Search

Your search keyword '"Chu, Yajing"' showing total 45 results
Start Over Author "Chu, Yajing" Search Limiters Available in Library Collection
45 results on '"Chu, Yajing"'

14. Hematopoietic IKBKE limits the chronicity of inflammasome priming and metaflammation

Author

Patel, Meghana N., Bernard, William G., Milev, Nikolay B., Cawthorn, William P., Figg, Nichola, Hart, Dan, Prieur, Xavier, Virtue, Sam, Hegyi, Krisztina, Bonnafous, Stephanie, Bailly-Maitre, Beatrice, Chu, Yajing, Griffin, Julian L., Mallat, Ziad, Considine, Robert V., Tran, Albert, Gual, Philippe, Takeuchi, Osamu, Akira, Shizuo, Vidal-Puig, Antonio, Bennett, Martin R., and Sethi, Jaswinder K.

Published
2015

16. Additional file 1 of Polyclonal evolution of Fanconi anemia to MDS and AML revealed at single cell resolution

Author

Chang, Lixian, Cui, Zejia, Shi, Deyang, Chu, Yajing, Wang, Bichen, Wan, Yang, Ma, Qiuyi, Zhang, Ranran, Li, Haoyuan, Cheng, Xuelian, Cheng, Tao, Zhu, Xiaofan, Li, Cheng, and Yuan, Weiping

Abstract

Additional file 1: Table S1. The mutation results in bone marrow and peripheral blood samples from patient P1001 at different stages. Table S2. Primers for single-cell targeted sequencing. Table S3. Antibodies for FACS experiments. Material methods. Including Whole genome analysis, Clonal analysis, and Single-cell targeted sequencing.

Published
2022
Full Text
View/download PDF

21. Rheb1-Deficient Neutrophils Promote Hematopoietic Stem/Progenitor Cell Proliferation via Mesenchymal Stem Cells

Author

Gao, Juan, primary, Hou, Shuaibing, additional, Yuan, Shengnan, additional, Wang, Yuxia, additional, Gao, Yanan, additional, Sun, Xiaolu, additional, Wang, Weili, additional, Chu, Yajing, additional, Zhou, Yuan, additional, Feng, Xiaoming, additional, Luo, Hongbo R., additional, Cheng, Tao, additional, Shi, Jun, additional, Yuan, Weiping, additional, and Wang, Xiaomin, additional

Published
2021
Full Text
View/download PDF

22. Biological characterization of MLL-NRIP3 fusion gene induced leukemia

Author

XiaoFan Zhu, WeiPing Yuan, HuiDong Guo, Chu Yajing, Tao Cheng, and Yangpeng Chen

Subjects
Myeloid leukemia, Chromosomal translocation, Cell cycle, Biology, medicine.disease, Fusion gene, Leukemia, Haematopoiesis, hemic and lymphatic diseases, medicine, Cancer research, Pharmacology (medical), Progenitor cell, Stem cell, neoplasms
Abstract

Leukemia, originating from hematopoietic stem or progenitor cells, is a malignant proliferative tumor which seriously endangers human health and survival. It is the most common childhood malignancy with an increasing proportion of malignancy in adults. Acute myeloid leukemia (AML) involving MLL (mixed lineage leukemia, MLL-r ) translocation is recognized as an aggressive form of hematopoietic malignancies that exhibit a blockade of differentiation, disruption of genetic and epigenetic regulation, and poor prognosis. Although MLL-NRIP3 fusion gene has been reported recently in establishing leukemia mouse model and its effect on leukemia progression in MLL-r mouse model has also been demonstrated, its leukemia biological characteristics were still not well characterized. Here we investigate the basic biological phenotypes of two MLL-r mouse models ( MLL-AF9 and MLL-NRIP3 ), including: the survival of recipient mice transplanted with leukemia cells; the migration and adhesion abilities of leukocyte cells; the number and the function of leukemia stem cells (LSCs), cell cycle and cell apoptosis, and investigate whether the surface markers of LSCs reported previously are equally applicable to MLL-NRIP3 leukemia cells. The results showed that the survival time of MLL-NRIP3 recipient mice was longer than that of MLL-AF9 . The migration ability of MLL-NRIP3 leukemia cells was less capable than MLL-AF9 , while adhesion was stronger than MLL-AF9 cells. Cell cycle and cell apoptosis of two MLL-r leukemia cells basically had no difference. C olony - forming unit assay and limiting dilution assay both revealed that MLL-AF9 leukemia had a higher number of functional LSCs than MLL-NRIP3 . In summary, MLL-NRIP3 induced leukemia is a low LSCs-enriched MLL-r .

