IndraLab

Statements


CYLD inhibits SMAD3. 15 / 21
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"Because Akt is known as the major upstream regulator of GSK3beta XREF_BIBR XREF_BIBR, we investigated whether Akt mediates CYLD induced degradation of Smad3."

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"These data suggest that CYLD decreases Smad3 stability in a DUB activity dependent manner."

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"This interesting result thus led us to determine whether Akt is critically involved in mediating CYLD induced degradation of Smad3 by first examining the effect of Akt knockdown on Smad3 protein stability."

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"CYLD decreases Smad3 stability by inhibiting Akt."

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"On the basis that carboxy terminus of CHIP has been shown to mediate Smad3 degradation XREF_BIBR XREF_BIBR, we first determined whether CHIP mediates CYLD induced Smad3 degradation by using siCHIP."

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"Moreover, CYLD decreases Smad3 stability by deubiquitinating K63 polyubiquitinated Akt."

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"Together, these data suggest that CYLD decreases Smad3 stability and TGF-beta-signalling by inhibiting Akt."

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"Moreover, CYLD decreases Smad3 protein stability by directly deubiquitinating K63 polyubiquitinated Akt, which, in turn, leads to activation of GSK3beta (XREF_FIG)."

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"Because CYLD is a known deubiquitinating enzyme (DUB) XREF_BIBR XREF_BIBR XREF_BIBR XREF_BIBR XREF_BIBR XREF_BIBR XREF_BIBR XREF_BIBR, we investigated whether CYLD induced Smad3 degradation depends on its deubiquitinating activity."

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"Because E3 ubiquitin ligase has a critical role in mediating Smad3 degradation XREF_BIBR and CYLD is known as a deubiquitinase XREF_BIBR XREF_BIBR XREF_BIBR, we hypothesized that CYLD may decrease Smad3 stability via regulating an E3 ubiquitin ligase."

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"We thus determined whether GSK3beta is involved in mediating CYLD induced Smad3 degradation."

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"Nonetheless, these data suggest that CYLD decreases Smad3 protein stability via negatively regulating Akt."

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"Interestingly, CYLD decreases Smad3 stability by directly deubiquitinating K63 polyubiquitinated Akt."

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"CYLD decreases Smad3 stability via Akt-GSK3beta-CHIP pathway."

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"To further determine whether CYLD inhibits TGF-beta-signalling by likely targeting Smad3, we next evaluated the effect of CYLD knockdown in Smad3 deficient MEF cells."