fgfr inhibitor infigratinib Search Results


fgfr inhibitor infigratinib  (LC Laboratories)
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LC Laboratories fgfr inhibitor infigratinib
a-b) Enrichment of knockouts whose distribution is significantly altered across pseudospace, and therefore EMT progression, in our spontaneous (11,908 cells) (a) and TGF-ß-driven (9,951 cells) (b) conditions. The distribution of cells expressing sgRNAs against EMT genes was compared to the distribution of NTC controls using Chi square (empirically determined FDR < 10%). For targets whose distribution is altered enrichment across each region was determined by calculating the odds ratio. c) Percent E-cadherin (top panels) or vimentin (bottom panels) positive cells in MCF10A colonies exposed to MEK (U0126) and PI3K (LY294002) inhibition after spontaneous (left panels) or TGF-ß-driven (right panels) EMT. Error bars denote standard deviation from the mean (n = 3, two-tailed Student’s t test). d) Percent E-cadherin (top panels) or vimentin (bottom panels) positive cells in MCF10A colonies exposed to EGFR (Erlotinib), MET (Crizotinib), <t>FGFR</t> <t>(Infigratinib)</t> and ITGAV (Cilengitide) inhibition after spontaneous (left panels) or TGF-ß-driven (right panels) EMT. Error bars denote standard deviation from the mean (at left: spontaneous EMT control/EGFRi/ITGAVi n = 7, METi/FGFRi n = 4 independent samples; at right: TGF-ß-driven EMT control n = 4, EGFRi/METi/FGFRi/ITGAVi n = 3 independent samples, two-tailed Student’s t test). e) Inferred EMT regulatory network and putative regulators identified in this study. f) Model depicting the MEK dependent EMT regulatory checkpoint created and its effects on the development of intermediate EMT phenotypes.
Fgfr Inhibitor Infigratinib, supplied by LC Laboratories, used in various techniques. Bioz Stars score: 90/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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a-b) Enrichment of knockouts whose distribution is significantly altered across pseudospace, and therefore EMT progression, in our spontaneous (11,908 cells) (a) and TGF-ß-driven (9,951 cells) (b) conditions. The distribution of cells expressing sgRNAs against EMT genes was compared to the distribution of NTC controls using Chi square (empirically determined FDR < 10%). For targets whose distribution is altered enrichment across each region was determined by calculating the odds ratio. c) Percent E-cadherin (top panels) or vimentin (bottom panels) positive cells in MCF10A colonies exposed to MEK (U0126) and PI3K (LY294002) inhibition after spontaneous (left panels) or TGF-ß-driven (right panels) EMT. Error bars denote standard deviation from the mean (n = 3, two-tailed Student’s t test). d) Percent E-cadherin (top panels) or vimentin (bottom panels) positive cells in MCF10A colonies exposed to EGFR (Erlotinib), MET (Crizotinib), FGFR (Infigratinib) and ITGAV (Cilengitide) inhibition after spontaneous (left panels) or TGF-ß-driven (right panels) EMT. Error bars denote standard deviation from the mean (at left: spontaneous EMT control/EGFRi/ITGAVi n = 7, METi/FGFRi n = 4 independent samples; at right: TGF-ß-driven EMT control n = 4, EGFRi/METi/FGFRi/ITGAVi n = 3 independent samples, two-tailed Student’s t test). e) Inferred EMT regulatory network and putative regulators identified in this study. f) Model depicting the MEK dependent EMT regulatory checkpoint created and its effects on the development of intermediate EMT phenotypes.

Journal: Nature genetics

Article Title: A pooled single-cell genetic screen identifies regulatory checkpoints in the continuum of the epithelial-to-mesenchymal transition

doi: 10.1038/s41588-019-0489-5

Figure Lengend Snippet: a-b) Enrichment of knockouts whose distribution is significantly altered across pseudospace, and therefore EMT progression, in our spontaneous (11,908 cells) (a) and TGF-ß-driven (9,951 cells) (b) conditions. The distribution of cells expressing sgRNAs against EMT genes was compared to the distribution of NTC controls using Chi square (empirically determined FDR < 10%). For targets whose distribution is altered enrichment across each region was determined by calculating the odds ratio. c) Percent E-cadherin (top panels) or vimentin (bottom panels) positive cells in MCF10A colonies exposed to MEK (U0126) and PI3K (LY294002) inhibition after spontaneous (left panels) or TGF-ß-driven (right panels) EMT. Error bars denote standard deviation from the mean (n = 3, two-tailed Student’s t test). d) Percent E-cadherin (top panels) or vimentin (bottom panels) positive cells in MCF10A colonies exposed to EGFR (Erlotinib), MET (Crizotinib), FGFR (Infigratinib) and ITGAV (Cilengitide) inhibition after spontaneous (left panels) or TGF-ß-driven (right panels) EMT. Error bars denote standard deviation from the mean (at left: spontaneous EMT control/EGFRi/ITGAVi n = 7, METi/FGFRi n = 4 independent samples; at right: TGF-ß-driven EMT control n = 4, EGFRi/METi/FGFRi/ITGAVi n = 3 independent samples, two-tailed Student’s t test). e) Inferred EMT regulatory network and putative regulators identified in this study. f) Model depicting the MEK dependent EMT regulatory checkpoint created and its effects on the development of intermediate EMT phenotypes.

Article Snippet: The MEK inhibitor U0126, the PI3K inhibitor LY294002, the EGFR inhibitor erlotinib, the MET inhibitor crizotinib and the FGFR inhibitor infigratinib were purchased from LC Laboratories and resuspended in DMSO.

Techniques: Expressing, Inhibition, Standard Deviation, Two Tailed Test