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UCHL1 activates TGFB. 19 / 19
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"Functionally, exosomal UCHL1 stimulates breast cancer migration and extravasation by facilitating TGFβ signaling [ 72 ]."
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"UCHL1 + exosomes upregulate TGFbeta signaling and serves as blood-based biomarker for aggressive breast cancer ."
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"In the most aggressive triple-negative breast cancer [loss of estrogen receptor (ER), progesterone receptor and HER2 expression], overexpression of UCH-L1 promotes TGF-β signaling-induced metastasis by inhibiting degradation of the TGF-β type I receptor and its downstream effector molecule SMAD2 (29)."
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"This confirmed the existence of OGN /UCHL1 in our spatial samples and further supported the role of BMP and TGFβ signals in early HF development.Overall, our results revealed two differentiation trajectories, one from OGN /UCHL1 cells→TC1→TC2 leading to normal Pc formation, the other from OGN /UCHL1 cells→TC1→TC3 leading to epithelial development."
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"UCHL-1 promotes TGF-β activation, while the depletion of UCHL-1 attenuates TGF-β signaling."
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"Here, we show that the deubiquitinating enzyme UBH-1 in Caenorhabditis elegans and its human homolog, ubiquitin C-terminal hydrolase-L1 (UCH-L1), stimulate DAF-7 and TGF-beta signaling, suggesting that this mode of regulation of TGF-beta signaling is conserved across animal species."
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"In several systems, including a zebrafish xenograft model, the authors provide evidence that exosomes enriched in UCHL1 upregulated TGF-β signalling in receptor cells via transfer from exosomes, facilitating migration and extravasation of breast cancer cells [54]."
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"Here, we show that the deubiquitinating enzyme UBH-1 in Caenorhabditis elegans and its human homolog, ubiquitin C-terminal hydrolase-L1 (UCH-L1), stimulate DAF-7 and TGF-beta signaling, suggesting that this mode of regulation of TGF-beta signaling is conserved across animal species."
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"The authors showed that UBH-1 in Caenorhabditis elegans and its human homolog UCHL1 promotes DAF-7/ TGF-β signalling, indicating that the mechanism of TGF-β signalling is conserved among animal species [67]."
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"Overexpression of UCH-L1, but not of UCH-L3 (the other human homolog of UBH1) or of the catalytic mutant UCH L1C90A, enhanced TGF-beta and SMAD-induced transcriptional activity, indicating that the deubiquitination activity of UCH-L1 is indispensable for enhancing TGF-beta and SMAD signaling."
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"In addition, TGF-β signalling is enhanced by overexpression of UCHL1 but not the mutant UCHL1-C90A, indicating that catalytic activity of UCHL1 is mandatory for enhancing TGF-β signalling."
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"These results indicate that UCH-L1 activity supports DAF-7 and TGF-beta signaling and suggest that UCH-L1 's deubiquitination activity is a potential therapeutic target for managing lung cancer."
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"In a contrasting analysis, Liu et al. proposed that UCHL1 promotes breast cancer metastasises by deubiquitinating and stabilising TGFβR1 and SMAD2 in TNBC by maintaining the TGF-β signalling pathway [54], with UCHL1 inhibition using a cyanpyrrolidine-based covalent inhibitor 6RK73 or genetic knockdown antagonising TGF-β signalling in TNBC models."
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"Mechanistically , we found UCHL1 could promote the transforming growth factor-beta ( TGFbeta ) - SMAD canonical signaling pathway by protecting the cell surface TGFbeta type I receptor and its downstream intracellular effector SMAD2 from proteasomal degradation ."
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"Similarly, IMP-1710 could be employed as a tool to study UCHL1-mediated TGF-β signaling in non-cancer contexts, such as cardiac remodeling [99]."
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"Overexpression of UCH-L1, but not of UCH-L3 (the other human homolog of UBH1) or of the catalytic mutant UCH-L1 C90A, enhanced TGF-beta and SMAD-induced transcriptional activity, indicating that the deubiquitination activity of UCH-L1 is indispensable for enhancing TGF-beta and SMAD signaling."
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"A recent finding reveals that within the uterus during early pregnancy of mice, UCHL1 is specifically expressed in decidual cells [24]; however, the roles of UCHL1 have not been explored in miscarriage related to impaired decidualization.In the present study, we found that the expression of UCHL1 was dramatically decreased in decidua from patients suffering miscarriage, accompanied by aberrant decidualization indicated by the downregulation of decidual markers IGFBP1 and PRL [25] and decreased dNKs due to reduced production of CXCL12, IL15 and TGF-β from DSCs."
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"These results indicate that UCH-L1 activity supports DAF-7 and TGF-beta signaling and suggest that UCH-L1 's deubiquitination activity is a potential therapeutic target for managing lung cancer."
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"In particular, UCHL1 promotes TGF-β signal transduction by acting on the TGF-β signaling pathway and Smad2 signaling pathway, thus inducing breast cancer cell metastasis [12]."
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