IndraLab

Statements

USP4 activates TGFB. 19 / 19
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"The DUBs USP4, USP11, USP15, and UCH37 have previously been demonstrated to modulate TGF-beta pathway activity by directly deubiquitinating the TbetaRI, resulting in increased TbetaRI stability (XREF_FIG) XREF_BIBR XREF_BIBR XREF_BIBR XREF_BIBR."
26435193
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"USP4 can enhance TGF-beta signaling by directly interacting with TbetaRI / ALK5 ."
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"USP4 promotes TGF-beta signals by stabilizing TGF-betatype I rceptor (TbetaRIota) [XREF_BIBR]."
24798342
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"In addition to these newly identified nuclear functions, both USP4 and USP15 are well known to function in the cytosol, i.e. USP4 modulates the Wnt and beta-catenin, NF-kappaB, p53 and TGF-beta signaling pathways while USP15 performs functions in the TGF-beta receptor and NF-kappaB signaling pathways."
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"By promoting activation of the relaxin and TGF-beta 1/Smad2/matrix metalloproteinase 9 axis and transcriptional repression activity of HDAC2, USP4 induces breast cell invasion, migration, and proliferation both in vitro and in vivo."
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"Collectively, our results support the concept that dysregulation of miR-148a is associated with the poor prognosis of HCC and may account for the tumor progression to advanced stages, and that, of the newly identified targets, USP4 overexpression may contribute to HCC progression towards more aggressive feature presumably by facilitating TGF-beta signaling pathways, growth advantage and migrating capability."
24798342
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"USP4, when overexpressed, potently enhanced TGF-beta signaling."
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"However, when it comes to tumor metastasis, USP4 can promote breast cancer cells metastasis by activating TGF-β1/Smad2/matrix metalloproteinase-9 signaling pathway [ 33 ]."
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"USP4 can serve as a double-edged sword in tumor progression because it functions as a tumor suppressor in lung cancer by indirectly circumventing stemness [56], while USP4 promotes TNBC metastasis by enhancing TGF-β signaling and inducing the suppressive activity of Tregs [87, 119]."
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"USP4 promotes invasion of breast cancer cells via Relaxin and TGF-beta 1/Smad2/MMP -9 signal."
27049265
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"The hypothesis that drove this study was that USP4 might also mediate the TGF-beta signal transduction pathway in hypertrophic scar fibroblasts."
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"In a previous study on breast cancer, USP4 was shown to promote TGF-β signaling and to cooperate with AKT signaling to promote cancer cell EMT, migration, and invasion [27]."
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"USP4 modulates tumor growth factor TGF-β signaling to regulate immunosuppressive pathways in the tumor microenvironment."
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"For example, USP4 drives breast cancer cell invasion via Relaxin/TGF-β1/Smad2/MMP-9 (matrix metallopeptidase 9) signalling [93] and promotes hepatocellular carcinoma metastasis by enhancing TGF-β sign[MISSING/INVALID CREDENTIALS: limited to 200 char for Elsevier]"
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"Of the newly identified two targets of miR-148a (i.e., USP4 and S1P1), USP4 overexpression contributed to HCC progression toward more aggressive feature by facilitating TGF-beta signaling pathways, growth advantage and migrating capability."
26682240
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"Both USP15 and USP4 stimulate TGF-beta signaling by deubiquitylating and stabilizing two key signaling molecules in this pathway, TGF-beta receptor I (TbetaRI) and R-SMADs, suggesting that these two closely related DUBs act in concert to modulate central signaling processes that are involved in oncogenesis and innate immunity."
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"USP4 silencing was found to decrease significantly TGFβ–induced cellular proliferation and expression of the TGF–β receptor I, as observed upon treatment with vialinin A."
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"Ubiquitin specific protease 4 (USP4) augments TGF-beta signaling through the prevention of TGF-beta RI degradation."
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"LncRNA H19 targets miR-148a, increases deubiquitinating enzyme USP4 expression, activates the TGF-β signaling pathway in hepatic stellate cells and hepatocytes, and exacerbates hepatic fibrosis 180."
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