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Adhesion via CD43 induces Syk activation and cell proliferation in TF-1 cells.

作者信息

Miura Y, Mizutani C, Nishihara T, Hishita T, Yanagi S, Tohyama Y, Ichiyama S, Yamamura H, Uchiyama T, Tohyama K

机构信息

Department of Hematology and Oncology, Graduate School of Medicine, Kyoto University, Sakyo-ku, Kyoto 606-8507, Japan.

出版信息

Biochem Biophys Res Commun. 2001 Oct 19;288(1):80-6. doi: 10.1006/bbrc.2001.5729.

Abstract

The effect of adhesion via CD43 (leukosialin, sialophorin) on cell proliferation and phosphorylation signaling were examined in a growth factor-dependent hematopoietic progenitor cell line, TF-1. TF-1 cells promptly resulted in death after withdrawal of growth factors. However, the viable cell number increased when TF-1 cells were cultured on anti-CD43 monoclonal antibody-coated plates. In this case, sustained activation of protein tyrosine kinase Syk and extracellular signal-regulated kinase (Erk) 1/2 were detected. Overexpression of exogenous Syk on TF-1 cells by the adenovirus vector system induced enhancement of the cell proliferation accompanied with enhancement of the Erk activation by a dominant-positive effect. The signal transducer and activator of transcription (STAT) 5 seemed not to be associated with the CD43-mediated cell proliferation. These results indicated that adhesion via CD43 induces the proliferation of TF-1 cells in the absence of growth factors in part by Syk-dependent Erk 1/2 signaling.

摘要

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