Molecular association of CD98, CD29, and CD147 critically mediates monocytic U937 cell adhesion.
Molecular association of CD98, CD29, and CD147 critically mediates monocytic U937 cell adhesion.
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DOI:
10.4196/kjpp.2016.20.5.515
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发表时间:
2016-09
期刊:
影响因子:
--
通讯作者:
Cho JY
中科院分区:
文献类型:
--
作者:
Kim MY;Cho JY
Adhesion events of monocytes represent an important step in inflammatory responses induced by chemokines. The β1-integrin CD29 is a major adhesion molecule regulating leukocyte migration and extravasation. Although several adhesion molecules have been known as regulators of CD29, the molecular interactions between CD29 and its regulatory adhesion molecules (such as CD98 and CD147) have not been fully elucidated. Therefore, in this study, we examined whether these molecules are functionally, biochemically, and cell-biologically associated using monocytic U937 cells treated with aggregation-stimulating and blocking antibodies, as well as enzyme inhibitors. The surface levels of CD29, CD98, and CD147 (but not CD43, CD44, and CD82) were increased. The activation of CD29, CD98, and CD147 by ligation of them with aggregation-activating antibodies triggered the induction of cell-cell adhesion, and sensitivity to various enzyme inhibitors and aggregation-blocking antibodies was similar for CD29-, CD98-, and CD147-induced U937 cell aggregation. Molecular association between these molecules and the actin cytoskeleton was confirmed by confocal microscopy and immunoprecipitation. These results strongly suggest that CD29 might be modulated by its biochemical and cellular regulators, including CD98 and CD147, via the actin cytoskeleton.
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影响因子:
6
作者:
Kim CH;Park J;Kim M
通讯作者:
Kim M
影响因子:
--
作者:
Khayati F;Pérez-Cano L;Maouche K;Sadoux A;Boutalbi Z;Podgorniak MP;Maskos U;Setterblad N;Janin A;Calvo F;Lebbé C;Menashi S;Fernandez-Recio J;Mourah S
通讯作者:
Mourah S
影响因子:
6
作者:
Italiani P;Boraschi D
通讯作者:
Boraschi D
影响因子:
3.7
作者:
Chiang YJ;Ho KC;Sun CT;Chiu JJ;Lee FJ;Liao F;Yang-Yen HF;Yen JJ
通讯作者:
Yen JJ
影响因子:
20.3
作者:
Cho, JY;Fox, DA;Chain, B
通讯作者:
Chain, B