IndraLab

Statements


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"In addition, OTUB1 enhances glycolysis and epithelial-mesenchymal transition of endometriosis cells, leading to promote proliferation, migration, and invasion of endometriosis cells."

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"Taken together, OTUB1 promotes the proliferation and migration of endometriosis cells."

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"Together, OTUB1 promotes epithelial-mesenchymal transition in endometriosis cells."

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"In summary, OTUB1 promotes the development of endometriosis by up-regulating HSF1."

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"We also find that OTUB1 promotes the growth and invasion of endometriosis cells."

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"In conclusion, OTUB1 promotes glycolysis in endometriosis cells."

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"Thus, the knockdown of OTUB1 inhibits the development of endometriosis in vivo."

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"The results confirmed that OTUB1 promoted EMT in endometriosis, which is consistent with our previous findings (Figures 8G and 8H)."

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"In this study, OTUB1 enhanced the proliferation, migration, and invasion of endometriosis cells."

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"Our data showed that overexpression of OTUB1 altered the expression levels of EMT-related factors and promotes EMT in endometriosis cells."

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"The results showed that OTUB1 deletion inhibited the growth of endometriosis lesions.In summary, our study identifies a HSF1 new binding partner-OTUB1, which promotes its protein stability via deubiquitination."

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"The results further show that OTUB1 promotes the development of endometriosis in vivo and in vitro (Figure 8I)."

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"In this study, we demonstrate that OTUB1 promotes the development of endometriosis via deubiquitination of HSF1."