Search research articles

ABOUT JoVE

Overview Leadership Blog JoVE Help Center

AUTHORS

Publishing Process Editorial Board Scope & Policies Peer Review FAQ Submit

LIBRARIANS

Testimonials Subscriptions Access Resources Library Advisory Board FAQ

RESEARCH

JoVE Journal Methods Collections JoVE Encyclopedia of Experiments Archive

EDUCATION

JoVE Core JoVE Business JoVE Science Education JoVE Lab Manual Faculty Resource Center Faculty Site

Terms & Conditions of Use

Related Concept Videos

Plasticity

Plasticity

Plasticity is the property where an object loses its elasticity and undergoes irreversible deformation, even after the deformation forces are eliminated. If a material deforms irreversibly without increasing stress or load, then this is called ideal plasticity. For example, when a force is applied to an aluminum rod, it changes its shape, but it does not return to its original shape once the force is removed. Plastic deformation or ductility is thus a permanent deformation or change in the...

Neuroplasticity

Neuroplasticity

Neuroplasticity reflects the brain's remarkable capacity to adapt and evolve, responding dynamically to learning, experiences, or injury by reorganizing its neural circuitry. This reorganization involves creating new neural connections and refining old ones through a series of biological processes that contribute to the brain's lifelong development and adaptability.

Cellular Adaptation III: Hyperplasia

Cellular Adaptation III: Hyperplasia

Hyperplasia is an increase in the number of cells in a tissue or organ due to enhanced cell division. It is an adaptive, controlled response to stimuli such as injury, hormones, or stress, involving mitosis to produce genetically identical cells and support tissue repair and regeneration.Tissue CapacityCertain tissues, including the epidermis, intestinal epithelium, bone marrow, and fibroblasts, have a high potential for hyperplasia. Others, such as bone, cartilage, and smooth muscle, show...

Loss of Tumor Suppressor Gene Functions

Loss of Tumor Suppressor Gene Functions

Tumor suppressor genes are normal genes that can slow down cell division, repair DNA mistakes, or program the cells for apoptosis in case of irreparable damage. Hence, they play an essential role in preventing the proliferation of damaged cells.
When the tumor suppressor genes develop mutations or are lost, cells start growing out of control, leading to cancer. However, a single functional copy of the tumor suppressor gene is enough for the cells to maintain their normal functions and cell...

Loss of Tumor Suppressor Gene Functions

Loss of Tumor Suppressor Gene Functions

Tumor suppressor genes are normal genes that can slow down cell division, repair DNA mistakes, or program the cells for apoptosis in case of irreparable damage. Hence, they play an essential role in preventing the proliferation of damaged cells.
When the tumor suppressor genes develop mutations or are lost, cells start growing out of control, leading to cancer. However, a single functional copy of the tumor suppressor gene is enough for the cells to maintain their normal functions and cell...

Cellular Adaptation I: Introduction and Atrophy

Cellular Adaptation I: Introduction and Atrophy

Cells can adapt to environmental changes to maintain function and avoid injury, a process called cellular adaptation. Adapted cells exist in a reversible intermediate state with changes in size, number, phenotype, metabolism, or function. These responses help cells meet altered physiological or pathological demands; for example, enlargement of breast and uterine tissues during pregnancy. Early adaptations may enhance function, but persistent stress eventually causes tissue damage.Types of...

You might also read

Related Articles

Articles linked to this work by shared authors, journal, and citation graph.

Sort by

Same author

Derivation and external validation of a prognostic nomogram for human epidermal growth factor receptor 2 negative early young breast cancer in women.

Discover oncology·2026

Same author

Glucose‑driven TRIB3 enhances the tumorigenic potential of colon cancer via the PI3K/AKT pathway.

Molecular medicine reports·2026

Same author

Glecirasib with or without cetuximab in previously treated locally advanced or metastatic colorectal cancer with KRAS<sup>G12C</sup> mutation (JAB-21822-1002 and JAB-21822-1007): two open-label, non-randomised phase 1/2 trials.

The lancet. Gastroenterology & hepatology·2025

Same author

Fe-Co LDH/MoP heterostructure with Fe and Co as intercalants for oxygen evolution electrocatalysis.

