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Vps34 inhibitor 1

Manufactured by Cayman Chemical
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VPS34 Inhibitor 1 is a selective and potent inhibitor of the phosphatidylinositol 3-kinase VPS34. It inhibits VPS34 activity in a concentration-dependent manner.

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Lab products found in correlation

Pi 3 p dic8, by Echelon Biosciences (2 mentions) 3 methyladenine 3 ma, by InvivoGen (2 mentions) Vps34 in1, by Cayman Chemical (2 mentions) 60mer dsdna, by DNA-Technology (2 mentions) Brefeldin a bfa, by Merck Group (2 mentions) 2 3 cgamp, by Biolog (2 mentions) Bafilomycin a1, by InvivoGen (2 mentions)

2 protocols using vps34 inhibitor 1

1

Diverse Cell Lines and Viral Models for STING Pathway Research

Cited 1 time
Check if the same lab product or an alternative is used in the 5 most similar protocols
The cell lines used for the study were iBMDC-MycSTING, THP-1, Vero cells, HEK-293T cells, HaCaT, HeLa cells, and Human foreskin fibroblasts (HFF). The choice of cell models depended on the experiments; e.g. THP-1 cells express high levels of cytokines and were used to evaluate gene expression, while HeLa cells have a large cytoplasm and were often the cell line of choice for immunofluorescence. SAVI patient-derived fibroblasts cells were obtained as described previously14 (link). Human blood-derived monocytes were isolated from normal healthy blood donor buffy coats obtained from Aarhus University Hospital Blood Bank. Human primary fibroblasts were obtained from healthy donors from Department of Dermatology and Venereology, Aarhus University Hospital. The viruses used were HSV-1 (Strain F+, and McKrae), HSV-2 (strain 333), Sendai virus (strain Cantrell). The reagents used were 2’3’-cGAMP (BIOLOG), 60mer dsDNA (DNA technology), PI(3)P diC8 (Echelon), phorbol 12-myristate 13-acetate (PMA, Sigma), Brefeldin A (BFA, Sigma), Bafilomycin A1(BafA1, InvivoGen), 3-Methyladenine (3-MA, InvivoGen), VPS34 Inhibitor 1 (VPS34 IN1, Cayman).
Zhang B.C., Nandakumar R., Reinert L.S., Huang J., Laustsen A., Gao Z.L., Sun C.L., Jensen S.B., Troldborg A., Assil S., Berthelsen M.F., Scavenius C., Zhang Y., Windross S.J., Olagnier D., Prabakaran T., Bodda C., Narita R., Cai Y., Zhang C.G., Stenmark H., Doucet C.M., Noda T., Guo Z., Goldbach-Mansky R., Hartmann R., Chen Z.J., Enghild J.J., Bak R.O., Thomsen M.K, & Paludan S.R. (2020). STEEP mediates STING ER exit and activation of signaling. Nature immunology, 21(8), 868-879.
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2

Diverse Cell Lines and Viral Models for STING Pathway Research

Cited 1 time
Check if the same lab product or an alternative is used in the 5 most similar protocols
The cell lines used for the study were iBMDC-MycSTING, THP-1, Vero cells, HEK-293T cells, HaCaT, HeLa cells, and Human foreskin fibroblasts (HFF). The choice of cell models depended on the experiments; e.g. THP-1 cells express high levels of cytokines and were used to evaluate gene expression, while HeLa cells have a large cytoplasm and were often the cell line of choice for immunofluorescence. SAVI patient-derived fibroblasts cells were obtained as described previously14 (link). Human blood-derived monocytes were isolated from normal healthy blood donor buffy coats obtained from Aarhus University Hospital Blood Bank. Human primary fibroblasts were obtained from healthy donors from Department of Dermatology and Venereology, Aarhus University Hospital. The viruses used were HSV-1 (Strain F+, and McKrae), HSV-2 (strain 333), Sendai virus (strain Cantrell). The reagents used were 2’3’-cGAMP (BIOLOG), 60mer dsDNA (DNA technology), PI(3)P diC8 (Echelon), phorbol 12-myristate 13-acetate (PMA, Sigma), Brefeldin A (BFA, Sigma), Bafilomycin A1(BafA1, InvivoGen), 3-Methyladenine (3-MA, InvivoGen), VPS34 Inhibitor 1 (VPS34 IN1, Cayman).
Zhang B.C., Nandakumar R., Reinert L.S., Huang J., Laustsen A., Gao Z.L., Sun C.L., Jensen S.B., Troldborg A., Assil S., Berthelsen M.F., Scavenius C., Zhang Y., Windross S.J., Olagnier D., Prabakaran T., Bodda C., Narita R., Cai Y., Zhang C.G., Stenmark H., Doucet C.M., Noda T., Guo Z., Goldbach-Mansky R., Hartmann R., Chen Z.J., Enghild J.J., Bak R.O., Thomsen M.K, & Paludan S.R. (2020). STEEP mediates STING ER exit and activation of signaling. Nature immunology, 21(8), 868-879.
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