Evidence map›Paper›PMID 36625497›Full record

ArticleJournal of neurochemistry2023

The effects of KTKEGV repeat motif and intervening ATVA sequence on α-synuclein solubility and assembly.

Lisa Brontesi, Thibaut Imberdis, Nagendran Ramalingam, Ulf Dettmer

Open access · greenAbstract read
In one paragraph

Article in Journal of neurochemistry, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.

0numbers the graph read from it
0cells of the map it votes in
4citing papers in PubMed
0.8field-weighted citation impact, top 27% of its field
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

4 citing papers in PubMed, 4 citations in OpenAlex.

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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

4 authors at 1 institution in 1 country.

Lisa BrontesiAnn Romney Center for Neurologic Diseases, Department of Neurology, Brigham and Women's Hospital and Harvard Medical School, Boston, Massachusetts, USA.
Thibaut ImberdisAnn Romney Center for Neurologic Diseases, Department of Neurology, Brigham and Women's Hospital and Harvard Medical School, Boston, Massachusetts, USA.
Nagendran RamalingamAnn Romney Center for Neurologic Diseases, Department of Neurology, Brigham and Women's Hospital and Harvard Medical School, Boston, Massachusetts, USA.ORCID 0000-0002-9459-3593
Ulf DettmerAnn Romney Center for Neurologic Diseases, Department of Neurology, Brigham and Women's Hospital and Harvard Medical School, Boston, Massachusetts, USA.ORCID 0000-0001-6676-0107
Brigham and Women's Hospital · US

Funding

Polo-like-kinase-2-dependent α-Synuclein Serine-129 Phosphorylation: a Physiological RoleDuring Synaptic ActivityRF1NS122880 · NINDS · BRIGHAM AND WOMEN'S HOSPITAL · PI DETTMER, ULF, RAMALINGAM, NAGENDRAN · 2022 to 2022
$2.1M
Stabilizing native α-synuclein homeostasis to prevent insoluble α-synuclein aggregatesR01NS099328 · NINDS · BRIGHAM AND WOMEN'S HOSPITAL · PI DETTMER, ULF · 2017 to 2021
$1.9M
Contrasting pathomechanisms of membrane versus cytosol alpha-synuclein excessR21NS121826 · NINDS · BRIGHAM AND WOMEN'S HOSPITAL · PI DETTMER, ULF · 2021 to 2021
$505k
NINDS NIH HHS R01 NS099328NINDS NIH HHS R21 NS121826NINDS NIH HHS RF1 NS122880
6 · The paper itself

Abstract

Alpha-synuclein (αS), the key protein in Parkinson's disease, is typically described as an intrinsically disordered protein. Consistent with this notion, several context-dependent folding states may coexist in neurons. Unfolded soluble monomers, helical monomers at membranes and helical multimers (soluble or at membranes) have all been reported and may be in an equilibrium with each other. We previously found that αS can be stabilized in its membrane-associated monomeric form by genetically increasing the hydrophobicity of the membrane-embedded half of the αS helix. αS amphipathic helix formation at membranes is governed by up to nine 11-amino acid repeats with the core motif KTKEGV. However, this repeat is only imperfectly conserved; for example, it consists of KAKEGV in repeat #1, KTKEQV in repeat #5, and AVVTGV in the poorly conserved repeat #6. Here we explored the effect of perfecting the αS core repeat to nine times KTKEGV ("9KV") and found by sequential protein extraction that this engineered mutant accumulates in the cytosolic phase of neural cells. Intact-cell cross-linking trapped a part of the cytosolic portion at multimeric positions (30, 60, 80, 100 kDa). Thus, compared to wild-type αS, αS 9KV seems less prone to populating the membrane-associated monomeric form. Removing the "ATVA" intervening amino-acid sequence between repeats 4 and 5 slightly increased cytosolic localization while adding "ATVA" in between all repeats 1-8 caused αS to be trapped as a monomer in membrane fractions. Our results contribute to an ongoing debate on the dynamic structure of αS, highlighting that wild-type αS is unlikely to be fully multimeric/monomeric or fully cytosolic/membrane-associated in cells, but protein engineering can create αS variants that preferentially adopt a certain state. Overall, the imperfect nature of the KTKEGV repeat motifs and the presence of ATVA in between repeats 4 and 5 seem to prevent a strong cytosolic localization of αS and thus play a major role in the protein's ability to dynamically populate cytosolic vs. membrane-associated and monomeric vs. multimeric states.

Indexed as

alpha-SynucleinParkinson DiseaseAmino Acid SequenceHumansMutationSolubilityalpha-Synucleinalpha-synucleinmembrane bindingmultimerneurotoxicityParkinson's diseasetetramer

Identifiers

PMID36625497
PMCPMC10211470
OpenAlexW4315436581

What OpenQuestion holds

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Read underepoch 390

Registered trials

None linked

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.