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| 1 | BubR1 phosphorylates CENP-E as a switch enabling the transition from lateral association to end-on capture of spindle microtubules显示文摘Error-free mitosis depends on accurate chromosome attachment to spindle microtubules, powered congression of those chromosomes, their segregation in anaphase, and assembly of a spindle midzone at mitotic exit. The centromere-associated kinesin motor CENP-E, whose binding partner is BubR1, has been implicated in congression of misaligned chromosomes and the transition from lateral kinetochore-microtubule association to end-on capture. Although previously proposed to be a pseudokinase, here we report the structure of the kinase domain of Drosophila melanogaster BubR1, revealing its folding into a conformation predicted to be catalytically active. BubR1 is shown to be a bona fide kinase whose phosphorylation of CENP-E switches it from a laterally attached microtubule motor to a plus-end microtubule tip tracker. Computational modeling is used to identify bubristatin as a selective BubR1 kinase antagonist that targets the αN1 helix of N-terminal extension and αC helix of the BubR1 kinase domain. Inhibition of CENP-E phosphorylation is shown to prevent proper microtubule capture at kinetochores and, surprisingly, proper assembly of the central spindle at mitotic exit. Thus, BubR1-mediated CENP-E phosphorylation produces a temporal switch that enables transition from lateral to end-on microtubule capture and organization of microtubules into stable midzone arrays. | Yuejia Huang Lin Lin Xing Liu Sheng Ye Phil Y. Yao Wenwen Wang Fengrui Yang Xinjiao Gao Junying Li Yin Zhang Jiancun Zhang Zhihong Yang Xu Liu Zhenye Yang Jianye Zang Maikun Teng Zhiyong Wang Ke Ruan Xia Ding Lin Li Don W. Cleveland Rongguang Zhang Xuebiao Yao | 2019 | Cell Research2019，29，7： | 8 |
| 2 | Effects of manganous sulphate on root growth,cell division,and nucleoli of Allium cepa显示文摘The effects of different concentrations of manganous sulphate on root growth,cell division, chromosome and nucleus morphplogy and nucleoli in root tip-cells of Allium cepa L. were studied. The concentrations of manganous sulphate used were 10-7,10-6,10-5 ,10-4,10-3, 10-2 and 10-1mol/L. The results indicated that manganese had a stimulatory effect on the root growth at lower concentrations (10-7 to 10-4mol/L). With increasing the concentration of Mn (10-3 to 10-1mol/L) and duration of treatment,manganese inhibited root growth and cell division, and had toxic effects on chromosomes,nuclei and nucleoli. Manganese Could induce mitotic irregularities,comprising c-mitosis,anaphase bridges and chromosome stickiness. The nuclei became irregular in shape and many micronuclei were scattered in the cytoplasm. Some similar silver-stained particulate materials were found scattered in the nucleus in root tip cells. The possible mechanism behind these phenomena is also briefly discussed. | 刘东华 蒋悟生 王威 翟林 | 1994 | 华北农学报1994，9，S2： | 6 |
| 3 | Cyclin A2:At the crossroads of cell cycle and cell invasion显示文摘Cyclin A2 is an essential regulator of the cell division cycle through the activation of kinases that participate to the regulation of S phase as well as the mitotic entry. However,whereas its degradation by the proteasome in mid mitosis was thought to be essential for mitosis to proceed,recent observations show that a small fraction of cyclin A2 persists beyond metaphase and is degraded by autophagy. Its implication in the control of cytoskeletal dynamics and cell movement has unveiled its role in the modulation of Rho A activity. Since this GTPase is involved in both cell rounding early in mitosis and later,in the formation of the cleavage furrow,this suggests that cyclin A2 is a novel actor in cytokinesis. Taken together,these data point to this cyclin as a potential mediator of cell-niche interactions whose dysregulation could be taken as a hallmark of metastasis. | Abdelhalim Loukil Caroline T Cheung Nawal Bendris Bénédicte Lemmers Marion Peter Jean Marie Blanchard | 2015 | World Journal of Biological Chemistry2015，6，4： | 6 |
