Compounds > inositol-1-4-5-trisphosphate

inositol-1-4-5-trisphosphate and Hemorrhage

inositol-1-4-5-trisphosphate has been researched along with Hemorrhage* in 2 studies

Other Studies

2 other study(ies) available for inositol-1-4-5-trisphosphate and Hemorrhage

Article	Year
ALOX12 mutation in a family with dominantly inherited bleeding diathesis. Journal of human genetics, 2021, Volume: 66, Issue:8 The arachidonic acid (AA) cascade plays a significant role in platelet aggregation. AA released from membrane phospholipids is metabolized by cyclooxygenase (COX) pathway to thromboxane A Topics: 15-Hydroxy-11 alpha,9 alpha-(epoxymethano)prosta-5,13-dienoic Acid; Arachidonate 12-Lipoxygenase; Arachidonic Acid; Blood Coagulation Disorders, Inherited; Blood Platelets; Calcium; Disease Susceptibility; Genetic Predisposition to Disease; GTP Phosphohydrolases; Hemorrhage; High-Throughput Nucleotide Sequencing; Humans; Inositol 1,4,5-Trisphosphate; Mutation; Pedigree; Phospholipase C beta; Platelet Aggregation; Prostaglandin-Endoperoxide Synthases; Signal Transduction; Thromboxane A2	2021
Defective platelet activation in G alpha(q)-deficient mice. Nature, 1997, Sep-11, Volume: 389, Issue:6647 Platelets are small disc-shaped cell fragments which undergo a rapid transformation when they encounter vascular damage. They become more spherical and extrude pseudopodia, their fibrinogen receptors are activated, causing them to aggregate, they release their granule contents, and eventually form a plug which is responsible for primary haemostasis. Activation of platelets is also implicated in the pathogenesis of unstable angina, myocardial infarction and stroke. Here we show that platelets from mice deficient in the alpha-subunit of the heterotrimeric guanine-nucleotide-binding protein Gq are unresponsive to a variety of physiological platelet activators. As a result, G alpha(q)-deficient mice have increased bleeding times and are protected from collagen and adrenaline-induced thromboembolism. We conclude that G alpha(q) is essential for the signalling processes used by different platelet activators and that it cannot be replaced by G alpha(i) or the beta gamma subunits of the heterotrimeric G proteins. G alpha(q) may thus be a new target for drugs designed to block the activation of platelets. Topics: Animals; Calcium; Enzyme Activation; GTP-Binding Proteins; Hemorrhage; In Vitro Techniques; Inositol 1,4,5-Trisphosphate; Mice; Mice, Inbred C57BL; Mutation; Platelet Activation; Signal Transduction; Thromboembolism; Type C Phospholipases	1997

Article

Year

ALOX12 mutation in a family with dominantly inherited bleeding diathesis.

Journal of human genetics, 2021, Volume: 66, Issue:8

The arachidonic acid (AA) cascade plays a significant role in platelet aggregation. AA released from membrane phospholipids is metabolized by cyclooxygenase (COX) pathway to thromboxane A

Topics: 15-Hydroxy-11 alpha,9 alpha-(epoxymethano)prosta-5,13-dienoic Acid; Arachidonate 12-Lipoxygenase; Arachidonic Acid; Blood Coagulation Disorders, Inherited; Blood Platelets; Calcium; Disease Susceptibility; Genetic Predisposition to Disease; GTP Phosphohydrolases; Hemorrhage; High-Throughput Nucleotide Sequencing; Humans; Inositol 1,4,5-Trisphosphate; Mutation; Pedigree; Phospholipase C beta; Platelet Aggregation; Prostaglandin-Endoperoxide Synthases; Signal Transduction; Thromboxane A2

2021

Defective platelet activation in G alpha(q)-deficient mice.

Nature, 1997, Sep-11, Volume: 389, Issue:6647

Platelets are small disc-shaped cell fragments which undergo a rapid transformation when they encounter vascular damage. They become more spherical and extrude pseudopodia, their fibrinogen receptors are activated, causing them to aggregate, they release their granule contents, and eventually form a plug which is responsible for primary haemostasis. Activation of platelets is also implicated in the pathogenesis of unstable angina, myocardial infarction and stroke. Here we show that platelets from mice deficient in the alpha-subunit of the heterotrimeric guanine-nucleotide-binding protein Gq are unresponsive to a variety of physiological platelet activators. As a result, G alpha(q)-deficient mice have increased bleeding times and are protected from collagen and adrenaline-induced thromboembolism. We conclude that G alpha(q) is essential for the signalling processes used by different platelet activators and that it cannot be replaced by G alpha(i) or the beta gamma subunits of the heterotrimeric G proteins. G alpha(q) may thus be a new target for drugs designed to block the activation of platelets.

Topics: Animals; Calcium; Enzyme Activation; GTP-Binding Proteins; Hemorrhage; In Vitro Techniques; Inositol 1,4,5-Trisphosphate; Mice; Mice, Inbred C57BL; Mutation; Platelet Activation; Signal Transduction; Thromboembolism; Type C Phospholipases

1997