(Q41334764)

29 September 2017

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title

Resolution of chronic inflammation by therapeutic induction of apoptosis (English)

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29 September 2017

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Anderson GP

1

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29 September 2017

publication date

1 December 1996

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Trends in Pharmacological Sciences

29 September 2017

published in

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29 September 2017

volume

17

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29 September 2017

issue

12

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29 September 2017

page(s)

438-442

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Macrophage phagocytosis of aging neutrophils in inflammation. Programmed cell death in the neutrophil leads to its recognition by macrophages

29 September 2017

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A potential mechanism of "cross-talk" between the p55 tumor necrosis factor receptor and Fas/APO1: proteins binding to the death domains of the two receptors also bind to each other

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Fas transduces activation signals in normal human T lymphocytes

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FAS-induced apoptosis is mediated via a ceramide-initiated RAS signaling pathway

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7 January 2021

FADD, a novel death domain-containing protein, interacts with the death domain of Fas and initiates apoptosis

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7 January 2021

FAP-1: a protein tyrosine phosphatase that associates with Fas

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T cell receptor-induced Fas ligand expression in cytotoxic T lymphocyte clones is blocked by protein tyrosine kinase inhibitors and cyclosporin A

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Bcl-2 is an inner mitochondrial membrane protein that blocks programmed cell death

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7 January 2021

ICE/CED3-like proteases as therapeutic targets for the control of inappropriate apoptosis

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Fas(CD95)/FasL interactions required for programmed cell death after T-cell activation.

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Extracellular Matrix Proteins Regulate Morphologic and Biochemical Properties of Tracheal Gland Serous Cells through Integrins

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7 January 2021

Eosinophil hematopoietins antagonize the programmed cell death of eosinophils. Cytokine and glucocorticoid effects on eosinophils maintained by endothelial cell-conditioned medium

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Activation of the Fas receptor on lung eosinophils leads to apoptosis and the resolution of eosinophilic inflammation of the airways

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Expansion of cytokine-producing CD4-CD8- T cells associated with abnormal Fas expression and hypereosinophilia.

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7 January 2021

10.1016/S0165-6147(96)01004-8

Identifiers

DOI

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29 September 2017

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