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

Reporter Genes

Reporter Genes

Reporter genes are a type of protein-coding gene that are often tagged to a gene of interest. Once inside a target cell, reporter genes usually produce visually identifiable characteristics like fluorescence and luminescence when expressed along with the gene of interest. Thus, reporter genes “report” the presence or absence of genes of interest in an organism, determine the gene expression pattern, or track the physical location of a DNA segment or protein in the cell.

Cell Specific Gene Expression

Cell Specific Gene Expression

Multicellular organisms contain a variety of structurally and functionally distinct cell types, but the DNA in all the cells originated from the same parent cells. The differences in the cells can be attributed to the differential gene expression. Liver cells, whose functions include detoxification of blood, production of bile to metabolize fats, and synthesis of proteins essential for metabolism, must express a specific set of genes to perform their functions. Gene expression also varies with...

Cell Specific Gene Expression

Cell Specific Gene Expression

Constitutive and Regulated Gene Expression

Constitutive and Regulated Gene Expression

Gene expression in prokaryotes is governed by constitutive and regulated systems, allowing cells to balance the production of essential proteins with adaptive responses to environmental changes.Constitutive Gene ExpressionConstitutive, or housekeeping, genes are continuously expressed as they encode proteins vital for fundamental cellular processes. These include enzymes for glycolysis, ribosomal components for protein synthesis, and proteins involved in DNA replication. Their constant...

You might also read

Related Articles

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

Sort by

Same author

Autoantibodies in Patients With Arrhythmogenic Cardiomyopathy Activate GSK-3β, Resulting in a Loss of Cardiomyocyte Cohesion.

Acta physiologica (Oxford, England)·2026

Same author

Apremilast improves cardiomyocyte cohesion and arrhythmia in different models for arrhythmogenic cardiomyopathy.

Stem cell research & therapy·2025

Same author

BRCA1 and BRCA2 gene expression: p53- and cell cycle-dependent repression requires RB and DREAM.

Cell death and differentiation·2025

Same author

Capoeira and Its Effects on Health-Related Outcomes-A Systematic Review.

Journal of integrative and complementary medicine·2025

Same author

CeDaD-a novel assay for simultaneous tracking of cell death and division in a single population.

Cell death discovery·2025

Same author

HDAC activity is dispensable for repression of cell-cycle genes by DREAM and E2F:RB complexes.

Nature communications·2024

Search research articles

Related Experiment Video

Updated: Oct 31, 2025

Mutagenesis and Analysis of Genetic Mutations in the GC-rich KISS1 Receptor Sequence Identified in Humans with Reproductive Disorders

Mutagenesis and Analysis of Genetic Mutations in the GC-rich KISS1 Receptor Sequence Identified in Humans with Reproductive Disorders

Published on: September 4, 2011

Ki-67 gene expression.

Sigrid Uxa¹, Paola Castillo-Binder¹, Robin Kohler¹

¹Molecular Oncology, Medical School, University of Leipzig, Leipzig, Germany.

Cell Death and Differentiation

|June 29, 2021

Summary

This summary is machine-generated.

The MKI67 gene, which codes for the cancer marker Ki-67, is tightly regulated during the cell cycle. Its expression peaks in G2/M phases, influenced by transcription factors and tumor suppressors like p53.

More Related Videos

Characterization of In Vitro Differentiation of Human Primary Keratinocytes by RNA-Seq Analysis

Characterization of In Vitro Differentiation of Human Primary Keratinocytes by RNA-Seq Analysis

Published on: May 16, 2020

An In Vitro Protocol for Evaluating MicroRNA Levels, Functions, and Associated Target Genes in Tumor Cells

An In Vitro Protocol for Evaluating MicroRNA Levels, Functions, and Associated Target Genes in Tumor Cells

Published on: May 21, 2019

Related Experiment Videos

Last Updated: Oct 31, 2025

Mutagenesis and Analysis of Genetic Mutations in the GC-rich KISS1 Receptor Sequence Identified in Humans with Reproductive Disorders

Mutagenesis and Analysis of Genetic Mutations in the GC-rich KISS1 Receptor Sequence Identified in Humans with Reproductive Disorders

Published on: September 4, 2011

Characterization of In Vitro Differentiation of Human Primary Keratinocytes by RNA-Seq Analysis

Characterization of In Vitro Differentiation of Human Primary Keratinocytes by RNA-Seq Analysis

Published on: May 16, 2020

An In Vitro Protocol for Evaluating MicroRNA Levels, Functions, and Associated Target Genes in Tumor Cells

An In Vitro Protocol for Evaluating MicroRNA Levels, Functions, and Associated Target Genes in Tumor Cells

Published on: May 21, 2019

Area of Science:

Molecular Biology
Cell Cycle Regulation
Cancer Biology

Background:

Ki-67 (encoded by MKI67) is a crucial cancer marker.
Understanding MKI67 gene expression control is vital for cancer research.

Purpose of the Study:

To elucidate the regulatory mechanisms of MKI67 gene expression during the cell cycle.
To investigate the role of transcription factors and tumor suppressors in MKI67 regulation.

Main Methods:

Analysis of MKI67 promoter elements (CHR, CDE).
Study of transcription factor binding (DREAM, B-MYB-MuvB, FOXM1-MuvB).
Utilized knockout cell models and knockdown experiments.

Main Results:

MKI67 expression peaks in G2/M phase, driven by B-MYB-MuvB and FOXM1-MuvB binding.
DREAM repressor complexes downregulate MKI67 in G0/G1.
RB tumor suppressor cooperates with DREAM/MuvB.
p53 tumor suppressor indirectly represses MKI67 via p21/CDKN1A.

Conclusions:

A model for cell cycle-dependent MKI67 transcription involving DREAM, MuvB complexes, and RB is proposed.
p53 activation and DNA damage induce MKI67 repression through p21/CDKN1A.
These findings provide insights into MKI67 regulation in normal and cancer cells.