Jove
Visualize
Contact Us
JoVE
x logofacebook logolinkedin logoyoutube logo
ABOUT JoVE
OverviewLeadershipBlogJoVE Help Center
AUTHORS
Publishing ProcessEditorial BoardScope & PoliciesPeer ReviewFAQSubmit
LIBRARIANS
TestimonialsSubscriptionsAccessResourcesLibrary Advisory BoardFAQ
RESEARCH
JoVE JournalMethods CollectionsJoVE Encyclopedia of ExperimentsArchive
EDUCATION
JoVE CoreJoVE BusinessJoVE Science EducationJoVE Lab ManualFaculty Resource CenterFaculty Site
Terms & Conditions of Use
Privacy Policy
Policies

Related Concept Videos

Inhibition of Cdk Activity02:34

Inhibition of Cdk Activity

5.1K
The orderly progression of the cell cycle depends on the activation of Cdk protein by binding to its cyclin partner. However, the cell cycle must be restricted when undergoing abnormal changes. Most cancers correlate to the deregulated cell cycle, and since Cdks are a central component of the cell cycle, Cdk inhibitors are extensively studied to develop anticancer agents. For instance, cyclin D associates with several Cdks, such as Cdk 4/6, to form an active complex. The cyclin D-Cdk4/6 complex...
5.1K
RNA Editing02:23

RNA Editing

9.3K
RNA editing is a post-transcriptional modification where a precursor mRNA (pre-mRNA) nucleotide sequence is changed by base insertion, deletion, or modification. The extent of RNA editing varies from a few hundred bases, in mitochondrial DNA of trypanosomes, to a just single base, in nuclear genes of mammals. Even a single base change in the pre-mRNA can convert a codon for one amino acid into the codon for another amino acid or a stop codon. This type of re-coding can significantly affect the...
9.3K
Anaphase Promoting Complex00:50

Anaphase Promoting Complex

3.0K
The stepwise destruction of specific proteins is necessary for the progression and completion of the cell cycle. Such proteins are ubiquitinated by ubiquitin ligases and then subsequently destroyed by the proteasome. The SCF (Skp1/Cullin/F-box) and the anaphase-promoting complex (APC) are two important ubiquitin ligases involved in cell cycle progression. While SCF is active throughout the cell cycle, APC gets activated during metaphase to anaphase transition. Cdc20 or Cdh1 binds to APC and...
3.0K
DNA Damage can Stall the Cell Cycle02:37

DNA Damage can Stall the Cell Cycle

9.6K
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...
9.6K
Separation of Sister Chromatids02:17

Separation of Sister Chromatids

3.9K
At the transition from prophase to metaphase, there is a reduction in cohesion along the chromosomal arms, resulting in the resolution of sister chromatids. However, residual cohesin connections remain to hold the sister chromatids together until the transition from metaphase to anaphase. The residual connection prevents any premature separation of sister chromatids, blocking the risks of aneuploidy within the daughter cells.
At the onset of anaphase, separase, a proteolytic enzyme, is...
3.9K
Negative Regulator Molecules01:23

Negative Regulator Molecules

36.7K
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.
36.7K

You might also read

Related Articles

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

Sort by
Same author

Spaceflight multi-omics reveals vulnerabilities of human germ cell development.

Science advances·2026
Same author

Closed-loop motor imagery brain-computer interface-assisted training for upper limb rehabilitation after subacute stroke: clinical and electroencephalographic outcomes from a randomized pilot trial.

Frontiers in neurology·2026
Same author

Management of Engraftment Arrhythmias Associated with Human Induced Pluripotent Stem Cell-Derived Cardiomyocytes Transplantation.

Heart rhythm·2026
Same author

Structural and dynamic insights into the allosteric activation of p38α MAP kinase via specific docking interactions.

Communications biology·2026
Same author

Resveratrol Promotes Goat Myoblast Differentiation via PROX1-Mediated Inhibition of NOTCH Signaling.

The Journal of nutrition·2026
Same author

Effects of motor imagery brain-computer interface task on quantitative EEG features in patients with prolonged disorders of consciousness.

Frontiers in neuroscience·2026

Related Experiment Video

Updated: Oct 22, 2025

Author Spotlight: Establishing CENP-E Knockout HeLa Cells – A Novel Approach to Study Kinesin-7 CENP-E Biology and its Inhibitors
11:49

Author Spotlight: Establishing CENP-E Knockout HeLa Cells – A Novel Approach to Study Kinesin-7 CENP-E Biology and its Inhibitors

Published on: June 23, 2023

904

RNA editing restricts hyperactive ciliary kinases.

