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USP8 binds N-HER2. 6 / 6
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"The stabilized MALAT1 inhibits ubiquitin-proteasomal degradation of the N-HER2 by affecting the interaction of deubiquitinase USP8 and N-HER2, thereby promoting N-HER2 accumulation."
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"The IP and IB analysis found that HER2 and USP8 bound each other, especially N-HER2 (Fig. 3E), and USP8 mainly inhibited N-HER2 ubiquitination (Fig. 3F)."
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"The upregulated MALAT1, additionally, affects the binding between the deubiquitinase USP8 and N-HER2, inhibits the N-HER2 ubiquitin proteasomal degradation and promotes N-HER2 accumulation."
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"We also found that PAK5 WT but not PAK5 KM enhanced the interaction between deubiquitinase USP8 and N-HER2 (Fig. 6K)."
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"PAK5 promotes the recruitment of USP8 for N-HER2 to inhibit N-HER2 ubiquitination degradation thought lncRNA MALAT1, leading to N-HER2 accumulation.N -methyladenosine (m A) modifications, the most prevalent form of epigenetic modification in RNA, intricately linked to cell proliferation, metastasis, metabolism, and therapeutic resistance [22]."
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"The upregulated MALAT1 enhances the binding between USP8 and N-HER2, inhibiting the N-HER2 ubiquitin proteasomal degradation and promoting N-HER2 accumulation, PAK5 induces HER2 accumulation by inhibiting N-HER2 ubiquitination degradation via stabilization of MALAT1, which occurs through PAK5-mediated phosphorylation of METTL14, thereby playing a crucial role in breast cancer targeted trastuzumab resistance.Although previous results suggest promoting function for PAK5 in breast cancer, definitive evidence related to drug resistance in breast cancer has been lacking until this study was performed."
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