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| 1 | Acetytation of ACAP4 regutates CCL18-elicited breast cancer cell migration and invasion显示文摘Tumor metastasis represents the main causes of cancer-related death.Our recent study showed that chemokine CCL18 secreted from tumor-associated macrophages regulates breast tumor metastasis,but the underlying mechanisms remain less clear.Here, we show that ARF6 GTPase-activating protein ACAP4 regulates CCL18-elicited breast cancer cell migration via the acetyltransferase PCAF-mediated acetylation.CCL18 stimulation elicited breast cancer cell migration and invasion via PCAF-dependent acetylation.ACAP4 physically interacts with PCAF and is a cognate substrate of PCAF during CCL18 stimulation.The acetylation site of ACAP4 by PCAF was mapped to Lys311 by mass spectrometric analyses.Importantly,dynamic acetylation of ACAP4 is essential for CCL18-induced breast cancer cell migration and invasion,as overexpression of the persistent acetylation-mimicking or nonacetylatable ACAP4 mutant blocked CCL18-elicited cell migration and invasion.Mechanistically,the acetylation of ACAP4 at Lys311 reduced the lipid-binding activity of ACAP4 to ensure a robust and dynamic cycling of ARF6-ACAP4 complex with plasma membrane in response to CCL18 stimulation.Thus,these results present a previously undefined mechanism by which CCL18-elicited acetylation of the PH domain controls dynamic interaction between ACAP4 and plasma membrane during breast cancer cell migration and invasion. | Xiaoyu Song Wei Liu Xiao Yuan Jiying Jiang Wanjuan Wang McKay Mullen Xuannv Zhao Yin Zhang Fusheng Liu Shihao Du Adeel Rehman Ruijun Tian Jian Li Andra Frost Zhenwei Song Hadiyah-Nicole Green Calmour Henry Xing Liu Xia Ding Dongmei Wang Xuebiao Yao | 2018 | Journal of Molecular Cell Biology2018，10，6： | 3 |
| 2 | Modeling of COVID-19 disease disparity in gastric organoids reveals the spatiotemporal dynamics of SARS-CoV-2 infectivity显示文摘Dear Editor,The promptness and continuous expansion of the coronavirus disease 2019(COVID-19)pandemic,elicited by severe acute respiratory syndrome coronavirus 2(SARS-CoV-2)and its variants,has presented an unprecedented impact on human health(WHO Coronavirus(COVID-19)Dashboard,2021).Although vaccination has attenuated the severe symptoms,there is no specific antiviral medication available for preventing the viral spread(Drayman et al.,2021). | Wenwen Wang Fengrui Yang Jie Lin Saravanakumar Muthusamy Shihao Du McKay Mullen Fatima Garba Wanjuan Wang Xu Liu Tao Li Zhihong Yang Xia Ding Felix Aikhionbare Xinjiao Gao Zhikai Wang Xing Liu Xuebiao Yao | 2022 | Journal of Molecular Cell Biology2022，14，2： | 1 |
| 3 | Numerical Simulation of Two-Phase Flow in Glutenite Reservoirs for Optimized Deployment in Horizontal Wells显示文摘It is known that the pore media characteristics of glutenite reservoirs are different from those of conventional sandstone reservoirs.Low reservoir permeability and naturally developed microfractures make water injection in this kind of reservoir very difficult.In this study,new exploitation methods are explored.Using a real glutenite reservoir as a basis,a three-dimensional fine geological model is elaborated.Then,combining the model with reservoir performance information,and through a historical fitting analysis,the saturation abundance distribution of remaining oil in the reservoir is determined.It is shown that,using this information,predictions can be made about whether the considered reservoir is suitable for horizontal well fracturing or not.The direction,well length,well spacing and productivity of horizontal well are also obtained. | Yuhui Zhou Shichang Ju Qijun Lyu Hongfei Chen Xuebiao Du Aiping Zheng Wenshun Chen Ning Li | 2023 | Fluid Dynamics & Materials Processing2023，19，1： | 0 |
