Zobrazeno 1 - 10
of 13
pro vyhledávání: '"Wei Xi Cao"'
Autor:
Chunli Li, Haixia Wang, Yajuan Li, Wenli Feng, Meng Shi, Xi Chen, Xiao-Zhong Wang, Wei-Xi Cao
Publikováno v:
Cellular Signalling. 25:2604-2612
The oncogenic BCR/ABL tyrosine kinase induces constitutive enhanced "spontaneous" DNA damage and unfaithful repair in Philadelphia chromosome positive leukemia cells. Here, we investigated the changes of protein profile in H2O2-induced DNA damage/rep
Autor:
Liang Zhong, Wei-Xi Cao, Wenli Feng, Qing Xiao, Jianping Wen, Zhenglan Huang, Haixia Wang, Kun Tao, Yajuan Li
Publikováno v:
Experimental Cell Research. 319:1094-1101
MicroRNAs (miRNAs) are small RNAs that regulate gene expression posttranscriptionally and are critical for many cellular pathways. Recent evidence has shown that aberrant miRNA expression profiles and unique miRNA signaling pathways are present in ma
Autor:
Jing Shi, Wen Li Feng, Ya Juan Li, Ying Yuan, Zhi Peng, Wei Xi Cao, Hong Wei Luo, Jing Rong Deng, Hai Xia Wang
Publikováno v:
The International Journal of Biochemistry & Cell Biology. 44:861-868
Emergence of resistance to imatinib mesylate complicates the treatment of chronic myeloid leukemia (CML). Second-generation tyrosine kinase inhibitors are capable to overcome resistance mediated by most mutations except T315I. As this mutation is cau
Autor:
Zhi-guang Tu, Xiaozhong Wang, Wei-Jun Bai, Zong-Gan Huang, Shi-Qiao Zhao, Mei Shi, Wei-Xi Cao, Jian-Ming Zeng, Wen-Li Feng
Publikováno v:
DNA and Cell Biology. 30:71-78
The protein signal transducer and activator of transcription 5 (STAT5) of the JAK/STAT pathway is constitutively activated because of its phosphorylation by tyrosine kinase activity of fusion protein BCR-ABL in chronic myelogenous leukemia (CML) cell
Autor:
Zheng-lan Huang, Hui Li, Xin Wang, An-ya Dai, Wen-li Feng, Qing Xiao, Kun Tao, Miao Gao, Fang Wang, Wei-Xi Cao
Publikováno v:
Cellular signalling. 27(10)
Bcr/Abl fusion protein is a hallmark of human chronic myeloid leukemia (CML). The protein can activate various signaling pathways to make normal cells transform malignantly and thus to facilitate tumorigenesis. It has been reported that heat shock pr
Autor:
Jing, Shi, Jing, Hu, Qing, Xiao, Zhi, Peng, Wei-xi, Cao, Qiu-ping, Luo, Fang, Wang, Wen-li, Feng
Publikováno v:
Nan fang yi ke da xue xue bao = Journal of Southern Medical University. 31(11)
To construct a recombinant adenovirus vector for SH2-DED fusion gene and assess its inhibitory effect on the proliferation of K562 cells.SH2-DED fusion gene and its mutant SH2mt-DED were amplified by splicing PCR and cloned into pAdTrack-CMV plasmid
Autor:
Gui Ling Mo, Wenli Feng, Yi Xin Zhan, Ya Juan Li, Zong Ping Mo, Zheng Yu Zeng, Chaohui Hu, Chang Shun Yu, Wei Xi Cao
Publikováno v:
Clinical chemistry and laboratory medicine. 50(4)
Background The aim of this study was to establish a sensitive method that can detect the presence of not only the common but also the unusual or unknown α-globin gene deletions for screening of α-thalassemia. We used quantitative multiplex PCR of s
Autor:
Shi Qiao Zhao, Wei Jun Bai, Xiao-Zhong Wang, Shi Feng Huang, Wen Li Feng, Ya Juan Li, Zong Gan Huang, Jian Ming Zeng, Wei Xi Cao
Publikováno v:
International journal of molecular medicine. 28(2)
Deregulated activity of the BCR-ABL tyrosine kinase encoded by the Bcr-Abl oncogene represents an important therapeutic target for all the chronic myelogenous leukemia (CML) phases. In this study, we sought to identify targeted PKR activation by Bcr-
Autor:
Wei-Xi Cao, Zhi Peng, Jing Shi, Shi-Feng Huang, Wenli Feng, Ying Yuan, Hong-Wei Luo, Chun-li Li, Zong-Gan Huang
Publikováno v:
Oncology reports. 25(5)
The persistence of Bcr-Abl-positive cells in patients on imatinib therapy indicates that inhibition of the Bcr-Abl kinase activity alone might not be sufficient to eradicate the leukemia cells. Many downstream effectors of Bcr-Abl have been described
Publikováno v:
Zhonghua xue ye xue za zhi = Zhonghua xueyexue zazhi. 30(5)
To observe the effect of recombinant adenovirus-mediated wild-type p53 gene on the number and proteins of centrosome in K562 cells. To explore the possibility of application of wild-type p53 gene therapy in the treatment of chronic myeloid leukemia.T