関連する実験動画

Updated: Jul 21, 2026

A Novel In vitro Model for Studying the Interactions Between Human Whole Blood and Endothelium
06:27

A Novel In vitro Model for Studying the Interactions Between Human Whole Blood and Endothelium

Published on: November 21, 2014

血液凝固の改訂モデルにおけるXI因子の活性化

D Gailani1, G J Broze

  • 1Department of Medicine, Jewish Hospital, Washington University Medical Center, St. Louis, MO 63110.

Science (New York, N.Y.)
|September 2, 1991
PubMed
まとめ

トロンビンは,因子XIIaではなく,血液凝固因子XIの主要な活性化因子である. この改訂された凝固モデルでは,XI因子の活性化におけるトロンビンの重要な役割が強調され,出血障害の研究に影響を与えています.

さらに関連する動画

Analyzing the Interaction of Fluorescent-Labeled Proteins with Artificial Phospholipid Microvesicles using Quantitative Flow Cytometry08:26

Analyzing the Interaction of Fluorescent-Labeled Proteins with Artificial Phospholipid Microvesicles using Quantitative Flow Cytometry

Published on: April 6, 2022

Extracellular Vesicle Tissue Factor Activity Assay03:53

Extracellular Vesicle Tissue Factor Activity Assay

Published on: December 29, 2023

関連する概念動画

Intracellular Signaling Affects Focal Adhesions01:17

Intracellular Signaling Affects Focal Adhesions

Integrins act both as extracellular input receivers and as intracellular processing activators. As their name suggests, integrins are entirely integrated into the membrane structure. Their hydrophobic membrane-spanning regions interact with the phospholipid bilayer's hydrophobic region. These membrane receptors provide extracellular attachment sites for effectors like hormones and growth factors. They activate intracellular response cascades when their effectors are bound and active.
Some...
Extrinsic and Intrinsic Pathways of Hemostasis01:20

Extrinsic and Intrinsic Pathways of Hemostasis

Blood clotting or coagulation involves extrinsic and intrinsic pathways, which ultimately merge into the common pathway, forming a fibrin clot.
The Extrinsic Pathway
The extrinsic pathway of coagulation is typically initiated by tissue damage that exposes blood to tissue factor (TF), a protein released by the damaged tissue cells outside the blood vessels—this interaction with TF triggers biochemical reactions involving specific clotting factors. The key player here is Factor VII, which forms a...
Clot Retraction and Fibrinolysis01:16

Clot Retraction and Fibrinolysis

After a fibrin clot is formed, the next step is clot retraction, a vital process facilitated by platelet contractile proteins, such as actin and myosin. These proteins pull the fibrin strands closer together and condense the clot. This action reduces the size of the clot, creating a smaller, denser structure that effectively seals off the damaged vessel. Clot retraction consolidates the clot and helps with wound healing by bringing the edges of the damaged blood vessel closer together.