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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...
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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

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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...
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Proteins can undergo many types of post-translational modifications, often in response to changes in their environment. These modifications play an important role in the function and stability of these proteins. Covalently linked molecules include functional groups, such as methyl, acetyl, and phosphate groups, and also small proteins, such as ubiquitin. There are around 200 different types of covalent regulators that have been identified.
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Related Experiment Video

Updated: May 9, 2026

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

TXNIP interacts with hEcd to increase p53 stability and activity.

Hyun-Woo Suh1, Sohyun Yun, Haeyoung Song

  • 1Immunotherapy Research Center, Korea Research Institute of Bioscience and Biotechnology, Yuseong-gu, Daejeon 305-806, Republic of Korea.

Biochemical and Biophysical Research Communications
|July 25, 2013
PubMed
Summary

Thioredoxin interacting protein (TXNIP) interacts with human ecdysoneless (hEcd) to stabilize p53 protein levels. This interaction enhances p53 activity, promoting cell death in response to stress stimuli.

Keywords:
Cell deathMdm2TRXTXNIPhEcdhuman ecdysonelessmurine double minute-2p53thioredoxinthioredoxin interacting protein

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Last Updated: May 9, 2026

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

Detection of Aggregation-Prone Behavior in Mutant P53 V157F Breast Cancer Cells Using Multipoint Thioflavin T Fluorescence
04:56

Detection of Aggregation-Prone Behavior in Mutant P53 V157F Breast Cancer Cells Using Multipoint Thioflavin T Fluorescence

Published on: December 30, 2025

Area of Science:

  • Molecular Biology
  • Cell Biology
  • Cancer Research

Background:

  • The p53 protein is a critical tumor suppressor involved in cell cycle arrest and apoptosis.
  • Human ecdysoneless (hEcd) is known to stabilize p53 and enhance its transcriptional activity.

Purpose of the Study:

  • To investigate the role of thioredoxin interacting protein (TXNIP) in the hEcd-p53 regulatory pathway.
  • To elucidate the mechanism by which TXNIP influences p53 stability and activity.

Main Methods:

  • Co-immunoprecipitation assays to confirm protein interactions.
  • Western blotting to assess p53 ubiquitination and protein levels.
  • Cell viability assays (e.g., using actinomycin D) to evaluate the functional impact of TXNIP and hEcd.

Main Results:

  • TXNIP was found to interact with hEcd.
  • TXNIP inhibits MDM2-mediated p53 ubiquitination, thereby stabilizing p53.
  • Overexpression of TXNIP and hEcd increased cell death, while their knockdown reduced it, particularly in MCF-7 cells.

Conclusions:

  • TXNIP acts as a novel regulator within the hEcd-MDM2-p53 regulatory loop.
  • The TXNIP-hEcd interaction contributes to p53 stabilization and enhanced tumor suppressor activity.
  • This pathway represents a potential therapeutic target for cancer treatment.