Yi‐Qun Zhan

Beijing Proteome Research Center

Author Statistics

Papers

Citation

H-Index

i-10 index

Research Trends

Author Order

Document Type

Co-Authors

Chang‐Yan Li

Beijing Proteome Research Center

Chang‐Hui Ge

Anhui Medical University

Xiaoming Yang

Beijing Proteome Research Center

Miao Yu

Beijing Proteome Research Center

Rong‐Hua Yin

Beijing Proteome Research Center

Wang‐Xiang Xu

Shanghai Institute of Planned Parenthood Research

Xiaoming Yang

First Affiliated Hospital of Zhengzhou University

Xiaoming Dong

Shaanxi Normal University

Liujun Tang

Beijing Proteome Research Center

Hui Chen

Reproductive & Genetic Hospital CITIC-Xiangya

Cooperative Institutions

Beijing Proteome Research Center

Beijing Radiation Center

Shanghai Jiao Tong University

Chinese Academy of Medical Sciences & Peking Union Medical College

Tianjin University

Chinese Academy of Sciences

Anhui Medical University

Academy of Military Medical Sciences

Sun Yat-sen University

Nanjing Medical University

Author Statistics

Papers

Citation

H-Index

i-10 index

Research Field

Specific Expression and Regulation of Hepassocin in the Liver and Down-regulation of the Correlation of HNF1α with Decreased Levels of Hepassocin in Human Hepatocellular Carcinoma

Journal of Biological Chemistry (2009)

Haitao Yu Miao Yu Chang‐Yan Li Yi‐Qun Zhan Wang‐Xiang Xu

Chromatin immunoprecipitation

Hepatocyte nuclear factors

10.1074/jbc.m806393200

Cite

Citations (56)

Pharmacological targeting of NLRP3 deubiquitination for treatment of NLRP3-associated inflammatory diseases

Science Immunology (2021)

Guang‐Ming Ren Jian Li Xiaochun Zhang Yu Wang Yang Xiao

Thiolutin, an inhibitor of the BRISC deubiquitinating enzyme complex, specifically and potently inhibits NLRP3 inflammasome activation.

Deubiquitinating enzyme

10.1126/sciimmunol.abe2933

Cite

Citations (61)

EWSR1 regulates mitosis by dynamically influencing microtubule acetylation

Figshare (2016)

Yilong Wang Hui Chen Yi‐Qun Zhan Rong‐Hua Yin Chang‐Yan Li

EWSR1, participating in transcription and splicing, has been identified as a translocation partner for various transcription factors, resulting in translocation, which in turn plays crucial roles in tumorigenesis. Recent studies have investigated the role of EWSR1 in mitosis. However, the effect of EWSR1 on mitosis is poorly understood. Here, we observed that depletion of EWSR1 resulted in cell cycle arrest in the mitotic phase, mainly due to an increase in the time from nuclear envelope breakdown to metaphase, resulting in a high percentage of unaligned chromosomes and multipolar spindles. We also demonstrated that EWSR1 is a spindle-associated protein that interacts with α-tubulin during mitosis. EWSR1 depletion increased the cold-sensitivity of spindle microtubules, and decreased the rate of spindle assembly. EWSR1 regulated the level of microtubule acetylation in the mitotic spindle; microtubule acetylation was rescued in EWSR1-depleted mitotic cells following suppression of HDAC6 activity by its specific inhibitor or siRNA treatment. In summary, these results suggest that EWSR1 regulates the acetylation of microtubules in a cell cycle-dependent manner through its dynamic location on spindle MTs, and may be a novel regulator for mitosis progress independent of its translocation.

10.6084/m9.figshare.3462932

Cite

Citations (0)

ABRO1 promotes NLRP3 inflammasome activation through regulation of NLRP3 deubiquitination

The EMBO Journal (2019)

Guang‐Ming Ren Xuanyi Zhang Yang Xiao Wen Zhang Yu Wang

10.15252/embj.2018100376

Cite

Citations (125)

Silencing of EDAG Induces Degradation of NPM1 and Sensitivity to Chemotherapeutic Drug in Acute Myeloid Leukemia Patients

ACTA AGRONOMICA SINICA (2013)

Weiwei Zheng Yang Yang Meijiang Zhang Xiaoming Dong Liujun Tang

NPM1

Degradation

10.3724/sp.j.1206.2013.00069

Cite

Citations (1)

EDAG promotes the expansion and survival of human CD34+ cells

PLoS ONE (2018)

Ke Zhao Weiwei Zheng Xiaoming Dong Rong‐Hua Yin Rui Gao

EDAG is multifunctional transcriptional regulator primarily expressed in the linloc-kit+Sca-1+ hematopoietic stem cells (HSC) and CD34+ progenitor cells. Previous studies indicate that EDAG is required for maintaining hematopoietic lineage commitment balance. Here using ex vivo culture and HSC transplantation models, we report that EDAG enhances the proliferative potential of human cord blood CD34+ cells, increases survival, prevents cell apoptosis and promotes their repopulating capacity. Moreover, EDAG overexpression induces rapid entry of CD34+ cells into the cell cycle. Gene expression profile analysis indicate that EDAG knockdown leads to down-regulation of various positive cell cycle regulators including cyclin A, B, D, and E. Together these data provides novel insights into EDAG in regulation of expansion and survival of human hematopoietic stem/progenitor cells.

