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Videos de Conceptos Relacionados

Overview of Cell Death01:30

Overview of Cell Death

7.4K
Cell death is an essential process where the body gets rid of old or damaged cells. Cell proliferation and death need to be balanced, as an imbalance between the two may lead to cancer or autoimmune diseases.
Cell death was observed in the early 19th century, but there was no experimental evidence to prove it. In 1842, Carl Vogt first discovered cell death in a metamorphic toad; however, it was not termed ‘cell death.’ Scientists discovered different cell death pathways only in the...
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Negative Regulator Molecules01:23

Negative Regulator Molecules

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Positive regulators allow a cell to advance through cell cycle checkpoints. Negative regulators have an equally important role as they terminate a cell’s progression through the cell cycle—or pause it—until the cell meets specific criteria.
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The Extrinsic Apoptotic Pathway01:17

The Extrinsic Apoptotic Pathway

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The extrinsic apoptotic pathway is initiated when extracellular death-inducing signals, such as specific cytokines, activate the death receptors expressed on the cell surface. The immune cells involved in this pathway are natural killer cells (NK cells) and cytotoxic T-lymphocytes. NK cells are critical in innate immune response, while cytotoxic T-lymphocytes are associated with adaptive immune response. These cells recognize specific receptors expressed on the altered cells and activate...
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Replicative Cell Senescence02:15

Replicative Cell Senescence

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Replicative cell senescence is a property of cells that allows them to divide a finite number of times throughout the organism's lifespan while preventing excessive proliferation. Replicative senescence is associated with the gradual loss of the telomere — short, repetitive DNA sequences found at the end of the chromosomes. Telomeres are bound by a group of proteins to form a protective cap on the ends of chromosomes. Embryonic stem cells express telomerase — an enzyme that adds...
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DNA Damage can Stall the Cell Cycle02:37

DNA Damage can Stall the Cell Cycle

9.2K
In response to DNA damage, cells can pause the cell cycle to assess and repair the breaks. However, the cell must check the DNA at certain critical stages during the cell cycle. If the cell cycle pauses before DNA replication, the cells will contain twice the amount of DNA. On the other hand, if cells arrest after DNA replication but before mitosis, they will contain four times the normal amount of DNA. With a host of specialized proteins at their disposal,cells must use the right protein at...
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Molecular Factors Affecting Cell Division01:27

Molecular Factors Affecting Cell Division

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Several external and internal factors influence the initiation and inhibition of cell division. For instance, the death of nearby cells or the release of human growth hormone (hGH) promotes cell division. In contrast, lack of hGH or crowding of cells can inhibit cell division.
Several proteins function as internal regulators to ensure each cell cycle stage is completed faithfully before proceeding to the next. Regulator molecules may act directly or influence the activity or production of other...
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Video Experimental Relacionado

Updated: Jul 25, 2025

Strategies for Tracking Anastasis, A Cell Survival Phenomenon that Reverses Apoptosis
12:55

Strategies for Tracking Anastasis, A Cell Survival Phenomenon that Reverses Apoptosis

Published on: February 16, 2015

18.1K

Detener la muerte celular

D Grahame Hardie1

  • 1School of Life Sciences, University of Dundee, Dundee, Scotland, UK.

Science (New York, N.Y.)
|June 29, 2023
PubMed
Resumen

La señalización de estrés energético se opone a las vías programadas de muerte celular como la necroptosis. Este descubrimiento revela un nuevo mecanismo que regula el destino celular durante los desafíos metabólicos.

Área de la Ciencia:

  • Biología celular
  • El metabolismo
  • Inmunología

Sus antecedentes:

  • La muerte celular necroptótica es una forma regulada de necrosis.
  • Los niveles de energía celular influyen en las vías de supervivencia y muerte celular.

Objetivo del estudio:

  • Investigar el papel de la detección del estrés energético en la regulación de la necroptosis.
  • Para identificar las vías de señalización que vinculan el estado metabólico con la muerte celular.

Principales métodos:

  • Se utilizaron modelos de cultivo celular.
  • Empleó técnicas de biología molecular para estudiar las vías de señalización.
  • Se evaluaron los marcadores de muerte celular y los indicadores metabólicos.

Principales resultados:

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Detecting Anastasis In Vivo by CaspaseTracker Biosensor
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Detecting Anastasis In Vivo by CaspaseTracker Biosensor

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Identification of Intracellular Signaling Events Induced in Viable Cells by Interaction with Neighboring Cells Undergoing Apoptotic Cell Death
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Identification of Intracellular Signaling Events Induced in Viable Cells by Interaction with Neighboring Cells Undergoing Apoptotic Cell Death

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Last Updated: Jul 25, 2025

Strategies for Tracking Anastasis, A Cell Survival Phenomenon that Reverses Apoptosis
12:55

Strategies for Tracking Anastasis, A Cell Survival Phenomenon that Reverses Apoptosis

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Detecting Anastasis In Vivo by CaspaseTracker Biosensor
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Detecting Anastasis In Vivo by CaspaseTracker Biosensor

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Identification of Intracellular Signaling Events Induced in Viable Cells by Interaction with Neighboring Cells Undergoing Apoptotic Cell Death
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Identification of Intracellular Signaling Events Induced in Viable Cells by Interaction with Neighboring Cells Undergoing Apoptotic Cell Death

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  • Se identificó una vía de señalización específica activada por el estrés energético.
  • Se encontró que esta vía inhibe los mediadores clave de la necroptosis.
  • La inhibición de la necroptosis está correlacionada con los niveles de energía celular.

Conclusiones:

  • El estado de energía celular regula activamente la muerte celular necroptótica.
  • Se describe un nuevo eje de señalización que conecta la detección de energía con el control de la muerte celular.
  • Esta vía representa un objetivo potencial para modular la muerte celular en la enfermedad.