Evidence map›Paper›PMID 42638611›Full record

ReviewBiochemical Society transactions2026

Functional amyloids as molecular switches: emerging roles in diverse signalling pathways.

Jessica A Buchanan, Brayden C Williams, Megan Steain, Margaret Sunde

Abstract readReview
In one paragraph

Review in Biochemical Society transactions, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

0numbers the graph read from it
0cells of the map it votes in
0citing 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

0 citing papers in PubMed.

No citing paper in PubMed yet.

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.

Jessica A Buchanan *School of Medical Sciences, Sydney Nano and Sydney Infectious Diseases, The University of Sydney, Sydney, NSW 2006, Australia.ORCID 0000-0002-8263-3850
Brayden C Williams *School of Medical Sciences, Sydney Nano and Sydney Infectious Diseases, The University of Sydney, Sydney, NSW 2006, Australia.ORCID 0009-0007-2713-8084
Megan SteainSchool of Medical Sciences, Charles Perkins Centre and Sydney Infectious Diseases, The University of Sydney, Sydney, NSW 2006, Australia.ORCID 0000-0002-7631-4204
Margaret SundeSchool of Medical Sciences, Sydney Nano and Sydney Infectious Diseases, The University of Sydney, Sydney, NSW 2006, Australia.ORCID 0000-0002-0150-3203

Funding

DHAC | National Health and Medical Research Council (NHMRC) APP2019231DHAC | National Health and Medical Research Council (NHMRC) APP2047845
6 · The paper itself

Abstract

Across all domains of life, functional amyloid fibrils serve structural, storage and signalling functions. In signalling pathways, assembly into the amyloid state constitutes a rapid and cooperative molecular switch that can reorganise protein function, promote multivalent interactions, and amplify downstream responses through templated self-propagation. Advances in the understanding of functional amyloids as regulators of signalling highlight their tailored structural properties and biological consequences. The nucleation-dependent polymerisation of amyloid enables sensitive control over activation thresholds, while the repetitive fibrillar architecture concentrates functional domains to enhance avidity and cooperativity. Controlled mechanisms for assembly, compartmentalisation and reversibility prevent inappropriate persistence or activity. These features underpin diverse signalling systems, including the RIPK1:RIPK3 necrosome in mammalian necroptosis, fungal prion-based cell-death pathways and prion-like regulatory systems in yeast and metazoans that modulate translation, development and cellular memory. Functional amyloids represent a versatile and evolutionarily conserved mechanism for molecular signalling and offer opportunities for the design of programmable amyloid-based switches with potential applications in therapeutics and synthetic biology.

Indexed as

AmyloidSignal TransductionAnimalsHumansPrionsAmyloidPrionsfibrilsfunctional amyloidsignaling

Identifiers

PMID42638611
PMCPMC13506858

What Socratic holds

Textmetadata
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 Socratic graph.