UBE2T/CDC42/CD276 signaling axis mediates brain metastasis of triple-negative breast cancer via lysosomal autophagy by Lin Li, Rong Fu, Yan Chen, Jin Yao, Xiaobing Jiang, Tao Liang, Jun jun Li, Qian zhi Chen, Liang Liang Shi, Ming Xing Xie, Xin Wei Qiao, Qi Hong Cheng, Min Jie Wang

“…Finally, animal experimental results also showed that inhibition of UBE2T elevated the TNBC sensitivity to immune checkpoint CD276 blockade and inhibited BrM of TNBC.Conclusions In conclusion, our results indicate a new mechanism whereby UBE2T-mediated ubiquitination positively controls the UBE2T/CDC42/CD276 axis to upregulate tumor cell expression of CD276 and thereby impair CD8+ T cells function, ultimately leading to tumor cell immune escape and BrM.…”
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IL-17 triggers PD-L1 gene transcription in NSCLC cells via TRIM31-dependent MEF2C K63-linked polyubiquitination by Shuai Ying, Ningxia Wu, Yuting Ruan, Wen Ge, Pei Ma, Tongpeng Xu, Yongqian Shu, Yingwei Wang, Wen Qiu, Chenhui Zhao

“…Co-IP/IB was used to examine the interaction between MEF2C and PD-L1, including MEF2C ubiquitination. IHC staining was carried out to analyse the expression of IL-17RA, MEF2C, TRIM31, and PD-L1 in NSCLC tissue arrays. …”
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The Legionella pneumophila effector PieF modulates mRNA stability through association with eukaryotic CCR4−NOT by Harley O'Connor Mount, Malene L. Urbanus, Francesco Zangari, Anne-Claude Gingras, Alexander W. Ensminger

“…With a host range that spans billions of years of evolution (from protists to humans), the interaction between L. pneumophila and its hosts frequently involves conserved eukaryotic pathways (protein translation, ubiquitination, membrane trafficking, autophagy, and the cytoskeleton). …”
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EPIGENETICS TODAY AND TOMORROW by B. F. Vanyushin

“…The most known epigenetic mechanisms (signals) are enzymatic DNA methylation, the histone code (various enzymatic histone modifications including acetylation, methylation, phosphorylation, ubiquitination and others), and gene silencing mediated by small RNAs (miRNA, siRNA). …”
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Tp53 determines the spatial dynamics of M1/M2 tumor-associated macrophages and M1-driven tumoricidal effects by Yi-Jing Hsiao, Min-Shu Hsieh, Gee-Chen Chang, Yin-Chen Hsu, Chia-Yu Wang, Yan-Ming Chen, Yi-Ling Chen, Pan-Chyr Yang, Sung-Liang Yu

“…This activation facilitates p53-STAT1 interactions, reduces the interaction between p53 and MDM2, and subsequently decreases p53 ubiquitination. M1 CM inhibited tumorigenesis, and silencing p53 reduced the anti-tumor efficacy of polyinosinic:polycytidylic acid (poly I:C) in vivo. …”
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TRAF2 and RIPK1 redundantly mediate classical NFκB signaling by TNFR1 and CD95-type death receptors by Jennifer Wagner, David Vredevoogd, Xin Yu, Dong Lu, Daniel S. Peeper, Heike M. Hermanns, Jin Wang, Harald Wajant, Daniela Siegmund

“…Complex Ia and Ib may furthermore interact and cooperate to ubiquitinate RIPK1 resulting in a modified complex Ia/b preventing complex Ia and Ib to convert to the established TNFR1-induced cytotoxic complexes IIa and IIb.…”
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Disruption of tumor-intrinsic PGAM5 increases anti-PD-1 efficacy through the CCL2 signaling pathway by Yan Li, Hong Wang, Xiaoyang Li, Yuan He, Huiquan Liu, Dong Han, Ting Mei, Yixuan Li, Zilong Xu, Xiaoying Wei, Jianguo Wang, Peijie Zhou, Yuwen Wang, Ziye Li, Junhao Ning, Anlin Wang, Jingjing Cheng, Dong Qian

“…Mechanistically, in HCC cells PGAM5 deficiency inhibited mitochondria fission by promoting TRIM28 binding with DRP1, which increased ubiquitination and degradation of DRP1. Tumor-intrinsic PGAM5 deficiency mediated mitochondria fusion and reduced cytosolic mtDNA stress which attenuated TLR9 activation and downstream NF-κB-regulated CCL2 secretion. …”
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