Related Experiment Video

Updated: May 9, 2026

Purification of Ubiquitinated p53 Proteins from Mammalian Cells
10:55

Purification of Ubiquitinated p53 Proteins from Mammalian Cells

Published on: March 21, 2022

The p53-PUMA axis suppresses iPSC generation

Yanxin Li1, Haizhong Feng, Haihui Gu

  • 1State Key Laboratory of Experimental Hematology, Institute of Hematology and Blood Diseases Hospital, Center for Stem Cell Medicine, Chinese Academy of Medical Sciences and Peking Union Medical College, Nanjing Road No. 288, Tianjin 300020, China.

Nature Communications
|July 23, 2013
PubMed

Insights

The tumor suppressor p53 pathway, including PUMA, negatively impacts induced pluripotent stem cell generation. Targeting PUMA, not p21, may improve reprogramming efficiency for therapeutic applications.

Area of Science:

  • Cell biology
  • Stem cell research
  • Cancer biology

Background:

  • The mechanisms of induced pluripotent stem cell (iPSC) reprogramming are not fully understood.
  • The Trp53 (p53) pathway, known for its role in tumor suppression, can inhibit iPSC generation, partly through p21Cdkn1a (p21)-mediated cell cycle arrest.

Purpose of the Study:

  • To investigate the role of PUMA, a pro-apoptotic factor in the p53 pathway, in somatic cell reprogramming.
  • To compare the function of PUMA with p21 in the context of p53-mediated suppression of iPSC generation.

Main Methods:

  • Utilized mouse models deficient in PUMA, p21, and p53.
  • Assessed the impact of these genetic deficiencies on the efficiency of induced pluripotent stem cell induction.
  • Evaluated DNA damage and chromosomal aberrations in iPSCs derived from these mouse models.

Main Results:

  • PUMA acts as an independent mediator of p53's negative effect on iPSC induction.
  • PUMA deficiency enhanced iPSC survival, reducing DNA damage and chromosomal aberrations.
  • Conversely, loss of p21 or p53 led to opposite outcomes, hindering iPSC generation.

Conclusions:

  • PUMA represents a distinct and potentially more favorable therapeutic target within the p53 pathway for improving iPSC generation.
  • Targeting PUMA could have significant implications for advancing the therapeutic potential of iPSCs.

More Related Videos

Yeast As a Chassis for Developing Functional Assays to Study Human P5314:57

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 Fluorescence04:56

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

Published on: December 30, 2025

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...
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.
Somatic to iPS Cell Reprogramming01:29

Somatic to iPS Cell Reprogramming

Reprogramming alters the gene expression in somatic cells, transforming them into induced pluripotent stem (iPS) cells over several generations. Scientists can reprogram cells by introducing genes for four transcription factors—Oct4, Sox2, Klf4, and c-Myc (OSKM) by viral or non-viral methods. These factors are also known as Yamanaka factors after Shinya Yamanaka, who first generated iPS cells using mouse skin cells. Yamanaka was awarded the Nobel Prize in Physiology or Medicine in 2012 for this...
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...
iPS Cell Differentiation01:22

iPS Cell Differentiation

The ability of induced pluripotent stem cells or iPSCs to differentiate into most body cell types has stimulated repair and regenerative medicine research over the past few decades. iPSC-derived blood cells, hepatocytes, beta islet cells, cardiomyocytes, neurons, and other cell types can repair injuries or regenerate damaged tissue in diseases such as diabetes and neurodegenerative disorders.
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...