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| 1 | TBK1,a central kinase in innate immune sensing of nucleic acids and beyond显示文摘Sensing of intracellular and extracellular environments is one of the fundamental processes of cell.Surveillance of aberrant nucleic acids,derived either from invading pathogens or damaged organelle,is conducted by pattern recognition receptors(PRRs)including RIG-l-like receptors,cyclic GMP-AMP synthase,absent in melanoma 2,and a few members of tll-like receptors.TANK-binding kinase 1(TBK1),along with its close analogue I-kappa-B kinase epsilon,is a central kinase in innate adaptor complexes linking activation of PRRs to mobilization of transcriptional factors that transcribe proinflammatory cytokines,type I interferon(IFN-a/B),and myriads interferon stimulated genes.However,it still remains elusive for the precise mechanisms of activation and execution of TBK1 in signaling platforms formed by innate adaptors mitochondrial antiviral sig-naling protein(MAVS),stimulator of interferon genes protein(STING),and TIR-domain-containing adapter-inducing interferon-β(TRIF),as well as its complex regulations.An atlas of TBK1 substrates is in constant expanding,setting TBK1 as a key node of signaling network and a dominant player in contexts of cell biology,animal models,and human diseases.Here,we review recent advancements of activation,regulations,and functions of TBK1 under these physiological and pathological contexts. | Ruyuan Zhou Qian Zhang Pinglong Xu | 2020 | Acta Biochimica et Biophysica Sinica2020，52，7： | 3 |
| 2 | Intercellular transmission of cGAS-STING signaling in cancer显示文摘Cellular communication is necessary for organizing multicellular organisms,and is critical in tumorigenesis and progression.Immune and tumor cells use the cGAS-STING mechanism to sense and respond to genomic instability,DNA damage,and mitochondrial dysfunction induced by extra-and intracellular stresses. | Qirou Wu Xiaohong Leng Pinglong Xu | 2023 | Cancer Biology & Medicine2023，20，2： | 1 |
| 3 | Erratum to Intercellular transmission of cGAS-STING signaling in cancer显示文摘There are errors in Figure 1D1 on page 94.Specifically,RAB22A-induced autophagosomes were inadvertently marked in Figure 1D.We have revised Figure 1 to correct the errors.Of note,the errors do not impact the conclusion of this article.We apologize for the errors and for any resulting confusion. | Qirou Wu Xiaohong Leng Pinglong Xu | 2023 | Cancer Biology & Medicine2023，20，4： | 0 |
| 4 | Crumbs proteins stabilize the cone mosaics of photoreceptors and improve vision in zebrafish显示文摘Although the unique organization of vertebrate cone mosaics was first described long ago,both their underlying molecular basis and physiological significance are largely unknown.Here,we demonstrate that Crumbs proteins,the key regulators of epithelial apical polarity,establish the planar cellular polarity of photoreceptors in zebrafish.Via heterophilic Crb2a-Crb2b interactions,the apicobasal polarity protein Crb2b restricts the asymmetric planar distribution of Crb2a in photoreceptors.The planar polarized Crumbs proteins thus balance intercellular adhesions and tension between photoreceptors,thereby stabilizing the geometric organization of cone mosaics.Notably,loss of Crb2b in zebrafish induces a nearsightedness-like phenotype in zebrafish accompanied by an elongated eye axis and impairs zebrafish visual perception for predation.These data reveal a detailed mechanism for cone mosaic homeostasis via previously undiscovered apical-planar polarity coordination and propose a pathogenic mechanism for nearsightedness. | Qinlong Hao Mingjie Zheng Kechao Weng Yumei Hao Yao Zhou Yuchen Lin Feng Gao Ziqi Kou Shoji Kawamura Ke Yao Pinglong Xu Jinghai Chen Jian Zou | 2021 | Journal of Genetics and Genomics2021，48，1： | 0 |
| 5 | Imatinib blocks tyrosine phosphorylation of Smad4 and restores TGF-β growth-suppressive signaling in BCR-ABL1-positive leukemia显示文摘Loss of TGF-β-mediated growth suppression is a major contributor to the development of cancers,best exemplified by loss-offunction mutations in genes encoding components of the TGF-βsignaling pathway in colorectal and pancreatic cancers.Alternatively,gain-of-function oncogene mutations can also disrupt antiproliferative TGF-βsignaling.However,the molecular mechanisms underlying oncogene-induced modulation of TGF-βsignaling have not been extensively investigated.Here,we show that the oncogenic BCR-ABL1 of chronic myelogenous leukemia(CML)and the cellular ABL1 tyrosine kinases phosphorylate and inactivate Smad4 to block antiproliferative TGF-βsignaling.Mechanistically,phosphorylation of Smad4 at Tyr195,Tyr301,and Tyr322 in the linker region interferes with its binding to the transcription co-activator p300/CBP,thereby blocking the ability of Smad4 to activate the expression of cyclin-dependent kinase(CDK)inhibitors and induce cell cycle arrest.In contrast,the inhibition of BCR-ABL1 kinase with Imatinib prevented Smad4 tyrosine phosphorylation and re-sensitized CML cells to TGF-β-induced antiproliferative and pro-apoptotic responses.Furthermore,expression of phosphorylation-site-mutated Y195F/Y301F/Y322F mutant of Smad4 in Smad4-null CML cells enhanced antiproliferative responses to TGF-β,whereas the phosphorylation-mimicking Y195E/Y301E/Y322E mutant interfered with TGF-βsignaling and enhanced the in vivo growth of CML cells.These findings demonstrate the direct role of BCR-ABL1 tyrosine kinase in suppressing TGF-βsignaling in CML and explain how Imatinib-targeted therapy restored beneficial TGF-βanti-growth responses. | Lijing Wang Shuchen Gu Fenfang Chen Yi Yu Jin Cao Xinran Li Chun Gao Yanzhen Chen Shuchong Yuan Xia Liu Jun Qin Bin Zhao Pinglong Xu Tingbo Liang Hongyan Tong Xia Lin Xin-Hua Feng | 2023 | Signal Transduction and Targeted Therapy2023，8，4： | 0 |
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