The laminin receptor modulates granulocyte-macrophage colony-stimulating factor receptor complex formation and modulates its signaling

被引:23
作者
Chen, J
Càrcamo, JM
Bórquez-Ojeda, O
Erdjument-Bromage, H
Tempst, P
Golde, DW [1 ]
机构
[1] Cornell Univ, Weill Grad Sch Med Sci, Dept Pharmacol, New York, NY 10021 USA
[2] Mem Sloan Kettering Canc Ctr, Program Mol Pharmacol & Chem, New York, NY 10021 USA
[3] Mem Sloan Kettering Canc Ctr, Dept Clin Labs, New York, NY 10021 USA
[4] Mem Sloan Kettering Canc Ctr, Program Mol Biol, New York, NY 10021 USA
关键词
D O I
10.1073/pnas.2334584100
中图分类号
O [数理科学和化学]; P [天文学、地球科学]; Q [生物科学]; N [自然科学总论];
学科分类号
07 ; 0710 ; 09 ;
摘要
Basement membrane matrix proteins are known to up-regulate granulocyte-macrophage colony-stimulating factor (GM-CSF) signaling in neutrophils and mononuclear phagocytes, but the mechanisms involved are poorly understood. We used the intracellular portion of the alpha subunit of the GM-CSF receptor(alphaGMR) to search for interacting proteins and identified the 67-kDa laminin receptor (LR), a nonintegrin matrix protein receptor expressed in several types of host defense cells and certain tumors, as a binding partner. LR was found to interact with the beta subunit of the GMR (betaGMR) as well. Whereas GM-CSF functions by engaging the aGMR and betaGMR into receptor complexes, LR inhibited GM-CSF-induced receptor complex formation. Laminin and fibronectin binding to LR was found to prevent the binding of betaGMR to LR and relieved the LR inhibition of GMR. These findings provide a mechanistic basis for enhancing host defense cell responsiveness to GM-CSF at transendothelial migration sites while suppressing it in circulation.
引用
收藏
页码:14000 / 14005
页数:6
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