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| 1 | Identification and primary genetic analysis of Arabidopsis stomatal mutants in response to multiple stresses显示文摘In response to variable environmental conditions, guard cells located in the leaf epidermis can integrate and cope with a multitude of complicated stimuli, thereby making stomata in an appro- priate state. However, many signaling components in guard cell signaling remain elusive. In our laboratory, a tool for non-invasive remote infrared thermal images was used to screen an ethyl methane sulfonate-mutagenized population for Arabidopsis stomatal response mutants under multiple stresses (ABA, H2O2, CO2, etc.). More than forty 'hot' or 'cold' mutants were isolated (above or below 0.5℃ in con- trast to normal plantlets). Identification and primary genetic analysis of these mutants show that they are monogenic recessive mutations and there exist distinct difference in stomata apertures compared to wild type. These mutants in response to various environmental stresses and hormones were comprehen- sively investigated, which enables us to further un- derstand the cross-talk in different signal transduction pathways. | SONG Yuwei KANG Yanli LIU Hao ZHAO Xiaoliang WANG Pengtao AN Guoyong ZHOU Yun MIAO Chen SONG Chunpeng | 2006 | Chinese Science Bulletin2006，51，21： | 11 |
| 2 | Oncogenic AURKA-enhanced N6-methyladenosine modification increases DROSHA mRNA stability to transactivate STC1 in breast cancer stem-like cells显示文摘RNase III DROSHA is upregulated in multiple cancers and contributes to tumor progression by hitherto unclear mechanisms.Here,we demonstrate that DROSHA interacts withβ-Catenin to transactivate STC1 in an RNA cleavage-independent manner,contributing to breast cancer stem-like cell(BCSC)properties.DROSHA mRNA stability is enhanced by N6-methyladenosine(m^(6)A)modification which is activated by AURKA in BCSCs.AURKA stabilizes METTL14 by inhibiting its ubiquitylation and degradation to promote DROSHA mRNA methylation.Moreover,binding of AURKA to DROSHA transcript further strengthens the binding of the m^(6)A reader IGF2BP2 to stabilize m^(6)A-modified DROSHA.In addition,wild-type DROSHA,but not an m^(6)A methylation-deficient mutant,enhances BCSC stemness maintenance,while inhibition of DROSHA m^(6)A modification attenuates BCSC traits.Our study unveils the AURKA-induced oncogenic m^(6)A modification as a key regulator of DROSHA in breast cancer and identifies a novel DROSHA transcriptional function in promoting the BCSC phenotype. | Fei Peng Jie Xu Bai Cui Qilan Liang Sai Zeng Bin He Hong Zou Manman Li Huan Zhao Yuting Meng Jin Chen Bing Liu Shasha Lv Peng Chu Fan An Zifeng Wang Junxiu Huang Yajing Zhan Yuwei Liao Jinxin Lu Lingzhi Xu Jin Zhang Zhaolin Su Zhiguang Li Fangjun Wang Eric W-FLam Quentin Liu | 2021 | Cell Research2021，31，3： | 9 |
| 3 | A New Bot- tleneck Detecting Approach to Productivity Im- provement of Knowledgeable Manufacturing System 显示文摘 | Yan Hongsen An Yuwei Shi Wenwu | 2010 | Journal of Intelligent Manufacturing2010，21，6： | 1 |
| 4 | EGFR signaling promotes nuclear translocation of plasma membrane protein TSPAN8 to enhance tumor progression via STAT3-mediated transcription显示文摘TSPAN family of protei ns are gen erally con sidered to assemble as multimeric complexes on the plasma membra ne.Our previous work uncovered that TSPAN8 can translocate into the nucleus as a membrane-free form,a process that requires TSPAN8 palmitoylation and association with cholesterol to promote its extraction from the plasma membrane and subsequent binding with 14-3-30 and importin-p.However,what upstream signal(S)regulate(s)the nuclear translocation of TSPAN8,the potential function of TSPAN8 in the n ucleus,and the un derlying molecular mechanisms all remai n unclear.Here,we dem on strate that,epidermal growth factor receptor(EGFR)signaling induces TSPAN8 nuclear translocation by activating the kinase AKTZ which in turn directly phosphorylates TSPAN8 at Ser129,an event essential for its binding with 14-3-30 and importin B1.In the nucleus,phosphorylated TSPAN8 interacts with STAT3 to enhance its chromatin occupancy and therefore regulates transcription of downstream cancer-promoting genes,such as MYC,BCL2,MMP9,etc.The EGFR-AKT-TSPAN8-STAT3 axis was found to be hyperactivated in multiple human cancers,and associated with aggressive phe no type and dismal prog nosis.We further developed a humanized mono clonal antibody hT8Ab4 that specifically recognizes the large extracellular loop of TSPAN8(TSPAN8-LEL),thus being able to block the extract!on of TSPAN8 from the plasma membrane and consequently its nuclear localization.Importantly,both in vitro and in vivo studies demonstrated an antitumor effect of hT8Ab4.Collectively,we discovered an unconventional function of TSPAN8 and dissected the underlying molecular mechanisms,which not only showcase a new layer of biological complexity of traditional membrane proteins,but also shed light on TSPAN8 as a novel therapeutic target for refractory cancers. | Xiaoqing Lu Liwei An Guangjian Fan Lijuan Zang Weiyi Huang Junjian Li Jun Liu Weiyu Ge Yuwei Huang Jingxuan Xu Shaoqian Du Tianhao Zhou Huijing Yin Li Yu Shi Jiao Hongxia Wang | 2022 | Cell Research2022，32，4： | 1 |
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