| 4 | The enigmatic ERH protein:its role in cell cycle,RNA splicing and cancer显示文摘Enhancer of rudimentary homolog(ERH)is a small,highly conserved protein among eukaryotes.Since its discovery nearly 20 years ago,its molecular function has remained enigmatic.It has been implicated to play a role in transcriptional regulation and in cell cycle.We recently showed that ERH binds to the Sm complex and is required for the mRNA splicing of the mitotic motor protein CENP-E.Fur-thermore,cancer cells driven by mutations in the KRAS oncogene are particularly sensitive to RNAi-mediated suppression of ERH function,and ERH expression is inversely correlated with survival in colorectal cancer pa-tients whose tumors harbor KRAS mutation.These recent fi ndings indicate that ERH plays an important role in cell cycle through its mRNA splicing activity and is critically required for genomic stability and cancer cell survival. | Meng-Tzu Weng Ji Luo | 2013 | Protein & Cell2013，4，11： | 6 |
| 5 | LRIF1 interacts with HPla to coordinate accurate chromosome segregation during mitosis显示文摘Heterochromatin protein 1α (HP1α)regulates chromatin specification and plasticity during cell fate decision.Different structural determinants account for HP1α Localization and function during cell division cycle.Our earlier study showed that centromeric Localization of HP1α depends on the epigenetic mark H3K9me3 in interphase,while its centromeric location in mitosis relies on uncharacterized PXVXL-containing factors.Here,we identified a PXVXL-containing protein,Ligand-dependent nuclear receptorinteracting factor 1 (LRIF1),which recruits HPla to the centromere of mitotic chromosomes and its interaction with HP1α is essential for accurate chromosome segregation during mitosis.LRIF1 interacts directly with HPla chromoshadow domain via an evolutionariLy conserved PXVXL motif within its C-terminus.Importantly,the LRIF1-HPla interaction is critical for Aurora B activity in the inner centromere.Mutation of PXVXL motif of LRIF1 Leads to defects in HPla centromere targeting and aberrant chromosome segregation.These findings reveal a previously unrecognized direct Link between LRIF1 and HP1α in centromere plasticity control and illustrate the critical role of LRIF1-HP1α interaction in orchestrating accurate cell division. | Saima Akram Fengrui Yang Junying Li Gregory Adams Yingying Liu Xiaoxuan Zhuang Lingluo Chu Xu Liu Nerimah Emmett Winston Thompson McKay Mullen Saravana Muthusamy Wenwen Wang Fei Mo Xing Liu | 2018 | Journal of Molecular Cell Biology2018，10，6： | 5 |
| 6 | Using a GFP-gene fusion technique to study the cell cycle-dependent distribution of calmodulin in living cells显示文摘In this study, a green fluorescent protein (GFP)-calmodulin (CaM) fusion gene method was used to examine the distribution of calmodulin during various stages of cell cycle. First, it was found that the distribution of CaM in living cells changes with the cell cycle. CaM was found mainly in the cytoplasm during G1 phase. It began to move into the nucleus when the cell entered S phase. At G2 phase, CaM became more concentrated in the nucleus than in cytoplasm. Second, the accumulation of CaM in the nucleus during G2 phase appeared to be related to the onset of mitosis, since inhibiting the activation of CaM at this stage resulted in blocking the nuclear membrane breakdown and chromatin condensation. Finally, after the cell entered mitosis, a high concentration of CaM was found at the polar regions of the mitotic spindle. At this time, inhibiting the activity of CaM would cause a disruption of the spindle structure. The relationship between the stage-specific distribution of CaM and its function in | 李朝军 吕品 张东才 | 1999 | Science China(Life Sciences)1999，42，5： | 2 |
| 7 | “Stop Ne(c)king around”: How interactomics contributes to functionally characterize Nek family kinases显示文摘Aside from Polo and Aurora, a third but less studied kinase family involved in mitosis regulation is the never in mitosis-gene A(NIMA)-related kinases(Neks). The founding member of this family is the sole member NIMA of Aspergillus nidulans, which is crucial for the initiation of mitosis in that organism. All 11 human Neks have been functionally assigned to one of the three core functions established for this family in mammals:(1) centrioles/mitosis;(2) primary ciliary function/ciliopathies; and(3) DNA damage response(DDR). Recent findings, especially on Nek 1 and 8, showed however, that several Neks participate in parallel in at least two of these contexts: primary ciliary function and DDR. In the core