| 4 | Antagonizing the irreversible thrombomodulin-initiated proteolytic signaling alleviates age-related liver fibrosis via senescent cell killing显示文摘Cellular senescence is a stress-induced,stable cell cycle arrest phenotype which generates a pro-inflammatory microenvironment,leading to chronic inflammation and age-associated diseases.Determining the fundamental molecular pathways driving senescence instead of apoptosis could enable the identification of senolytic agents to restore tissue homeostasis.Here,we identify thrombomodulin(THBD)signaling as a key molecular determinant of the senescent cell fate.Although normally restricted to endothelial cells,THBD is rapidly upregulated and maintained throughout all phases of the senescence program in aged mammalian tissues and in senescent cell models.Mechanistically,THBD activates a proteolytic feed-forward signaling pathway by stabilizing a multi-protein complex in early endosomes,thus forming a molecular basis for the irreversibility of the senescence program and ensuring senescent cell viability.Therapeutically,THBD signaling depletion or inhibition using vorapaxar,an FDA-approved drug,effectively ablates senescent cells and restores tissue homeostasis in liver fibrosis models.Collectively,these results uncover proteolytic THBD signaling as a conserved pro-survival pathway essential for senescent cell viability,thus providing a pharmacologically exploitable senolytic target for senescence-associated diseases. | Christopher C.Pan Raquel Maeso-Díaz Tylor R.Lewis Kun Xiang Lianmei Tan Yaosi Liang Liuyang Wang Fengrui Yang Tao Yin Calvin Wang Kuo Du De Huang Seh Hoon Oh Ergang Wang Bryan Jian Wei Lim Mengyang Chong Peter B.Alexander Xuebiao Yao Vadim Y.Arshavsky Qi-Jing Li Anna Mae Diehl Xiao-Fan Wang | 2023 | Cell Research2023，33，7： | 0 |
| 5 | Methylation of PLK1 by SET7/9 ensures accurate kinetochore–microtubule dynamics显示文摘Faithful segregation of mitotic chromosomes requires bi-orientation of sister chromatids, which relies on the sensing of correct attachments between spindle microtubules and kinetochores. Although the mechanisms underlying PLK1 activation have been extensively studied, the regulatory mechanisms that couple PLK1 activity to accurate chromosome segregation are not well understood. In particular, PLK1 is implicated in stabilizing kinetochore–microtubule attachments, but how kinetochore PLK1 activity is regulated to avoid hyperstabilized kinetochore–microtubules in mitosis remains elusive. Here, we show that kinetochore PLK1 kinase activity is modulated by SET7/9 via lysine methylation during early mitosis. The SET7/9-elicited dimethylation occurs at the Lys191 of PLK1, which tunes down its activity by limiting ATP utilization. Overexpression of the non-methylatable PLK1 mutant or chemical inhibition of SET7/9 methyltransferase activity resulted in mitotic arrest due to destabilized kinetochore–microtubule attachments. These data suggest that kinetochore PLK1 is essential for stable kinetochore–microtubule attachments and methylation by SET7/9 promotes dynamic kinetochore–microtubule attachments for accurate error correction. Our findings define a novel homeostatic regulation at the kinetochore that integrates protein phosphorylation and methylation with accurate chromosome segregation for maintenance of genomic stability. | Ruoying Yu Huihui Wu Hazrat Ismail Shihao Du Jun Cao Jianyu Wang Tarsha Ward Fengrui Yang Ping Gui Mahboob Ali Lingluo Chu Fei Mo Qi Wang Youjun Chu Jianye Zang Yun Zhao Mingliang Ye Guowei Fang Peng RChen Zhen Dou Xinjiao Gao Wenwen Wang Xing Liu Xuebiao Yao | 2020 | Journal of Molecular Cell Biology2020，12，6： | 0 |
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