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Publication : PALLD Regulates Phagocytosis by Enabling Timely Actin Polymerization and Depolymerization.

First Author  Sun HM Year  2017
Journal  J Immunol Volume  199
Issue  5 Pages  1817-1826
PubMed ID  28739877 Mgi Jnum  J:251079
Mgi Id  MGI:6100180 Doi  10.4049/jimmunol.1602018
Citation  Sun HM, et al. (2017) PALLD Regulates Phagocytosis by Enabling Timely Actin Polymerization and Depolymerization. J Immunol 199(5):1817-1826
abstractText  PALLD is an actin cross-linker supporting cellular mechanical tension. However, its involvement in the regulation of phagocytosis, a cellular activity essential for innate immunity and physiological tissue turnover, is unclear. We report that PALLD is highly induced along with all-trans-retinoic acid-induced maturation of myeloid leukemia cells, to promote Ig- or complement-opsonized phagocytosis. PALLD mechanistically facilitates phagocytic receptor clustering by regulating actin polymerization and c-Src dynamic activation during particle binding and early phagosome formation. PALLD is also required at the nascent phagosome to recruit phosphatase oculocerebrorenal syndrome of Lowe, which regulates phosphatidylinositol-4,5-bisphosphate hydrolysis and actin depolymerization to complete phagosome closure. Collectively, our results show a new function for PALLD as a crucial regulator of the early phase of phagocytosis by elaborating dynamic actin polymerization and depolymerization.
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