section of this in-depth review, we report the current detailed functional knowledge on each of the 11 Neks. In the discussion, we return to the cross-connections among Neks and point out how our and other groups' functional and interactomics studies revealed that most Neks interact with protein partners associated with two if not all three of the functional contexts. We then raise the hypothesis that Neks may be the connecting regulatory elements that allow the cell to fine tune and synchronize the cellular events associated with these three core functions. The new and exciting findings on the Nek family open new perspectives and should allow the Neks to finally claim the attention they deserve in the field of kinases and cell cycle biology. | Gabriela Vaz Meirelles Arina Marina Perez Edmárcia Elisa de Souza Ferna Luisa Basei Priscila Ferreira Papa Talita Diniz Melo Hanchuk Vanessa Bomfim Cardoso Jrg Kobarg | 2014 | World Journal of Biological Chemistry2014，5，2： | 2 |
| 8 | Molecular basis of vasohibins-mediated detyrosination and its impact on spindle function and mitosis显示文摘α-Tubulin detyrosination, largely catalyzed by vasohibins, is involved in many microtubule (MT)-related cellular events. In this study, we identified a core heterodimeric complex of human small vasohibin-binding protein (SVBP) and vasohibin 1 (VASH1)(hereafter denoted as SVBP-VASH1) that catalyzes the detyrosination of a peptide derived from C-terminus of α-tubulin. We further solved the crystal structures of the SVBP-VASH1 heterodimer alone and in complex with either an inhibitor or a mutant substrate peptide. Our structural research, complemented by biochemical and mutagenesis experiments, resulted in identification of the key residues for VASH1 binding to SVBP and α-tubulin substrate. Our in vivo experiments reveal that MT detyrosination in general, as well as the interactions between SVBP, VASH1, and α-tubulin, are critical for spindle function and accurate chromosome segregation during mitosis. Furthermore, we found that the phenotypes caused by the depletion of vasohibins were largely rescued upon co-depletion of kinesin13/MCAK, suggesting the coordination between the MT depolymerase and MT detyrosination during mitosis. Thus our work not only provides structural insights into the molecular mechanism of α-tubulin detyrosination catalyzed by SVBP-bound vasohibins, but also uncovers the key role of vasohibins-mediated MT detyrosination in spindle morphology and chromosome segregation during mitosis. | Shanhui Liao Girish Rajendraprasad Na Wang Susana Eibes Jun Gao Huijuan Yu Gao Wu Xiaoming Tu Hongda Huang Marin Barisic Chao Xu | 2019 | Cell Research2019，29，7： | 2 |
| 9 | 胃的 Neuroendocrine 癌: 一份案例报告显示文摘 Neuroendocrine carcinoma(NEC)is a rare tumor,comprising<1%of stomach cancers.A 55-year-old woman was referred to our hospital with biopsy-proven gastric cancer.A shallow ulcerative lesion was detected in the lesser curvature of the lower body.It was suspected to be early gastric cancerⅡA+ⅡC type.Thus,endoscopic submucosal dissection was performed.She was subsequently diagnosed with NEC,which is aggressive and carries a poor prognosis.We conducted a radical resection and a laparoscopic-assisted distal gastrectomy.The tumor had infiltrated the subserosal layer and6/42 lymph nodes were involved.The mitotic index was16/10 high power fields and the Ki-67 labeling index was 26%-50%.The final diagnosis of NEC was made according to the World health Organization 2010 criteria.She was suspected of having jumping metastasis to the proximal margin.The patient was treated with an oral anticancer drug(5-flurouracil based drug)for2 years.The patient has been followed up for 3 years without recurrence. | Sang hyun Kang Kwang hee Kim Sang hyuk Seo Min Sung An Tae Kwun ha ha Kyung Park Ki Beom Bae Chang Soo Choi Sang hun Oh Young Kil Choi | 2014 | World Journal of Gastrointestinal Surgery2014，6，4： | 1 |
