This screen identified IWS1, POLE3, POLR1.ĭAPK1 loss triggers tumor invasion in colorectal tumor cells. To investigate host factors which promote HIV-1 latency, we conducted a genome-wide functional knockout screen using CRISPR-Cas9 in a HIV-1 latency cell line model. Rathore A, Iketani S, Wang P, Jia M, Sahi V, Ho DD The major barrier to a HIV-1 cure is the persistence of latent genomes despite treatment with antiretrovirals. Although filamentous actin (F-actin) increases MICAL1 monooxygenase activity, hydrogen peroxide (HO) is also generated in the absence of F-actin, suggesting that diffusi.ĬRISPR-based gene knockout screens reveal deubiquitinases involved in HIV-1 latency in two Jurkat cell models. The Molecule Interacting with CasL 1 (MICAL1) monooxygenase has emerged as an important regulator of cytoskeleton organization via actin oxidation. MICAL1 regulates actin cytoskeleton organization, directional cellmigration and the growth of human breast cancer cells as orthotopicxenograft tumours. Using our products in your publication? Let us know!

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