Cathepsin G activates protease-activated receptor-4 in human platelets (Q22253276)

GOA release 2020-03-11

signal transduction

1 reference

GOA release 2020-03-11

G R Sambrano

1

G R

Sambrano

1 reference

8 February 2023

W Huang

2

W

Huang

1 reference

8 February 2023

T Faruqi

3

T

Faruqi

1 reference

8 February 2023

S Mahrus

4

S

Mahrus

1 reference

8 February 2023

C Craik

5

C

Craik

1 reference

8 February 2023

S R Coughlin

6

S R

Coughlin

1 reference

Journal of Biological Chemistry

8 February 2023

language of work or name

English

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publication date

10 March 2000

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published in

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volume

275

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issue

10

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page(s)

6819-23

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17 The kinetics of reversible tight-binding inhibition

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Molecular cloning of a functional thrombin receptor reveals a novel proteolytic mechanism of receptor activation

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Susceptibility to infection and altered hematopoiesis in mice deficient in both P- and E-selectins

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Human neutrophil cathepsin G is a potent platelet activator

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Development of potent thrombin receptor antagonist peptides

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A dual thrombin receptor system for platelet activation

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Protease-activated receptor 3 is a second thrombin receptor in humans

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Cathepsin G binding to human platelets. Evidence for a specific receptor

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Intracellular Ca2+ rise in human platelets induced by polymorphonuclear-leucocyte-derived cathepsin G.

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Cathepsin G and thrombin: evidence for two different platelet receptors

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Molecular cloning of a potential proteinase activated receptor

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Cloning and characterization of human protease-activated receptor 4

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Proteolysis of the human platelet and endothelial cell thrombin receptor by neutrophil-derived cathepsin G.

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The cloned thrombin receptor is necessary and sufficient for activation of mitogen-activated protein kinase and mitogenesis in mouse lung fibroblasts. Loss of responses in fibroblasts from receptor knockout mice

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Human neutrophil elastase proteolytically activates the platelet integrin alphaIIbbeta3 through cleavage of the carboxyl terminus of the alphaIIb subunit heavy chain. Involvement in the potentiation of platelet aggregation

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Thrombin-induced events in non-platelet cells are mediated by the unique proteolytic mechanism established for the cloned platelet thrombin receptor

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Cell surface-bound elastase and cathepsin G on human neutrophils: a novel, non-oxidative mechanism by which neutrophils focus and preserve catalytic activity of serine proteinases

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Protease-activated receptors 1 and 4 mediate activation of human platelets by thrombin

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