| 10 | cGAS guards against chromosome endto-end fusions during mitosis and facilitates replicative senescence显示文摘As a sensor of cytosolic DNA, the role of cyclic GMP-AMP synthase (cGAS) in innate immune response is well established, yet how its functions in different biological conditions remain to be elucidated. Here, we identify cGAS as an essential regulator in inhibiting mitotic DNA double-strand break (DSB) repair and protecting short telomeres from end-to-end fusion independent of the canonical cGAS-STING pathway. cGAS associates with telomeric/subtelomeric DNA during mitosis when TRF1/TRF2/POT1 are deficient on telomeres. Depletion of cGAS leads to mitotic chromosome end-to-end fusions predominantly occurring between short telomeres. Mechanistically, cGAS interacts with CDK1 and positions them to chromosome ends. Thus, CDK1 inhibits mitotic non-homologous end joining (NHEJ) by blocking the recruitment of RNF8. cGAS-deficient human primary cells are defective in entering replicative senescence and display chromosome end-to-end fusions, genome instability and prolonged growth arrest. Altogether, cGAS safeguards genome stability by controlling mitotic DSB repair to inhibit mitotic chromosome end-to-end fusions, thus facilitating replicative senescence. | Xiaocui Li Xiaojuan Li Chen Xie Sihui Cai Mengqiu Li Heping Jin Shu Wu Jun Cui Haiying Liu Yong Zhao | 2022 | Protein & Cell2022，13，1： | 1 |
| 11 | Cell cycle dysregulation with overexpression of KIF2C/MCAK is a critical event in显示文摘Nasopharyngeal carcinoma(NPC)is a common malignant carcinoma of the head and neck,and the biological mechanisms underlying the pathogenesis of NPC remain not fully understood.In the present study,we systematically analyzed four independent NPC transcriptomic datasets and focused on identifying the critical molecular networks and novel key hub genes implicated in NPC.We found totally 170 common overlapping differentially expressed genes(DEGs)in the four NPC datasets.GO and KEGG pathway analysis revealed that cell cycle dysregulation is a critical event in NPC.Protein-protein interaction(PPl)network analysis identified a 15 hub-gene corenetwork with overexpressedkinesin family member2C(KIF2C)as a central regulator.Loss-of-function study demonstrated that knockdown of KiF2C significantly inhibited cell growth and cell motility,and delayed cell cycle progression,accompanied with dramatic mitotic defects in spindle formation in NPC cells.RNA-seq analysis revealed that KIF2c knockdown led to deregulation of various downstream genes.KiF2C could also regulate the AKT/mTOR pathways,and enhance paclitaxel sensitivity in NPC cells.Taken together,our results suggest that cell cycle dysregulation is a critical event during NPC pathogenesis and KIF2C is a novel key mitotic hub gene with therapeutic potential in NPC. | Xiaofeng Zuo Peixin Meng Yuxin Bao Chuntao Tao Yitao Wang Xianjun Liu Youquan Bu Jiang Zhu | 2023 | Genes & Diseases2023，10，1： | 1 |
| 12 | NDP52 tunes cortical actin interaction with astral microtubules for accurate spindle orientation显示文摘Oriented cell divisions are controlled by a conserved molecular cascade involving Gαi, LGN, and NuMA. Here, we show that NDP52 regulates spindle orientation via remodeling the polar cortical actin cytoskeleton. siRNA-mediated NDP52 suppression surprisingly revealed a ring-like compact subcortical F-actin architecture surrounding the spindle in prophase/prometaphase cells, which resulted in severe defects of astral microtubule growth and an aberrant spindle orientation. Remarkably, NDP52 recruited the actin assembly factor N-WASP and regulated the dynamics of the subcortical F-actin ring in mitotic cells. Mechanistically, NDP52 was found to bind to phosphatidic acid-containing vesicles, which absorbed cytoplasmic N-WASP to regulate local filamentous actin growth at the polar cortex. Our TIRFM analyses revealed that NDP52-containing vesicles anchored N-WASP and shortened the length of actin filaments in vitro. Based on these results we propose that NDP52-containing vesicles regulate cortical actin dynamics through N-WASP to accomplish a spatiotemporal regulation between astral microtubules and the actin network for proper spindle orientation and precise chromosome segregation. In this way, intracellular vesicles cooperate with microtubules and actin filaments to regulate proper mitotic progression. Since NDP52 is absent from yeast, we reason that metazoans have evolved an elaborate spindle positioning machinery to ensure accurate chromosome segregation in mitosis. | Huijuan Yu Fengrui Yang Peng Dong Shanhui Liao Wei R. Liu Gangyin Zhao Bo Qin Zhen Dou Zhe Liu Wei Liu Jianye Zang Jennifer Lippincott-Schwartz Xing Liu Xuebiao Yao | 2019 | Cell Research2019，29，8： | 1 |
