TAM receptors in apoptotic cell clearance, autoimmunity, and cancer
Published 2013 View Full Article
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Title
TAM receptors in apoptotic cell clearance, autoimmunity, and cancer
Authors
Keywords
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Journal
AUTOIMMUNITY
Volume 46, Issue 5, Pages 294-297
Publisher
Informa UK Limited
Online
2013-05-10
DOI
10.3109/08916934.2013.794515
References
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Note: Only part of the references are listed.- Retinal pigment epithelial cells use a MerTK-dependent mechanism to limit the phagocytic particle binding activity of αvβ5 integrin
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- Complement Component C1q Regulates Macrophage Expression of Mer Tyrosine Kinase To Promote Clearance of Apoptotic Cells
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- Epithelial cell-directed efferocytosis in the post-partum mammary gland is necessary for tissue homeostasis and future lactation
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- Increased plasma levels of the soluble Mer tyrosine kinase receptor in systemic lupus erythematosus relate to disease activity and nephritis
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- PMA up-regulates the transcription of Axl by AP-1 transcription factor binding to TRE sequences via the MAPK cascade in leukaemia cells
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- R428, a Selective Small Molecule Inhibitor of Axl Kinase, Blocks Tumor Spread and Prolongs Survival in Models of Metastatic Breast Cancer
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- Tubby and tubby-like protein 1 are new MerTK ligands for phagocytosis
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- TAM receptor ligands in lupus: Protein S but not Gas6 levels reflect disease activity in systemic lupus erythematosus
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- The receptor tyrosine kinase MerTK regulates dendritic cell production of BAFF
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- Antiphosphatidylserine Antibody Combined with Irradiation Damages Tumor Blood Vessels and Induces Tumor Immunity in a Rat Model of Glioblastoma
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- The Mer receptor tyrosine kinase is expressed on discrete macrophage subpopulations and mainly uses Gas6 as its ligand for uptake of apoptotic cells
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- Glucocorticoids Induce Protein S-Dependent Phagocytosis of Apoptotic Neutrophils by Human Macrophages
- (2009) A. McColl et al. JOURNAL OF IMMUNOLOGY
- Mertk Receptor Mutation Reduces Efferocytosis Efficiency and Promotes Apoptotic Cell Accumulation and Plaque Necrosis in Atherosclerotic Lesions of Apoe −/− Mice
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