Dongdong Li1,2,3,4, Yufan Liu1,2,3,4, Peishan Yi1,2,3,4

  • 1Tsinghua-Peking Center for Life Sciences, Tsinghua University, Beijing, China.

Science (New York, N.Y.)
|August 27, 2021
PubMed
Summary

Cells regulate hyperactive protein kinases using RNA editing. Mutations in ADR-2, an RNA adenosine deaminase, rescued ciliary defects caused by a hyperactive kinase, revealing a novel feedback mechanism.

More Related Videos

Identification of Cyclin-dependent Kinase 1 Specific Phosphorylation Sites by an In Vitro Kinase Assay
12:26

Identification of Cyclin-dependent Kinase 1 Specific Phosphorylation Sites by an In Vitro Kinase Assay

Published on: May 3, 2018

18.9K
CRISPR/Cas9 Editing of the C. elegans rbm-3.2 Gene using the dpy-10 Co-CRISPR Screening Marker and Assembled Ribonucleoprotein Complexes.
07:46

CRISPR/Cas9 Editing of the C. elegans rbm-3.2 Gene using the dpy-10 Co-CRISPR Screening Marker and Assembled Ribonucleoprotein Complexes.

Published on: December 11, 2020

6.1K

Related Experiment Videos

Last Updated: Oct 22, 2025

Author Spotlight: Establishing CENP-E Knockout HeLa Cells – A Novel Approach to Study Kinesin-7 CENP-E Biology and its Inhibitors
11:49

Author Spotlight: Establishing CENP-E Knockout HeLa Cells – A Novel Approach to Study Kinesin-7 CENP-E Biology and its Inhibitors

Published on: June 23, 2023

904
Identification of Cyclin-dependent Kinase 1 Specific Phosphorylation Sites by an In Vitro Kinase Assay
12:26

Identification of Cyclin-dependent Kinase 1 Specific Phosphorylation Sites by an In Vitro Kinase Assay

Published on: May 3, 2018

18.9K
CRISPR/Cas9 Editing of the C. elegans rbm-3.2 Gene using the dpy-10 Co-CRISPR Screening Marker and Assembled Ribonucleoprotein Complexes.
07:46

CRISPR/Cas9 Editing of the C. elegans rbm-3.2 Gene using the dpy-10 Co-CRISPR Screening Marker and Assembled Ribonucleoprotein Complexes.

Published on: December 11, 2020

6.1K

Area of Science:

  • Molecular Biology
  • Genetics
  • Cell Biology

Background:

  • Precise regulation of protein kinase activity is crucial for cellular function.
  • Dysregulated kinase activity, particularly hyperactivity, can lead to various cellular defects.
  • Mechanisms governing the control of hyperactive kinases are not fully understood.

Purpose of the Study:

  • To investigate the regulatory mechanisms controlling hyperactive protein kinases in *Caenorhabditis elegans*.
  • To identify genetic factors that can suppress the phenotypes associated with a constitutively active kinase.
  • To elucidate the role of RNA editing in kinase regulation.

Main Methods:

  • Generation of a constitutively active mitogen-activated protein kinase DYF-5 (DYF-5CA) in *C. elegans*.
  • Utilizing genetic suppressor screens to identify rescuing mutations.
  • Analyzing RNA transcription, RNA editing, mRNA splicing, and protein translation in affected animals.

Main Results:

  • Mutations in ADR-2 (RNA adenosine deaminase) rescued ciliary defects caused by DYF-5CA.
  • DYF-5CA induced abnormal transcription of antisense RNAs, forming double-stranded RNA with DYF-5CA mRNA.
  • ADR-2 ectopically edited the DYF-5CA mRNA, impairing splicing, blocking translation, and triggering mRNA decay.
  • This RNA editing-dependent feedback regulation was dependent on kinase hyperactivity and also observed for other ciliary kinases (NEKL-4/NEK10 and DYF-18/CCRK).

Conclusions:

  • Hyperactive kinases can be regulated by an RNA editing-dependent feedback mechanism.
  • ADR-2 plays a critical role in suppressing kinase hyperactivity through mRNA editing.
  • This regulatory pathway involving RNA editing represents a widespread mechanism for controlling ciliary kinases.