| 13 | Mps1 dimerization and multisite interactions with Ndc80 complex enable responsive spindle assembly checkpoint signaling显示文摘Error-free mitosis depends on accurate chromosome attachment to spindle microtubules,which is monitored by the spindle assembly checkpoint(SAC)signaling.As an upstream factor of SAC,the precise and dynamic kinetochore localization of Mps1 kinase is critical for initiating and silencing SAC signaling.However,the underlying molecular mechanism remains elusive.Here,we demonstrated that the multisite interactions between Mps1 and Ndc80 complex(Ndc80C)govern Mps1 kinetochore targeting.Importantly,we identified direct interaction between Mps1 tetratricopeptide repeat domain and Ndc80C.We further identified that Mps1 C-terminal fragment,which contains the protein kinase domain and C-tail,enhances Mps1 kinetochore localization.Mechanistically,Mps1 C-terminal fragment mediates its dimerization.Perturbation of C-tail attenuates the kinetochore targeting and activity of Mps1,leading to aberrant mitosis due to compromised SAC function.Taken together,our study highlights the importance of Mps1 dimerization and multisite interactions with Ndc80C in enabling responsive SAC signaling. | Ping Gui Divine M.Sedzro Xiao Yuan Sikai Liu Mohan Hei Wei Tian Najdat Zohbi Fangwei Wang Yihan Yao Felix O.Aikhionbare Xinjiao Gao Dongmei Wang Xuebiao Yao Zhen Dou | 2020 | Journal of Molecular Cell Biology2020，12，7： | 1 |
| 14 | The spindle assembly checkpoint:perspectives in tumorigenesis and cancer therapy显示文摘Loss or gain of chromosomes,a condition known as aneuploidy,is a common feature of tumor cells and has therefore been proposed as the driving force for tumorigenesis.Such chromosomal instability can arise during mitosis as a result of mis-segregation of the duplicated sister chromatids to the two daughter cells.In normal cells,missegregation is usually prevented by the spindle assembly checkpoint(SAC),a sophisticated surveillance mechanism that inhibits mitotic exit until all chromosomes have successfully achieved bipolar attachment to spindle microtubules.Complete abrogation of SAC activity is lethal to normal as well as to tumor cells,as a consequence of massive chromosome mis-segregation.Importantly,many human aneuploid tumor cells exhibit a weakened SAC activity that allows them to tolerate gains or losses of a small number of chromosomes;and interfering with this SAC residual activity may constitute a suitable strategy to kill cancer cells.This review focuses on the potential link between SAC and tumorigenesis,and the therapeutic strategy to target the SAC for cancer treatment. | Joana BARBOSA Ana Vanessa NASCIMENTO Juliana FARIA Patrícia SILVA Hassan BOUSBAA | 2011 | Frontiers in Biology2011，6，2： | 1 |
| 15 | Anti-tumor pharmacology of natural products targeting mitosis显示文摘Cancer has been an insurmountable problem in the history of medical science.The uncontrollable proliferation of cancer cells is one of cancers main characteristics,which is closely associated with abn ormal mitosis.Targeting mitosis is an effective method for cancer treatment.This review summarizes several natural products with anti-tumor effects related to mitosis,focusing on targeting microtubulin,inducing DNA damage,and modulating mitosis-associated kinases.Furthermore,the main disadvantages of several typical compounds,including drug resistance,toxicity to non-tumor tissues,and poor aqueous solubility and pharmacokinetic properties,are also discussed,together with strategies to address them.Improved understanding of cancer cell mitosis and natural products may pave the way to drug development for the treatment of cancer. | Manru Huang Caiyan Liu Yingying Shao Shiyue Zhou Gaoyong Hu Shuangshuang Yin Weiling Pu Haiyang Yu | 2022 | Cancer Biology & Medicine2022，19，6： | 1 |
| 16 | Effects of Zn^(2+) on root growth,cell division,and nucleoli of Allium cepa L.显示文摘EffectsofZn^(2+)onrootgrowth,celldivision,andnucleoliofAlliumcepaL.￥LiuDonghua;JiangWusheng;WangChunli(DepartmentofBiology,Ti?.. | Liu Donghua Jiang Wusheng Wang Chunli (Department of Biology, Tianjin Normal University,Tianjin 300074,China)Zhai Lin (Xinhua High School , Tianjin 300204,China) | 1996 | Journal of Environmental Sciences1996，8，1： | 0 |
