IndraLab

Statements


USP9X activates Notch. 6 / 8
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"Using a murine TNBC model, we show that USP9x knockdown abrogates Notch activation, reducing the production of the proinflammatory cytokines, C-C motif chemokine ligand 2 (CCL2) and interleukin-1 beta (IL-1β)."

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"The knockdown of USP9X abolishes Notch activation and reduces the production of pro-inflammatory cytokines, such as CCL2 and IL-1β."

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"Moreover, USP9X selectively promotes activation of the Notch developmental signaling pathway in triple-negative breast cancer, and small molecule EOAI3402143 (G9)-mediated USP9X inhibition specifically inhibits the Notch pathway, which leads to a remodeling of the tumor immune landscape and suppresses tumor growth (107)."

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"Loss of Usp9x disrupts cell adhesion, and components of the Wnt and Notch signaling pathways in neural progenitors."

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"Others have recently utilized LC-MS to identify nitric oxide-mediated S-nitrosylation of 217 proteins in cultured VICs, and subsequently demonstrated that S-nitrosylation of the deubiquitinase USP9X modulates NOTCH signaling in VICs, prevents murine valvular calcification, and is reduced in human valves with CAVD."

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"Usp9x promotes Notch signalling by antagonising the degradation of Mind bomb1, as well as activating Epsin in the signal sending cell XREF_BIBR, XREF_BIBR."