ArticleMolecular biology of the cell2024
The microvillar protocadherin CDHR5 associates with EBP50 to promote brush border assembly.
Article in Molecular biology of the cell, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
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Who cites it
6 citing papers in PubMed, 4 citations in OpenAlex.
- From immature to mature epithelium: unveiling structural dynamics and transcriptional programs in rainbow trout intestinal barrier.Veterinary research · 2026Article
- Plasma proteomics identifies proteins and pathways associated with incident migraine in 50,668 adults.The journal of headache and pain · 2026Article
- Integrated Multi-Omic Analysis Identifies Altered Colonic Brush Border Profile as a Key Feature of Microscopic Colitis.United European gastroenterology journal · 2026Article
- Protocadherin 20 Is a POU Class 2 Homeobox 3 Target Gene Required for Proper Tuft Cell Microvillus Organization.Cellular and molecular gastroenterology and hepatology · 2026Article
- Select autosomal dominant DFNA11 deafness variants activate Myo7A targeting in epithelial cells.Journal of cell science · 2025Article
- The poly-proline motifs found in the cytoplasmic tail of the brush border cadherin CDHR5 play a role in its ability to elongate microvilli.microPublication biology · 2025Article
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Authors and funding
11 authors at 1 institution in 1 country.
Funding
Abstract
Transporting epithelial cells of the gut and kidney interact with their luminal environment through a densely packed collection of apical microvilli known as a brush border (BB). Proper brush border assembly depends on the intermicrovillar adhesion complex (IMAC), a protocadherin-based adhesion complex found at the distal tips of microvilli that mediates adhesion between neighboring protrusions to promote their organized packing. Loss of the IMAC adhesion molecule Cadherin-related family member 5 (CDHR5) results in significant brush border defects, though the functional properties of this protocadherin have not been thoroughly explored. Here, we show that the cytoplasmic tail of CDHR5 contributes to its correct apical targeting and functional properties in an isoform-specific manner. Library screening identified the Ezrin-associated scaffolds EBP50 and E3KARP as cytoplasmic binding partners for CDHR5. Consistent with this, loss of EBP50 disrupted proper brush border assembly with cells exhibiting markedly reduced apical IMAC levels. Together, our results shed light on the apical targeting determinants of CDHR5 and further define the interactome of the IMAC involved in brush border assembly.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.