IndraLab

Statements

UCHL1 activates DNA-templated transcription. 6 / 6
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"UCHL1 plasma levels decrease after LDN-57444 treatment, suggesting the application of plasma UCHL1 as a treatment monitoring indicator.Increasing evidence shows that the nuclear pore complex regulates the nucleocytoplasmic transportation of key molecular factors to drive cancer progression.47 64 65 66 Inhibition of the nuclear pore complex induces cancer cell death.64 POM121 is highly expressed in multiple cancers and directly interacts with importin-β, a nuclear import machinery component, to regulate two oncogenic transcription factors, E2F1 and c-MYC, in advanced PC."
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"UCH-L1 forms endogenous complexes with beta-catenin, stabilizes it and up-regulates beta-catenin/TCF/Lef-dependent transcription."
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"In addition, UCH-L1 increases the ubiquitination and degradation of microphthalmia-related transcription factor (MITF) by binding to ubiquitinated MITF (64)."
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"Researchers found that NF-κB can bind to the promoter of ubiquitin carboxy-terminal hydrolase 1 (UCHL1) to promote its transcription, and UCHL1 in turn activates the NF-κB pathway, forming positive feedback 41."
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"Activation of NF-κB signaling by the inflammatory stimulator lipopolysaccharide and TNFα resulted in a decrease of UCH-L1 gene expression by inhibiting its transcription."
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"Histone modification of H3K4 trimethylation of CHGA and UCHL1 promoter were increased to activate their transcription through the signalling transduction such as Rho-GTPase, AKT and NFκB pathways."
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