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Related Concept Videos

Structure and Function of Platelets01:18

Structure and Function of Platelets

The cell fragments known as platelets are disc-shaped, with an average diameter of about 3 μm and a thickness of roughly 1 μm. They play a crucial role in the body's vascular clotting system, which also involves plasma proteins, blood cells, and blood vessel tissues.
Platelets are continually replenished, circulating in the bloodstream for 9-12 days before being removed by phagocytes, primarily in the spleen. A microliter of circulating blood contains between 150,000 and 450,000 platelets, with...
Regulation of Nuclear Protein Sorting01:45

Regulation of Nuclear Protein Sorting

Nuclear protein sorting regulates nucleus composition and gene expression, crucial for determining the fate of a eukaryotic cell. Hence, the entry and exit of molecules across the nuclear envelope is a tightly controlled process. Nuclear protein sorting can be inhibited by one of the following ways: 1) masking cargo signal sequences, 2) modifying the nuclear receptor's affinity for cargo, 3) controlling the nuclear pore size, 4) retaining the cargo during its transit to the cytosol or the...
Formation of the Platelet Plug01:22

Formation of the Platelet Plug

The platelet phase, the second stage of hemostasis, commences around 15-20 seconds after an injury. It follows and overlaps with the vascular phase, during which blood vessels constrict to minimize blood loss.
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Role of Hematopoietic Growth Factors01:28

Role of Hematopoietic Growth Factors

Hematopoietic growth factors are molecules that regulate the differentiation rate of hematopoietic stem cells (HSCs). Erythropoietin (EPO), primarily produced by the kidneys, plays a crucial role in erythrocyte production. When oxygen levels in the blood are low, EPO is released into the bloodstream, reaching the bone marrow, where it stimulates HSCs to differentiate and mature into erythrocytes, which are vital for oxygen transport.
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Additional Subnuclear Structures02:10

Additional Subnuclear Structures

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Related Experiment Video

Updated: Jun 17, 2026

Megakaryocyte Differentiation and Platelet Formation from Human Cord Blood-derived CD34+ Cells
09:46

Megakaryocyte Differentiation and Platelet Formation from Human Cord Blood-derived CD34+ Cells

Published on: December 27, 2017

Platelets and megakaryocytes contain functional nuclear factor-kappaB.

Sherry L Spinelli1, Ann E Casey, Stephen J Pollock

  • 1Department of Environmental Medicine, Box 850, University of Rochester School of Medicine and Dentistry, 601 Elmwood Avenue, Rochester, New York 14642, USA.

Arteriosclerosis, Thrombosis, and Vascular Biology
|January 1, 2010
PubMed
Summary
This summary is machine-generated.

Nuclear factor-kappaB (NF-kappaB) proteins are present in platelets and influence their function in blood clot formation. NF-kappaB inhibitors, used for inflammation and cancer, may affect platelet activity, suggesting NF-kappaB as a target for controlling platelet activation.

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Last Updated: Jun 17, 2026

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Leukodepletion Filters-Derived CD34+ Cells As a Cell Source to Study Megakaryocyte Differentiation and Platelet Formation
06:57

Leukodepletion Filters-Derived CD34+ Cells As a Cell Source to Study Megakaryocyte Differentiation and Platelet Formation

Published on: May 20, 2021

Area of Science:

  • Hematology
  • Molecular Biology
  • Cellular Biology

Background:

  • Nuclear factor-kappaB (NF-kappaB) is a transcription factor family known for regulating inflammation and cell survival.
  • NF-kappaB proteins, including inhibitor-kappaB (I-kappaB) and I-kappa kinase (IKK) molecules, are expressed in human megakaryocytes and platelets.

Purpose of the Study:

  • To investigate the presence and functional role of NF-kappaB proteins in megakaryocytes and platelets.
  • To determine the impact of NF-kappaB signaling on platelet functions crucial for vascular injury repair and thrombus formation.

Main Methods:

  • Human megakaryocytes and platelets were analyzed for NF-kappaB family member expression.
  • Platelet functions were assessed following exposure to NF-kappaB inhibitors, including BAY-11-7082, which inhibits I-kappaB-alpha phosphorylation.
  • Recombinant IKK-beta and I-kappaB-alpha proteins were added to treated platelets to evaluate functional restoration.

Main Results:

  • NF-kappaB inhibition impaired platelet functions such as lamellipodia formation, clot retraction, and thrombus stability.
  • Inhibition of I-kappaB-alpha phosphorylation by BAY-11-7082 caused platelets to revert from a spread to a spheroid morphology.
  • Restoration of platelet spreading was partially achieved by adding recombinant IKK-beta or I-kappaB-alpha, and active IKK-beta increased endogenous I-kappaB-alpha phosphorylation.

Conclusions:

  • The NF-kappaB family plays a significant, nonclassical role in regulating platelet function.
  • Platelets are sensitive to NF-kappaB inhibitors, which may have unintended consequences when these drugs are used for anti-inflammatory or anticancer therapies.
  • NF-kappaB represents a novel therapeutic target for modulating excessive platelet activation.