| 17 | Dynamic phosphorylation of CENP-N by CDK1 guides accurate chromosome segregation in mitosis显示文摘In mitosis,accurate chromosome segregation depends on the kinetochore,a supermolecular machinery that couples dynamic spin-dle microtubules to centromeric chromatin.However,the structure–activity relationship of the constitutive centromere-associated network(CCAN)during mitosis remains uncharacterized.Building on our recent cryo-electron microscopic analyses of human CCAN structure,we investigated how dynamic phosphorylation of human CENP-N regulates accurate chromosome segregation.Our mass spectrometric analyses revealed mitotic phosphorylation of CENP-N by CDK1,which modulates the CENP-L–CENP-N interaction for accurate chromosome segregation and CCAN organization.Perturbation of CENP-N phosphorylation is shown to prevent proper chromosome alignment and activate the spindle assembly checkpoint.These analyses provide mechanistic insight into a previously undefined link between the centromere–kinetochore network and accurate chromosome segregation. | Ran Liu Zhen Dou Tian Tian Xinjiao Gao Lili Chen Xiao Yuan Chunyue Wang Jiahe Hao Ping Gui McKay Mullen Felix Aikhionbare Liwen Niu Guoqiang Bi Peng Zou Xuan Zhang Chuanhai Fu Xuebiao Yao Jianye Zang Xing Liu | 2023 | Journal of Molecular Cell Biology2023，15，6： | 0 |
| 18 | Publisher Correction: Molecular basis of vasohibins-mediated detyrosination and its impact on spindle function and mitosis显示文摘In the initial published version of this article,there was an inadvertent omission from the Acknowledgements that work in the lab of MB is supported by grants from Danish Cancer Society Scientific Committee(KBVU;R146-A9322) and the Lundbeck Foundation (R215-2015-4081).This omission does not affect the description of the resuits or the conclusions of this work. The publisher apologizes for any inconvenience this has caused to the readers. | Shanhui Liao Girish Rajendraprasad Na Wang Susana Eibes Jun Gao Huijuan Yu Gao Wu Xiaoming Tu Hongda Huang Marin Barisic Chao Xu | 2019 | Cell Research2019，29，9： | 0 |
| 19 | Mitotic inactivation of the cGAS-MITA/STING pathways显示文摘The cyclic guanosine monophosphate-adenosine monophosphate synthase(cGAS)-mediator of interferon response factor 3 acti-vation/stimulator of interferon genes(MITA/STING)axis has emerged as a major pathway,which senses microbial or mislocated cellular DNA in the cytosol to trigger innate immune responses.cGAS senses cytosolic DNA without a preference of self-or nonself-DNA.How the cGAS-MITA/STING axis is inactivated upon nuclear envelope breakdown(NEBD)at mitotic entry in vertebrate cells to avoid self-DNA sensing remains unclear until very recently.In this review,we summarize the recent advances on how cGAS responds to chromosomes upon NEBD and the mechanisms involved in the inactivation of the cGAS-MITA/STING pathways in mitosis. | Li Zhong Hong-Bing Shu | 2021 | Journal of Molecular Cell Biology2021，13，10： | 0 |
| 20 | Acetylation of Nup62 by TIP60 ensures accurate chromosome segregation in mitosis显示文摘Stable transmission of genetic information during cell division requires faithful mitotic spindle assembly and chromosome segregation.In eukaryotic cells,nuclear envelope breakdown(NEBD)is required for proper chromosome segregation.Although a list of mitotic kinases has been implicated in NEBD,how they coordinate their activity to dissolve the nuclear envelope and protein machinery such as nuclear pore complexes was unclear.Here,we identified a regulatory mechanism in which Nup62 is acetylated by TIP60 in human cell division.Nup62 is a novel substrate of TIP60,and the acetylation of Lys432 by TIP60 dissolves nucleoporin Nup62-Nup58-Nup54 complex during entry into mitosis.Importantly,this acetylation-elicited remodeling of nucleoporin complex promotes the distribution of Nup62 to the mitotic spindle,which is indispensable for orchestrating correct spindle orientation.Moreover,suppression of Nup62 perturbs accurate chromosome segregation during mitosis.These results establish a previously uncharacterized regulatory mechanism in which TIP60-elicited nucleoporin dynamics promotes chromosome segregation in mitosis. | Hameed Akbar Jun Cao Dongmei Wang Xiao Yuan Manjuan Zhang Saravanakumar Muthusamy Xiaoyu Song Xu Liu Felix Aikhionbare Xuebiao Yao Xinjiao Gao Xing Liu | 2022 | Journal of Molecular Cell Biology2022，14，8： | 0 |
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