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Related Concept Videos

Abnormal Proliferation02:23

Abnormal Proliferation

Under normal conditions, most adult cells remain in a non-proliferative state unless stimulated by internal or external factors to replace lost cells. Abnormal cell proliferation is a condition in which the cell's growth exceeds and is uncoordinated with normal cells. In such situations, cell division persists in the same excessive manner even after cessation of the stimuli, leading to persistent tumors. The tumor arises from the damaged cells that replicate to pass the damage to the daughter...
The Intrinsic Apoptotic Pathway01:31

The Intrinsic Apoptotic Pathway

Internal cellular stress, such as cellular injury or hypoxia, triggers intrinsic apoptosis. The B-cell lymphoma 2 (Bcl-2) family of proteins are the primary regulators of the intrinsic apoptotic pathway. For example, during DNA damage, checkpoint proteins, such as Ataxia Telangiectasia Mutated (ATM protein) and Checkpoints Factor-2 (Chk2) proteins, are activated. These proteins phosphorylate p53 which further activates pro-apoptotic proteins, such as Bax, Bak, PUMA, and Noxa, and inhibits...
DNA Damage can Stall the Cell Cycle02:36

DNA Damage can Stall the Cell Cycle

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...
DNA Damage Can Stall the Cell Cycle02:36

DNA Damage Can Stall the Cell Cycle

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...
Interactions Between Signaling Pathways01:19

Interactions Between Signaling Pathways

Signaling cascades usually lack linearity. Multiple pathways interact and regulate one another, allowing cells to integrate and respond to diverse environmental stimuli.
Convergence and divergence, and cross-talk between signaling pathways
Two distinct signaling pathways can converge on a single functional unit, which may either be a single protein or a complex of proteins. The response is either functionally distinct or synergistic between the two pathways but different from the response...
PI3K/mTOR/AKT Signaling Pathway01:22

PI3K/mTOR/AKT Signaling Pathway

The mammalian target of rapamycin  (mTOR) is a serine/threonine kinase that regulates growth, proliferation, and cell survival in response to hormones, growth factors, or nutrient availability. This kinase exists in two structurally and functionally distinct forms: mTOR complex 1  (mTORC1) and mTOR complex 2  (mTORC2). The first form (mTORC1) is composed of a rapamycin-sensitive Raptor and proline-rich Akt substrate, PRAS40. In contrast,  mTORC2 consists of a rapamycin-insensitive companion...

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Related Experiment Video

Updated: Jun 6, 2026

Deacetylation Assays to Unravel the Interplay between Sirtuins (SIRT2) and Specific Protein-substrates
14:32

Deacetylation Assays to Unravel the Interplay between Sirtuins (SIRT2) and Specific Protein-substrates

Published on: February 27, 2016

SIRT2 down-regulation in HeLa can induce p53 accumulation via p38 MAPK activation-dependent p300 decrease, eventually

Yanze Li1, Haruka Matsumori, Yuji Nakayama

  • 1Division of Human Genome Science, Department of Molecular and Cellular Biology, School of Life Sciences, Faculty of Medicine, Tottori University, 86 Nishi-cho, Yonago, Tottori 683-8503, Japan.

Genes to Cells : Devoted to Molecular & Cellular Mechanisms
|November 10, 2010
PubMed
Summary
This summary is machine-generated.

Sirtuin 2 (SIRT2) down-regulation induces cancer cell apoptosis via p53 accumulation, suggesting SIRT2 as a novel cancer therapy target. This mechanism differs from its known role in cell division regulation.

Related Experiment Videos

Last Updated: Jun 6, 2026

Deacetylation Assays to Unravel the Interplay between Sirtuins (SIRT2) and Specific Protein-substrates
14:32

Deacetylation Assays to Unravel the Interplay between Sirtuins (SIRT2) and Specific Protein-substrates

Published on: February 27, 2016

Area of Science:

  • Molecular Biology
  • Cancer Research
  • Biochemistry

Background:

  • Sirtuin 2 (SIRT2) is an NAD+-dependent deacetylase involved in mitotic regulation and spindle checkpoint-mediated cell death.
  • Sirtuin inhibitors are investigated as anticancer agents, primarily targeting SIRT1's role in p53 deacetylation and cell survival.

Purpose of the Study:

  • To investigate a novel, non-mitotic function of SIRT2.
  • To explore SIRT2's potential as a molecular target for cancer therapy.

Main Methods:

  • Utilized siRNA to down-regulate SIRT2 expression in cancer cell lines (e.g., HeLa) and normal cells.
  • Assessed apoptosis induction and investigated the underlying molecular mechanisms involving p53, p38 MAPK, p300, and MDM2.

Main Results:

  • SIRT2 down-regulation induced apoptosis specifically in cancer cell lines, not in normal cells.
  • Apoptosis resulted from p53 accumulation, mediated by p38 MAPK-activated degradation of p300 and subsequent MDM2 degradation.

Conclusions:

  • SIRT2 possesses a novel function distinct from its role in mitotic regulation, capable of inducing cancer cell-specific apoptosis.
  • The findings establish SIRT2 as a promising molecular target for cancer therapy, providing a mechanistic basis for its therapeutic potential.