Evidence map›Paper›PMID 39447937›Full record

ArticleJournal of structural biology2024

Deletion within ameloblastin multitargeting domain reduces its interaction with artificial cell membrane.

Natalie C Kegulian, Janet Moradian-Oldak

Abstract read
In one paragraph

Article in Journal of structural biology, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.

0numbers the graph read from it
0cells of the map it votes in
2citing papers in PubMed
–field-weighted citation impact
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

2 citing papers in PubMed.

  1. Article
  2. Article
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

2 authors.

Natalie C KegulianCenter for Craniofacial Molecular Biology, Herman Ostrow School of Dentistry, University of Southern California, Los Angeles, CA 90033, USA.
Janet Moradian-OldakCenter for Craniofacial Molecular Biology, Herman Ostrow School of Dentistry, University of Southern California, Los Angeles, CA 90033, USA. Electronic address: joldak@usc.edu.

Funding

MATRIX-BASED MINERAL (MBM) ENAMEL BIOMIMETICSR01DE013414 · NIDCR · UNIVERSITY OF SOUTHERN CALIFORNIA · PI Janet Oldak · 2001 to 2026
$8.6M
A Peptide-Based Biomineralization Strategy for Tooth RepairR01DE027632 · NIDCR · UNIVERSITY OF SOUTHERN CALIFORNIA · PI OLDAK, JANET · 2019 to 2022
$1.6M
NIDCR NIH HHS R01 DE013414NIDCR NIH HHS R01 DE027632
6 · The paper itself

Abstract

In human, mutations in the gene encoding the enamel matrix protein ameloblastin (Ambn) have been identified in cases of amelogenesis imperfecta. In mouse models, perturbations in the Ambn gene have caused loss of enamel and dramatic disruptions in enamel-making ameloblast cell function. Critical roles for Ambn in ameloblast cell signaling and polarization as well as adhesion to the nascent enamel matrix have been supported. Recently, we have identified a multitargeting domain (MTD) in Ambn that interacts with cell membrane, with the majority enamel matrix protein amelogenin, and with itself. This domain includes an amphipathic helix (AH) motif that directly interacts with cell membrane. In this study, we analyzed the sequence of the MTD for evolutionary conservation and found high conservation among mammals within the MTD and particularly within the AH motif. We computationally predicted that the AH motif lost its hydrophobic moment upon deleting hydrophobic but not hydrophilic residues from the motif. Furthermore, we rationally designed peptides that encompassed the Ambn MTD and contained deletions of largely hydrophobic or hydrophilic stretches of residues. To assess their AH-forming and membrane-binding abilities, we combined those peptides with synthetic phospholipid membrane vesicles and performed circular dichroism, membrane leakage, and vesicle clearance measurements. Circular dichroism showed retention of α-helix formation in all peptides except the one with the largest deletion of eleven amino acids including seven that were hydrophobic. This same peptide variant failed to cause leakage or clearance of synthetic membranes, while smaller deletions yielded intermediate membrane interaction as measured by leakage and clearance assays. Our data revealed that deletion of key hydrophobic residues from the AH leads to the most dramatic loss of Ambn-membrane interaction. Pinpointing roles of residues within the MTD has important implications for the multifunctionality of Ambn.

Indexed as

Cell MembraneDental Enamel ProteinsAmino Acid MotifsAmino Acid SequenceAnimalsHumansHydrophobic and Hydrophilic InteractionsMembranes, ArtificialMiceProtein BindingProtein DomainsSequence DeletionAMBN protein, humanDental Enamel ProteinsMembranes, ArtificialAmeloblastinAmelogenesisAmphipathic helixEnamelIntrinsically disordered proteinsMembranes

Identifiers

PMID39447937
PMCPMC11784912

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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.