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3篇 您的检索式:作者名="Hongqi Teng"
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1Ubiquitination of Rheb governs growth factor-induced mTORC1 activation显示文摘Mechanistic target of rapamycin mTOR complex 1 (mTORC1)plays a key role in the integration of various environmental signals to regulate cell growth and metabolism,mTORC1 is recruited to the lysosome where it is activated by its interaction with GTP-bound Rheb GTPase.However,the regulatory mechanism of Rheb activity remains largely unknown.Here,we show that ubiquitination governs the nucleotide-bound status of Rheb.Lysosome-anchored E3 ligase RNF152 catalyzes Rheb ubiquitination and promotes its binding to the TSC complex.EGF enhances the deubiquitination of Rheb through AKT-dependent USP4 phosphorylation,leading to the release of Rheb from the TSC complex.Functionally,ubiquitination of Rheb is linked to mTORC1-mediated signaling and consequently regulates tumor growth.Thus,we propose a mechanistic model whereby Rheb-mediated mTORC1 activation is dictated by a dynamic opposing act between Rheb ubiquitination and deubiquitination that are catalyzed by RNF152 and USP4 respectively.Lu Deng Lei Chen Linlin Zhao Yan Xu Xiaoping Peng Xinbo Wang Lin Ding Jiali Jin Hongqi Teng Yanming Wang Weijuan Pan Fei Yu Lujian Liao Li Li Xin Ge Ping Wang 2019Cell Research2019,29,2:16
2Identification of Glutaminyl Cyclase isoenzyme isoQC as a regulator of SIRPα-CD47 axis显示文摘Dear Editor,Cancer cells often upregulate the expression of ligands for the inhibitory immune checkpoints receptor to escape anti-tumor immunity1. Targeting inhibitory immune checkpoints has become one of the most promising anticancer therapeutic inventions. Infiltration of myeloid cells, especially phagocytic cells, to tumors is often associated with chemotherapy resistance and progression of various cancer types. Phagocytosis of cancer cells is the major mechanism for these myeloid cells-mediated antitumor activity. However, many types of cancer cells express high level of ‘don’t eat me’ signals on the cell surface to escape the phagocytic cells-mediated antitumor immunity.Zhiqiang Wu Linjun Weng Tengbo Zhang Hongling Tian Lan Fang Hongqi Teng Wen Zhang Jing Gao Yun Hao Yaxu Li Hu Zhou Ping Wang 2019Cell Research2019,29,6:1
3ZRANB1 is an NBS1 deubiquitinase and a potential target to overcome radioresistance and PARP inhibitor resistance in triple-negative breast cancer显示文摘Poly(ADP-ribose)polymerase inhibitors(PARPi)are used to treat ovarian cancer and triple-negative breast cancer(TNBC)with defective homologous recombination repair pathways.However,de novo and acquired PARPi resistance limits clinical benefits.1 The MRE11-RAD50-NBS1(MRN)complex mediates the sensing,processing,and signaling of DNA double-strand breaks(DSBs)and plays important roles in the efficacy of PARPi and radiation treatment,2 and yet the mechanisms for the regulation and degradation of the MRN complex are not well understood.ZRANB1,also known as Trabid,is a breast cancer-promoting deubiquitinase that preferentially cleaves K29-,K33-,and K63-linked ubiquitin chains,3 but its role in therapy resistance remains unknown.Ying Mei Qinglei Hang Hongqi Teng Fan Yao Mei-Kuang Chen Mien-Chie Hung Yutong Sun Li Ma 2023Genes & Diseases2023,10,5:0
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