Small (Weinheim an der Bergstrasse, Germany)·2025

Same author

Hypoxic stimulation of DCLK1 transcription and alternative-promoter switching fuels tumor malignancy in clear cell renal cell carcinoma.

Cell death & disease·2025

Same author

Misdirected yet intact TREX1 exonuclease activity causes human cerebral and systemic small vessel disease.

Brain : a journal of neurology·2025

Search research articles

Related Experiment Video

Updated: Jun 10, 2026

Ex Utero Electroporation and Organotypic Slice Culture of Mouse Hippocampal Tissue

Ex Utero Electroporation and Organotypic Slice Culture of Mouse Hippocampal Tissue

Published on: March 4, 2015

Loss of Bright/ARID3a function promotes developmental plasticity.

Guangyu An¹, Cathrine A Miner, Jamee C Nixon

¹Immunobiology and Cancer Program, Oklahoma Medical Research Foundation, University of Oklahoma Health Sciences Center, Oklahoma City, Oklahoma, USA.

Stem Cells (Dayton, Ohio)

|August 4, 2010

Summary

Inhibiting the B-cell regulator Bright (ARID3a) enhances developmental plasticity in adult somatic cells. Loss of Bright function allows cells to express pluripotency markers and differentiate into multiple lineages.

More Related Videos

Assaying Circuit Specific Regulation of Adult Hippocampal Neural Precursor Cells

Assaying Circuit Specific Regulation of Adult Hippocampal Neural Precursor Cells

Published on: July 24, 2019

Experience-Dependent Remodeling of Juvenile Brain Olfactory Sensory Neuron Synaptic Connectivity in an Early-Life Critical Period

Experience-Dependent Remodeling of Juvenile Brain Olfactory Sensory Neuron Synaptic Connectivity in an Early-Life Critical Period

Published on: March 1, 2024

Related Experiment Videos

Last Updated: Jun 10, 2026

Ex Utero Electroporation and Organotypic Slice Culture of Mouse Hippocampal Tissue

Ex Utero Electroporation and Organotypic Slice Culture of Mouse Hippocampal Tissue

Published on: March 4, 2015

Assaying Circuit Specific Regulation of Adult Hippocampal Neural Precursor Cells

Assaying Circuit Specific Regulation of Adult Hippocampal Neural Precursor Cells

Published on: July 24, 2019

Experience-Dependent Remodeling of Juvenile Brain Olfactory Sensory Neuron Synaptic Connectivity in an Early-Life Critical Period

Experience-Dependent Remodeling of Juvenile Brain Olfactory Sensory Neuron Synaptic Connectivity in an Early-Life Critical Period

Published on: March 1, 2024

Area of Science:

Molecular Biology
Developmental Biology
Cell Biology

Background:

B-cell regulator of immunoglobulin heavy chain transcription (Bright)/ARID3a was initially identified in B lymphocytes.
Expression patterns and knockout lethality indicated broader biological roles beyond B-cell development.
Investigating Bright's function is crucial for understanding cellular plasticity and differentiation.

Purpose of the Study:

To investigate the role of Bright/ARID3a in regulating developmental plasticity.
To determine if inhibiting Bright in adult somatic cells can induce pluripotency-associated characteristics.
To explore the potential of Bright as a target for reprogramming somatic cells.

Main Methods:

Analysis of Bright-deficient mouse models.
Assessment of gene expression profiles for pluripotency markers.
In vitro expansion and differentiation assays of Bright-deficient cells.
Direct knockdown of human Bright in somatic cells.

Main Results:

Bright-deficient cells from two mouse models exhibited increased developmental plasticity.
These cells expressed pluripotency-associated genes, showed indefinite expansion, and underwent spontaneous multi-lineage differentiation.
Knockdown of human Bright resulted in cell colonies capable of expressing multiple lineage markers.

Conclusions:

Functional inhibition of Bright/ARID3a significantly enhances developmental plasticity in adult somatic cells.
Repression of Bright confers new developmental options, enabling adult cells to acquire pluripotency-like features.
Bright/ARID3a represents a key molecular target for modulating somatic cell differentiation potential.