Focal adhesion kinase versus p53: apoptosis or survival?

Related Experiment Video

Updated: Jul 5, 2026

Knockdown of FAM83A to Verify Its Role in Cervical Cancer Cell Growth and Cisplatin Sensitivity
04:20

Knockdown of FAM83A to Verify Its Role in Cervical Cancer Cell Growth and Cisplatin Sensitivity

Published on: February 9, 2024

William G Cance1, Vita M Golubovskaya

  • 1Department of Surgery, University of Florida, School of Medicine, Gainesville, FL 32610, USA. cance@surgery.ufl.edu

Science Signaling
|May 22, 2008
PubMed

Insights

Focal adhesion kinase (FAK) sequesters the tumor suppressor p53, inhibiting apoptosis and promoting cell survival. This kinase-independent interaction reveals new insights into cell signaling and cancer research.

Area of Science:

  • Cell Biology
  • Molecular Biology
  • Biochemistry

Background:

  • Focal adhesion kinase (FAK) is a tyrosine kinase crucial for cell survival.
  • FAK interacts with numerous signaling partners, including the tumor suppressor p53.
  • p53 binds FAK's amino-terminal domain and promoter, inhibiting FAK transcription.

Purpose of the Study:

  • To investigate the biological implications of the kinase-independent interaction between FAK and p53.
  • To explore the role of FAK-p53 signaling in linking extracellular matrix signals to nuclear responses.
  • To understand FAK's function as a scaffold protein in cell survival pathways.

Main Methods:

  • Analysis of FAK and p53 interactions in human and mouse cells.
  • Investigating signal transduction pathways involving FAK and p53.
  • Studying the role of FAK as a scaffold protein.

Main Results:

  • The study highlights the biological significance of the kinase-independent FAK-p53 interaction.
  • FAK acts as a scaffold protein, sequestering proapoptotic proteins like p53.
  • This sequestration mechanism mediates cell survival.

Conclusions:

  • The kinase-independent interaction between FAK and p53 has significant biological implications.
  • FAK's role as a scaffold protein in sequestering p53 is critical for cell survival.
  • This research opens new avenues for cell signaling and cancer research.

More Related Videos

Identification of Intracellular Signaling Events Induced in Viable Cells by Interaction with Neighboring Cells Undergoing Apoptotic Cell Death09:18

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

Published on: December 27, 2016

Related Concept Videos

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...
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...
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...
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...