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

Amplifying Signals via Enzymatic Cascade01:22

Amplifying Signals via Enzymatic Cascade

8.5K
When a ligand binds to a cell-surface receptor, the receptor's intracellular domain changes shape, which may either activate its enzyme function or allow its binding to other molecules. The initial signal is amplified by most signal transduction pathways. This means that a single ligand molecule can activate multiple molecules of a downstream target. Proteins that relay a signal are most commonly phosphorylated at one or more sites, activating or inactivating the protein. Kinases catalyze...
8.5K
Transducer Mechanism: Enzyme-Linked Receptors01:27

Transducer Mechanism: Enzyme-Linked Receptors

2.5K
Enzyme-linked receptors are cell-surface receptors acting as an enzyme or associating with an enzyme intracellularly. They make excellent drug targets. Drugs can bind to the extracellular ligand-binding domain or directly affect their enzymatic domain and alter their activity.
Major types that are helpful drug targets include:
2.5K
MAPK Signaling Cascades01:07

MAPK Signaling Cascades

5.6K
Mitogen-activated protein kinase, or MAPK pathway, activates three sequential kinases to regulate cellular responses such as proliferation, differentiation, survival, and apoptosis. The canonical MAPK pathway starts with a mitogen or growth factor binding to an RTK. The activated RTKs stimulate Ras, which recruits Raf or MAP3 Kinase (MAPKKK), the first kinase of the MAPK signaling cascade. Raf further phosphorylates and activates MEK or MAP2 Kinases (MAPKK), which in turn phosphorylates MAP...
5.6K
Calmodulin-dependent Signaling01:16

Calmodulin-dependent Signaling

5.2K
Calmodulin (CaM) is a calcium-binding protein in eukaryotes that controls various calcium-regulated cellular processes. It has four calcium-binding sites that bind calcium to form the calcium-calmodulin ( Ca2+-CaM) complex. GPCR stimulation increases the calcium levels in the cells that bind to CaM and induces a conformational change.
The Ca2+-CaM complex does not have enzymatic activity by itself. Instead, the complex binds downstream target proteins, including membrane proteins or enzymes,...
5.2K
Intrinsically Disordered Proteins02:18

Intrinsically Disordered Proteins

17.9K
Intrinsically disordered proteins are a group of proteins that do not fold into specific three-dimensional structures. Their structural flexibility allows them to complement ordered proteins to perform functions that are inaccessible to rigid structures. They are more common in eukaryotes than prokaryotes and may either be exclusively intrinsically disordered or hybrid proteins, consisting of a mix of ordered and disordered regions. The absence of a rigid structure in these proteins can be...
17.9K
Enzyme-linked Receptors01:00

Enzyme-linked Receptors

78.6K
Enzyme-linked receptors are proteins that act as both receptor and enzyme, activating multiple intracellular signals. This is a large group of receptors that include the receptor tyrosine kinase (RTK) family. Many growth factors and hormones bind to and activate the RTKs.
Neurotrophin (NT) receptors are a family of RTKs, including trkA, trkB, and trkC (tropomyosin-related kinase) receptors. TrkA is specific for nerve growth factor (NGF), neurotrophin-6, and neurotrophin-7. TrkB binds...
78.6K

You might also read

Related Articles

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

Sort by
Same author

Targeting Sensory Neuropathies Through Neurotrophin-Based Approaches.

Cellular and molecular neurobiology·2026
Same author

Promoting Research Excellence in Down Syndrome: Proceedings of the 5th International Conference of the Trisomy 21 Research Society.

Neuromolecular medicine·2026
Same author

EEG-motor correlation as early Alzheimer's disease index in herpes simplex virus type-1-infected mice.

Brain communications·2026
Same author

Loss of Proteostasis and Early-Onset Neurodegeneration in Down Syndrome: From Mechanisms to Interventions.

Antioxidants (Basel, Switzerland)·2026
Same author

Next-generation multicolor indicators for in vivo imaging of norepinephrine.

Nature methods·2026
Same author

Herpes simplex virus-1 induces complement-mediated microglial phagocytosis of synapses in murine primary brain cultures and tissues.

Cell communication and signaling : CCS·2026
Same journal

Erratum for the Research Article "Assessing the health risks of rice cadmium content standards in China" by H. Chu <i>et al</i>.

