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Related Concept Videos

Thermosensation01:43

Thermosensation

Peripheral thermosensation is the perception of external temperature. A change in temperature (on the surface of the skin and other tissues) is detected by a family of temperature-sensitive ion channels called Transient Receptor Potential, or TRP, receptors. These receptors are located on free nerve endings. Those detecting cold temperatures are closer to the surface of the skin than the nerve endings detecting warmth. These thermoTRP channels, while temperature selective, have relatively...
Ligand-Gated Ion Channel Receptor: Gating Mechanism01:30

Ligand-Gated Ion Channel Receptor: Gating Mechanism

Ligand-gated ion channels are transmembrane proteins that play a vital role in intercellular communication and functions of the nervous system. They allow the influx of ions across the membrane once the neurotransmitter binds, allowing the subsequent transmission of electrical excitation across the neurons. Other ligand-gated ion channels, like the γ-aminobutyric acid (GABA) receptor, permit anions like chloride into the cells on the binding of the GABA molecule. Their entry into the cell...
Resting Membrane Potential01:24

Resting Membrane Potential

The relative difference in electrical charge, or voltage, between the inside and the outside of a cell membrane, is called the membrane potential. It is generated by differences in permeability of the membrane to various ions and the concentrations of these ions across the membrane.
The Inside of a Neuron is More Negative
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Feedback Inhibition00:46

Feedback Inhibition

Biochemical reactions are occurring constantly in cells, converting starting substances to different products, usually with the help of enzymes that speed the reactions. Without enzymes, it would take far too long for most reactions to occur to be useful to the cell!

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Related Experiment Video

Updated: May 31, 2026

Development of Inhibitors of Protein-protein Interactions through REPLACE: Application to the Design and Development Non-ATP Competitive CDK Inhibitors
10:33

Development of Inhibitors of Protein-protein Interactions through REPLACE: Application to the Design and Development Non-ATP Competitive CDK Inhibitors

Published on: October 26, 2015

Design of Inhibitory Peptides Based on TRPM4-KCTD5 Interaction.

Javiera Baeza1,2, Diego Maureira1, Mariela Gonzalez-Avendaño2

  • 1Núcleo Interdisciplinario de Biología y Genética, Instituto de Ciencias Biomédicas, Facultad de Medicina, Universidad de Chile, Santiago 8380453, Chile.

Journal of Chemical Information and Modeling
|May 29, 2026
PubMed
Summary
This summary is machine-generated.

Researchers designed peptides to block the TRPM4-KCTD5 interaction, a key driver in metastatic breast cancer. These peptides successfully reduced cancer cell invasion, offering a potential new therapeutic strategy.

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Method for Identifying Small Molecule Inhibitors of the Protein-protein Interaction Between HCN1 and TRIP8b
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Method for Identifying Small Molecule Inhibitors of the Protein-protein Interaction Between HCN1 and TRIP8b

Published on: November 11, 2016

Area of Science:

  • Molecular Biology
  • Cell Biology
  • Oncology

Background:

  • Transient Receptor Potential Melastatin 4 (TRPM4) channels are implicated in cytoskeletal rearrangement and cell migration, contributing to pathologies like fibrosis and metastatic cancer.
  • KCTD5 acts as a positive regulator of TRPM4, enhancing its calcium (Ca2+) sensitivity and influencing cell migration.
  • Elevated TRPM4 and KCTD5 expression correlates with poor prognosis in breast cancer, identifying their interaction as a potential therapeutic target.

Purpose of the Study:

  • To design and evaluate peptides targeting the TRPM4-KCTD5 protein-protein interaction.
  • To assess the therapeutic potential of these peptides in inhibiting TRPM4 activity and reducing cancer cell invasion.

Main Methods:

  • In silico peptide design based on the TRPM4-KCTD5 interface.
  • In vitro assays including bimolecular fluorescent complementation (BiFC), patch clamp electrophysiology, and intracellular sodium recordings.
  • Cell invasion assays using MDA-MB-231 breast cancer cells.

Main Results:

  • Designed peptides (TAT-TRPM4-HA, TAT-KCTD5-HA) disrupted the TRPM4-KCTD5 interaction, as shown by reduced BiFC signal.
  • Peptide treatment significantly decreased TRPM4-dependent sodium (Na+) influx and ion channel currents in HEK293 cells.
  • The TAT-TRPM4-HA peptide notably reduced cell invasion in MDA-MB-231 breast cancer cells.

Conclusions:

  • The developed peptides effectively inhibit the TRPM4-KCTD5 interaction.
  • Targeting the TRPM4-KCTD5 interface with peptides shows promise for reducing metastatic breast cancer cell invasion.
  • The TRPM4-KCTD5 interaction represents a viable therapeutic target for metastatic breast cancer treatment.