Published
2017

27. Rheb1 loss leads to increased hematopoietic stem cell proliferation and myeloid-biased differentiation in vivo

Author

Wang, Xiaomin, primary, Gao, Yanan, additional, Gao, Juan, additional, Li, Minghao, additional, Zhou, Mi, additional, Wang, Jinhong, additional, Pang, Yakun, additional, Cheng, Hui, additional, Yuan, Chase, additional, Chu, Yajing, additional, Jiang, Yu, additional, Zhou, Jianfeng, additional, Luo, Hongbo R., additional, Ju, Zhenyu, additional, Cheng, Tao, additional, and Yuan, Weiping, additional

Published
2018
Full Text
View/download PDF

29. Tet2 Regulates Osteoclast Differentiation by Interacting with Runx1 and Maintaining Genomic 5-Hydroxymethylcytosine (5hmC)

Author

Chu, Yajing, primary, Zhao, Zhigang, additional, Sant, David Wayne, additional, Zhu, Ganqian, additional, Greenblatt, Sarah M., additional, Liu, Lin, additional, Wang, Jinhuan, additional, Cao, Zeng, additional, Tho, Jeanette Cheng, additional, Chen, Shi, additional, Liu, Xiaochen, additional, Zhang, Peng, additional, Maciejewski, Jaroslaw P., additional, Nimer, Stephen, additional, Wang, Gaofeng, additional, Yuan, Weiping, additional, Yang, Feng-Chun, additional, and Xu, Mingjiang, additional

Published
2018
Full Text
View/download PDF

32. PDK1 plays a vital role on hematopoietic stem cell function

Author

Hu, Tianyuan, primary, Li, Cong, additional, Wang, Le, additional, Zhang, Yingchi, additional, Peng, Luyun, additional, Cheng, Hui, additional, Chu, Yajing, additional, Wang, Weili, additional, Ema, Hideo, additional, Gao, Yingdai, additional, Ju, Zhenyu, additional, Yang, Zhongzhou, additional, Wang, Xiaomin, additional, Cheng, Tao, additional, and Yuan, Weiping, additional

Published
2017
Full Text
View/download PDF

37. Mechanistic insights revealed by lipid profiling in monogenic insulin resistance syndromes

Author

Eiden, Michael, primary, Koulman, Albert, additional, Hatunic, Mensud, additional, West, James A., additional, Murfitt, Steven, additional, Osei, Michael, additional, Adams, Claire, additional, Wang, Xinzhu, additional, Chu, Yajing, additional, Marney, Luke, additional, Roberts, Lee D., additional, O’Rahilly, Stephen, additional, Semple, Robert K., additional, Savage, David B., additional, and Griffin, Julian L., additional

Published
2015
Full Text
View/download PDF

38. Hematopoietic IKBKE limits the chronicity of inflammasome priming and metaflammation

Author

Patel, Meghana N., primary, Bernard, William G., additional, Milev, Nikolay B., additional, Cawthorn, William P., additional, Figg, Nichola, additional, Hart, Dan, additional, Prieur, Xavier, additional, Virtue, Sam, additional, Hegyi, Krisztina, additional, Bonnafous, Stephanie, additional, Bailly-Maitre, Beatrice, additional, Chu, Yajing, additional, Griffin, Julian L., additional, Mallat, Ziad, additional, Considine, Robert V., additional, Tran, Albert, additional, Gual, Philippe, additional, Takeuchi, Osamu, additional, Akira, Shizuo, additional, Vidal-Puig, Antonio, additional, Bennett, Martin R., additional, and Sethi, Jaswinder K., additional

Published
2014
Full Text
View/download PDF

41. Acetylation Targets the M2 Isoform of Pyruvate Kinase for Degradation through Chaperone-Mediated Autophagy and Promotes Tumor Growth

Author

Lv, Lei, primary, Li, Dong, additional, Zhao, Di, additional, Lin, Ruiting, additional, Chu, Yajing, additional, Zhang, Heng, additional, Zha, Zhengyu, additional, Liu, Ying, additional, Li, Zi, additional, Xu, Yanping, additional, Wang, Gang, additional, Huang, Yiran, additional, Xiong, Yue, additional, Guan, Kun-Liang, additional, and Lei, Qun-Ying, additional

Published
2011
Full Text
View/download PDF

42. PBX3is Essential for Leukemia Stem Cell Maintenance in MLL-Rearranged Leukemia

Author

Guo, Huidong, Chu, Yajing, Wang, Le, Cheng, Hui, Wang, Weili, Wang, Xiaomin, Zhang, Xiaobing, Cheng, Tao, and Yuan, Weiping

Abstract

Acute myeloid leukemia (AML) with MLLtranslocation is recognized as a group of aggressive hematopoietic malignancies with poor prognosis. An atypical homeodomain protein family (TALE family, three-amino-acid loop extension) has been reported to be involved in leukemogenesis and leukemia progression. For example, MEIS1and PBX3were abnormally expressed in examined AML patient samples when compared with their normal counterparts. While MEIS1has been studied extensively, the precise role of PBX3in leukemia development is still largely unknown.

