z-7-oxozeaenol was purchased from Sigma Aldrich.

Augeri D.J., Langenfeld E., Castle M., Gilleran J.A, & Langenfeld J. (2016). Inhibition of BMP and of TGFβ receptors downregulates expression of XIAP and TAK1 leading to lung cancer cell death. Molecular Cancer, 15, 27.

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Melanoma cell lines and fibroblasts

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Pharmacological Compounds Evaluation

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LY294002, KU-0063794, AZD3463, SB505124, axitinib, tocilizumab and Bay 11-7085 were purchased from Selleck Chemicals (USA). Crenolanib (CP-868596) was purchased from MedChemExpress. AS101 was purchased from Cayman Chemical (USA). Stock solutions of compounds were prepared in DMSO and stored at −20°C or diluted in media for experiments.

Xin Y., Min P., Xu H., Zhang Z., Zhang Y, & Zhang Y. (2020). CD26 upregulates proliferation and invasion in keloid fibroblasts through an IGF-1-induced PI3K/AKT/mTOR pathway. Burns & Trauma, 8, tkaa025.

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