![]() Despite winning a great victory against the pirates in 1555, he quickly fell from power by running afoul of the domineering clique of Yan Song and Zhao Wenhua, and was executed by the Jiajing Emperor later in the same year.Ī native of Houguan county (侯官縣 present-day Fuzhou) of Fujian province, Zhang Jing was noted as a man of tall stature. At the height of his power, he was in charge of the military in six provinces, an unprecedented number in the Ming dynasty. As he climbed the ladder of Chinese bureaucracy, he became in charge of several provinces as supreme commander, and was involved in the conflicts such as the suppression of the Yao rebellions in the southwestern frontier and the defence of China from wokou pirates. Blood, 118: 368-379, 2011.Zhang Jing (張經 died 12 November 1555), going by the name Cai Jing ( 蔡經) for much of his life, was a Chinese official who served the Ming dynasty. Endogenous Oncogenic Nras Mutation Initiates Hematopoietic Malignancies in a Dose- and Cell Type-Dependent Manner. H., Ranheim, E., Chang, Q., and Zhang, J. Cis-Element Mutated in GATA2-Dependent Immunodeficiency Governs Hematopoiesis and Vascular Integrity. Signaling Profiling at the Single-Cell Level Identifies a Distinct Signaling Signature in Murine Hematopoietic Stem Cells. Du, J., Wang, J., Kong, G., Jiang, J., Zhang, J., Liu, Y., Tong, W., and Zhang, J.NrasG12D/+ Promotes Leukemogenesis by Aberrantly Regulating Hematopoietic Stem Cell Functions. K., Meloche, S., Damnernsawad, A., Zhang, J., and Zhang, J. Combined MEK and JAK Inhibition Abrogates Murine Myeloproliferative Neoplasm. R., Zhang, X., Juckett, M., Mattison, R., Damnernsawad, A., Zhang, J., Mulloy, J. Kong, G., Wunderlich, M., Yang, D., Ranheim, E. ![]() Oncogenic K-ras mutations further co-operate with additional genetic change(s) occurring in lineage-committed progenitors to initiate and maintain hematopoietic malignant phenotypes. Based on our preliminary results, we hypothesize that when oncogenic K-ras mutations act as the 1st hit in leukemogenesis, its primary target is HSCs. Using recipient mice transplanted with bone marrow cells expressing oncogenic K-ras from its endogenous promoter, we found that oncogenic K-ras mutations induce hematopoietic malignancies in multiple lineages. ![]() However, its precise roles in leukemogenesis and leukemia progression remain elusive. The oncogenic mutations in the K-ras gene are acquired either as the first genetic change (1st hit) during leukemogenesis or one of the later genetic changes during leukemia progression. K-ras is one of the most frequently mutated genes identified in human patients with various hematopoietic malignancies. One of the molecules we have been studying is K-ras. My laboratory focuses on studying the mechanisms underlying the normal as well as oncogenic self-renewal of stem cells using the hematopoietic compartment as a model system.
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