Published
2016
Full Text
View/download PDF

43. High Expression of Microtubule-associated Protein TBCB Predicts Adverse Outcome and Immunosuppression in Acute Myeloid Leukemia.

Author

Wang B, Wang W, Li Q, Guo T, Yang S, Shi J, Yuan W, and Chu Y

Abstract

Acute myeloid leukemia (AML) is a devastating blood cancer with high heterogeneity and ill-fated outcome. Despite numerous advances in AML treatment, the prognosis remains poor for a significant proportion of patients. Consequently, it is necessary to accurately and comprehensively identify biomarkers as soon as possible to enhance the efficacy of diagnosis, prognosis and treatment of AML. In this study, we aimed to identify prognostic markers of AML by analyzing the cohorts from TCGA-LAML database and GEO microarray datasets. Interestingly, the transcriptional level of microtubule-associated protein TBCB in AML patients was noticeably increased when compared with normal individuals, and this was verified in two independent cohorts (GSE9476 and GSE13159) and with our AML patients. Furthermore, univariate and multivariate regression analysis revealed that high TBCB expression was an independent poor prognostic factor for AML. GO and GSEA enrichment analysis hinted that immune-related signaling pathways were enriched in up-regulated DEGs between two populations separated by the median expression level of TBCB . By constructing a protein-protein interaction network, we obtained six hub genes, all of which are immune-related molecules, and their expression levels were positively linked to that of TBCB . In addition, the high expression of three hub genes was significantly associated with a poor prognosis in AML. Moreover, we found that the tumor microenvironment in AML with high TBCB expression tended to be infiltrated by NK cells, especially CD56 bright NK cells. The transcriptional levels of NK cell inhibitory receptors and their ligands were positively related to that of TBCB , and their high expression levels also predicted poor prognosis in AML. Notably, we found that the down-regulation of TBCB suppressed cell proliferation in AML cell lines by enhancing the apoptosis and cell cycle arrest. Finally, drug sensitivity prediction illustrated that cells with high TBCB expression were more responsive to ATRA and midostaurin but resistant to cytarabine, dasatinib, and imatinib. In conclusion, our findings shed light on the feasibility of TBCB as a potential predictor of poor outcome and to be an alternative target of treatment in AML., Competing Interests: Competing Interests: The authors have declared that no competing interest exists., (© The author(s).)

Published
2023
Full Text
View/download PDF

44. Rheb1 loss leads to increased hematopoietic stem cell proliferation and myeloid-biased differentiation in vivo .

Author

Wang X, Gao Y, Gao J, Li M, Zhou M, Wang J, Pang Y, Cheng H, Yuan C, Chu Y, Jiang Y, Zhou J, Luo HR, Ju Z, Cheng T, and Yuan W

Subjects
Animals, Cell Lineage genetics, Cell Proliferation, Gene Expression Profiling, Karyotype, Mice, Myeloproliferative Disorders etiology, Myeloproliferative Disorders metabolism, Myeloproliferative Disorders mortality, Myeloproliferative Disorders pathology, Neutrophils metabolism, Cell Differentiation genetics, Gene Deletion, Hematopoietic Stem Cells cytology, Hematopoietic Stem Cells metabolism, Myelopoiesis genetics, Ras Homolog Enriched in Brain Protein genetics
Abstract

Hematopoietic stem cells constitute a unique subpopulation of blood cells that can give rise to all types of mature cells in response to physiological demands. However, the intrinsic molecular machinery that regulates this transformative property remains elusive. In this paper, we demonstrate that small GTPase Rheb1 is a critical regulator of proliferation and differentiation of hematopoietic stem cells in vivo Rheb1 deletion led to increased phenotypic hematopoietic stem cell/hematopoietic progenitor cell proliferation under a steady state condition. Over-proliferating Rheb1-deficient hematopoietic stem cells were severely impaired in functional repopulation assays, and they failed to regenerate the blood system when challenged with hematopoietic ablation by sublethal irradiation. In addition, it was discovered that Rheb1 loss resulted in a lack of maturation of neutrophils / caused neutrophil immaturation by reducing mTORC1 activity, and that activation of the mTORC1 signaling pathway by mTOR activator 3BDO partially restored the maturation of Rheb1-deficient neutrophils. Rheb1 deficiency led to a progressive enlargement of the hematopoietic stem cell population and an eventual excessive myeloproliferation in vivo , including an overproduction of peripheral neutrophils and an excessive expansion of extramedullary hematopoiesis. Moreover, low RHEB expression was correlated with poor survival in acute myeloid leukemia patients with normal karyotype. Our results, therefore, demonstrate a critical and unique role for Rheb1 in maintaining proper hematopoiesis and myeloid differentiation., (Copyright © 2019 Ferrata Storti Foundation.)

Published
2019
Full Text
View/download PDF

Catalog

Books, media, physical & digital resources
See catalog results