Related Experiment Video

Updated: Dec 24, 2025

Yeast As a Chassis for Developing Functional Assays to Study Human P53
14:57

Yeast As a Chassis for Developing Functional Assays to Study Human P53

Published on: August 4, 2019

9.9K

DNAJB9 Inhibits p53-Dependent Oncogene-Induced Senescence and Induces Cell Transformation

Hyeon Ju Lee1, Yu-Jin Jung2, Seungkoo Lee3

  • 1Department of Biochemistry and Molecular Biology, Kangwon National University School of Medicine, Chuncheon 24341, Korea.

Molecules and Cells
|April 9, 2020
PubMed

Insights

DNAJB9 inhibits p53-dependent oncogene-induced senescence (OIS) and promotes cell transformation by interacting with p53 under strong mitogenic signals. This molecular chaperone

Area of Science:

  • Molecular biology
  • Cellular senescence
  • Oncogenesis

Background:

  • DNAJB9 is a molecular chaperone with incompletely understood cellular functions.
  • Strong mitogenic signals can trigger cellular responses like oncogene-induced senescence (OIS).

Purpose of the Study:

  • To investigate the cellular function of DNAJB9 under strong mitogenic signals.
  • To elucidate the role of DNAJB9 in oncogene-induced senescence and neoplastic transformation.

Main Methods:

  • Primary mouse fibroblasts were utilized.
  • Experiments involved oncogenic RAS activation.
  • Physical interactions between DNAJB9 and p53 were assessed.

Main Results:

  • DNAJB9 was found to inhibit p53-dependent OIS.
  • DNAJB9 induced neoplastic transformation in the presence of oncogenic RAS.
  • DNAJB9 physically interacts with p53, and this interaction is crucial for its functions.

Conclusions:

  • DNAJB9 promotes cell transformation by inhibiting p53-dependent OIS through physical interaction with p53.
  • Understanding DNAJB9's role in cell transformation provides insights into molecular chaperone function and oncogenesis.
Keywords:
DNAJB9RASp53senescencetransformation

More Related Videos

Techniques to Induce and Quantify Cellular Senescence06:51

Techniques to Induce and Quantify Cellular Senescence

Published on: May 1, 2017

34.7K
Induction and Validation of Cellular Senescence in Primary Human Cells08:18

Induction and Validation of Cellular Senescence in Primary Human Cells

Published on: June 20, 2018

17.8K

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...
5.0K
Negative Regulator Molecules01:23

Negative Regulator Molecules

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.
38.1K
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...
9.9K
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...
3.0K
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...
8.0K
Inhibition of Cdk Activity02:34

Inhibition of Cdk Activity

The orderly progression of the cell cycle depends on the activation of Cdk protein by binding to its cyclin partner. However, the cell cycle must be restricted when undergoing abnormal changes. Most cancers correlate to the deregulated cell cycle, and since Cdks are a central component of the cell cycle, Cdk inhibitors are extensively studied to develop anticancer agents. For instance, cyclin D associates with several Cdks, such as Cdk 4/6, to form an active complex. The cyclin D-Cdk4/6 complex...
5.5K