Evidence map›Paper›PMID 27648755›Full record

ArticlePrion2016

On the evolutionary trajectories of signal-transducing amyloids in fungi and beyond.

Asen Daskalov

Open access · goldAbstract read
In one paragraph

Article in Prion, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.

0numbers the graph read from it
0cells of the map it votes in
5citing papers in PubMed
0.5field-weighted citation impact, top 28% 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

5 citing papers in PubMed, 7 citations in OpenAlex.

  1. Article
  2. Review
  3. Review
  4. Review
  5. Regulated Forms of Cell Death in Fungi.Frontiers in microbiology · 2017
    Review
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

1 author at 1 institution in 1 country.

Asen Daskalova Department of Plant and Microbial Biology , University of California , Berkeley , CA , USA .
University of California, Berkeley · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

In the last decade, multiple reports have established that amyloids can bear important functional roles in a variety of biological processes and in distant taxonomic clades. In filamentous fungi, amyloids are involved in a signal transducing mechanism in which a group of NOD-like receptors (NLRs) controls downstream effector proteins to induce a programmed cell death reaction. A structurally characterized example of fungal signal-transducing amyloid is the prion-forming domain (PFD) of the HET-S toxin from Podospora anserina. Amyloid-mediated programmed cell death is equally reported in metazoans in the context of innate immunity and antiviral response. The cell death reaction, described as programmed necrosis, is dependent on an amyloid-forming RHIM motif (RIP homotypic interaction motif). An evolutionary link between the RHIM and the PFD signaling amyloids has been previously reported. Our recent study ties further the signaling amyloids in fungi and metazoans, reporting a fungal signal-transducing domain with amyloid and prion-like properties, which shows significant sequence similarity to the metazoan RHIM motif. Here, I discuss the expanding class of the signal-transducing amyloids and reflect on the possible evolutionary scenarios of their diversification.

Indexed as

Biological EvolutionSignal TransductionAmyloidImmunity, InnatePodosporaAmyloidfunctional amyloidHET-SNLRprionprogrammed cell deathRHIMsignal-transduction

Identifiers

PMID27648755
PMCPMC5105908
OpenAlexW2523382043

What OpenQuestion 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 OpenQuestion graph.