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[Abnormal Notch-Hes Signaling Pathways and Acute Leukemia -Review].
Gu, Zhen-Yang; Wang, Li; Gao, Chun-Ji.
Afiliação
  • Gu ZY; Department of Hematology, Chinese PLA Medical School & Chinese PLA General Hospital, Beijing 100853, China.
  • Wang L; Department of Hematology, Chinese PLA Medical School & Chinese PLA General Hospital, Beijing 100853, China.
  • Gao CJ; Department of Hematology, Chinese PLA Medical School & Chinese PLA General Hospital, Beijing 100853, China. E-mail: gaochunji@hotmail.com.
Zhongguo Shi Yan Xue Ye Xue Za Zhi ; 25(1): 240-243, 2017 Feb.
Article em Zh | MEDLINE | ID: mdl-28245409
ABSTRACT
The abnormal activation of Notch signaling is closely related to the development of acute leukemia (AL). The core elements of the Notch signaling system include Notch receptors, Notch ligands, CSL DNA-binding proteins, and effectors like target genes. Any factors, which affect ligands, receptors, signal transducers and effectors, can influence the signal transduction of Notch signaling greatly. Based on the role of Notch signaling in AL, several targeted drugs against Notch upstream signaling have been developed. However, due to the complexity and pleiotropic effects of Notch upstream signaling, these targeted drugs display strong side effects. Thus, Hes (Hairy Enhancer of Split) factors as a primary Notch effector, also play an important role in the pathogenesis of AL. This review summarizes recent progresses on Notch-Hes signaling in AL, hopping to provide references for further excavation of the Notch-Hes signaling, and lay foundations for developing the next generation of targeted drugs.
Assuntos

Texto completo: 1 Coleções: 01-internacional Base de dados: MEDLINE Assunto principal: Transdução de Sinais / Leucemia / Receptores Notch Limite: Humans Idioma: Zh Ano de publicação: 2017 Tipo de documento: Article

Texto completo: 1 Coleções: 01-internacional Base de dados: MEDLINE Assunto principal: Transdução de Sinais / Leucemia / Receptores Notch Limite: Humans Idioma: Zh Ano de publicação: 2017 Tipo de documento: Article