Cord blood

10.1371/journal.pone.0190794

Cite

Citations (10)

Hepassocin is required for hepatic outgrowth during zebrafish hepatogenesis

Biochemical and Biophysical Research Communications (2015)

Ming Gao Hui Yan Rong‐Hua Yin Qiang Wang Yi‐Qun Zhan

Morpholino

Liver Regeneration

Organogenesis

10.1016/j.bbrc.2015.05.121

Cite

Citations (11)

Hemgn Protects Hematopoietic Stem and Progenitor Cells Against Transplantation Stress Through Negatively Regulating IFN‐γ Signaling

Advanced Science (2021)

Ke Zhao Jin‐Fang Liu Yaxin Zhu Xiaoming Dong Rong‐Hua Yin

Abstract Hematopoietic stem and progenitor cells (HSPCs) possess the remarkable ability to regenerate the whole blood system in response to ablated stress demands. Delineating the mechanisms that maintain HSPCs during regenerative stresses is increasingly important. Here, it is shown that Hemgn is significantly induced by hematopoietic stresses including irradiation and bone marrow transplantation (BMT). Hemgn deficiency does not disturb steady‐state hematopoiesis in young mice. Hemgn −/‐ HSPCs display defective engraftment activity during BMT with reduced homing and survival and increased apoptosis. Transcriptome profiling analysis reveals that upregulated genes in transplanted Hemgn −/− HSPCs are enriched for gene sets related to interferon gamma (IFN‐ γ ) signaling. Hemgn −/− HSPCs show enhanced responses to IFN‐ γ treatment and increased aging over time. Blocking IFN‐ γ signaling in irradiated recipients either pharmacologically or genetically rescues Hemgn −/‐ HSPCs engraftment defect. Mechanistical studies reveal that Hemgn deficiency sustain nuclear Stat1 tyrosine phosphorylation via suppressing T‐cell protein tyrosine phosphatase TC45 activity. Spermidine, a selective activator of TC45, rescues exacerbated phenotype of HSPCs in IFN‐ γ ‐treated Hemgn −/− mice. Collectively, these results identify that Hemgn is a critical regulator for successful engraftment and reconstitution of HSPCs in mice through negatively regulating IFN‐ γ signaling. Targeted Hemgn may be used to improve conditioning regimens and engraftment during HSPCs transplantation.

Homing (biology)

10.1002/advs.202103838

Cite

Citations (5)

Over-expression of EDAG in the myeloid cell line 32D: Induction of GATA-1 expression and erythroid/megakaryocytic phenotype

Journal of Cellular Biochemistry (2010)

Yali Ding Chengwang Xu Zhi‐Dong Wang Yi‐Qun Zhan Wei Li

Abstract Erythroid differentiation‐associated gene (EDAG), a hematopoietic tissue‐specific transcription regulator, plays a key role in maintaining the homeostasis of hematopoietic lineage commitment. However, the mechanism and genes regulated by EDAG remain unknown. In this study, we showed that overexpression of EDAG in a myeloid cell line 32D led to an erythroid phenotype with increased number of benzidine‐positive cells and up‐regulation of erythroid specific surface marker TER119. The megakaryocytic specific marker CD61 was also induced significantly. Using a genome‐wide microarray analysis and a twofold change cutoff, we identified 332 genes with reduced expression and 288 genes with increased expression. Among up‐regulation genes, transcription factor GATA‐1 and its target genes including EKLF, NF‐E2, Gfi‐1b, hemogen, SCL, hemoglobin alpha, beta and megakaryocytic gene GPIX were increased. Silencing of EDAG by RNA interference in K562 cells resulted in down‐regulation of these genes. Taken together, EDAG functions as a positive regulator of erythroid/megakaryocytic differentiation in 32D cells associated with the induction of GATA‐1 and its target genes. J. Cell. Biochem. 110: 866–874, 2010. © 2010 Wiley‐Liss, Inc.

GATA1

10.1002/jcb.22597

Cite

Citations (14)

GPS2 promotes erythroid differentiation by control of the stability of EKLF protein

Blood (2020)

Wenbing Ma Xiaohan Wang Chang‐Yan Li Huan-Huan Tian Jie Zhang

Corepressor

GATA1

Ectopic expression

GPS2

10.1182/blood.2019003867

Cite

Citations (13)