Science advances·2026
Same journal

Erratum for the Research Article "Developmental regulation of Erk signaling by mitotic kinases" by F. Chen <i>et al</i>.

Science advances·2026
Same journal

Magnetically levitated metasurface enabling tangible and bidirectional human-machine interaction.

Science advances·2026
Same journal

A general photoinduced manganese-catalyzed platform for the sequential difunctionalization of [1.1.1]propellane.

Science advances·2026
Same journal

Turning sound and force into light with AlN:Mn<sup>2+</sup> mechanoluminescence.

Science advances·2026
Same journal

Extreme dominance of Earth-origin heavy ions in the intense ring current near the Earth during the May 2024 super geomagnetic storm.

Science advances·2026
See all related articles

Related Experiment Video

Updated: Jul 11, 2025

Assaying Protein Kinase Activity with Radiolabeled ATP
08:05

Assaying Protein Kinase Activity with Radiolabeled ATP

Published on: May 26, 2017

18.4K

Engineering memory with an extrinsically disordered kinase.

Cristian Ripoli1,2, Onur Dagliyan3, Pietro Renna1,2

  • 1Department of Neuroscience, Università Cattolica del Sacro Cuore, 00168 Rome, Italy.

Science Advances
|November 15, 2023
PubMed
Summary
This summary is machine-generated.

Researchers established a direct link between actin polymerization and memory encoding. Activating a specific protein kinase in mice enhanced memory and cognitive function, demonstrating a causal relationship.

More Related Videos

Deciphering the Structural Effects of Activating EGFR Somatic Mutations with Molecular Dynamics Simulation
15:05

Deciphering the Structural Effects of Activating EGFR Somatic Mutations with Molecular Dynamics Simulation

Published on: May 20, 2020

8.7K
A Guide to Production, Crystallization, and Structure Determination of Human IKK1/&#945;
11:27

A Guide to Production, Crystallization, and Structure Determination of Human IKK1/α

Published on: November 2, 2018

9.2K

Related Experiment Videos

Last Updated: Jul 11, 2025

Assaying Protein Kinase Activity with Radiolabeled ATP
08:05

Assaying Protein Kinase Activity with Radiolabeled ATP

Published on: May 26, 2017

18.4K
Deciphering the Structural Effects of Activating EGFR Somatic Mutations with Molecular Dynamics Simulation
15:05

Deciphering the Structural Effects of Activating EGFR Somatic Mutations with Molecular Dynamics Simulation

Published on: May 20, 2020

8.7K
A Guide to Production, Crystallization, and Structure Determination of Human IKK1/&#945;
11:27

A Guide to Production, Crystallization, and Structure Determination of Human IKK1/α

Published on: November 2, 2018

9.2K

Area of Science:

  • Neuroscience
  • Molecular Biology
  • Cognitive Science

Background:

  • Synaptic plasticity is fundamental for memory formation, involving neuronal communication.
  • Actin polymerization is associated with synaptic plasticity and dendritic spine stability.
  • The direct causal role of actin polymerization in memory encoding remains unclear.

Purpose of the Study:

  • To investigate the causal link between actin polymerization and memory encoding.
  • To determine if actin polymerization drives or is a consequence of learning.
  • To explore the therapeutic potential of modulating actin dynamics for cognitive enhancement.

Main Methods:

  • Utilized an engineered, extrinsically disordered form of the protein kinase LIMK1.
  • Administered the engineered LIMK1 in vivo to precisely target ADF/cofilin, an actin modifier.
  • Assessed long-term structural and functional changes in hippocampal dendritic spines and synaptic transmission.
  • Evaluated memory encoding and cognitive decline in aged mice.

Main Results:

  • Induced long-term enlargement of dendritic spines and enhanced synaptic transmission on command.
  • Demonstrated that in vivo activation of engineered LIMK1 improved memory encoding.
  • Observed a slowing of cognitive decline in aged mice with reduced cofilin phosphorylation.

Conclusions:

  • The study provides direct causal evidence linking actin-mediated synaptic transmission to memory.
  • Engineered memory through LIMK1 activation supports the role of actin dynamics as a driver of memory.
  • Modulating actin polymerization via LIMK1 presents a potential strategy for cognitive enhancement and mitigating age-related cognitive decline.