Related Experiment Video
Updated: Feb 21, 2026

07:16
Monitoring Hippo Signaling Pathway Activity Using a Luciferase-based Large Tumor Suppressor LATS Biosensor
Published on: September 13, 2018
20.7K
p53 shades of Hippo
Noa Furth1, Yael Aylon1, Moshe Oren1
1Department of Molecular Cell Biology, The Weizmann Institute, Rehovot, Israel.
Cell Death and Differentiation
|October 7, 2017
Summary
The p53 and Hippo pathways, crucial for genomic stability, interact intricately. Understanding their cross-talk is vital for deciphering cell regulation and developing cancer therapies.
Area of Science:
- Molecular Biology
- Cell Biology
- Cancer Research
Background:
- The p53 family (p53, p63, p73) and Hippo pathway regulate critical cellular processes including cell cycle, metabolism, development, and tumor suppression.
- Both pathways are essential for maintaining genomic fidelity and cellular homeostasis.
- Complex cross-talk exists between the p53 and Hippo pathways, with context-specific interactions ranging from collaborative to antagonistic.
Purpose of the Study:
- To review the interactions between the p53 and Hippo pathways.
- To focus on their roles in normal stem cells, development, apoptosis, senescence, and metabolism in cancer cells.
Main Methods:
- Literature review of existing research on p53-Hippo pathway interactions.
- Analysis of studies focusing on specific physiological contexts and cellular processes.
Main Results:
- The p53 and Hippo pathways exhibit complex, context-dependent regulatory networks.
- Interactions can be interdependent, collaborative, or antagonistic, influencing cellular outcomes.
- Disruptions in this network due to genetic/epigenetic alterations can lead to genomic instability and cancer.
Conclusions:
- A deeper understanding of p53-Hippo pathway cross-talk is necessary for comprehending normal cellular functions and disease pathogenesis.
- Elucidating these interactions can reveal novel therapeutic targets for cancer treatment.
More Related Videos
Related Concept Videos
Interactions Between Signaling Pathways
7.4K
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...
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...
7.4K
Hedgehog Signaling Pathway
10.2K
The Hedgehog gene (Hh) was first discovered due to its control of the growth of disorganized, hair-like bristles phenotype in Drosophila, much like hedgehog spines. Hh plays a crucial role in the development of organs and the maintenance of homeostasis in both invertebrates and vertebrates. However, while Drosophila has only one Hh protein, mammals have multiple functional Hedgehog proteins - Sonic (Shh), Desert (Dhh), and Indian Hedgehog (Ihh). All of these homologous proteins have adapted to...
10.2K
PI3K/mTOR/AKT Signaling Pathway
5.8K
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...
5.8K
Abnormal Proliferation
5.3K
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...
5.3K
DNA Damage can Stall the Cell Cycle
10.2K
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...
10.2K
DNA Damage Can Stall the Cell Cycle
3.2K
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...
3.2K

