Evidence map›Paper›PMID 25965669›Full record

ArticleScientific reports2015

Plasma Membrane Proteolipid 3 Protein Modulates Amphotericin B Resistance through Sphingolipid Biosynthetic Pathway.

Vinay K Bari, Sushma Sharma, Md Alfatah, Alok K Mondal, K Ganesan

Open access · goldAbstract read
In one paragraph

Article in Scientific reports, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.

0numbers the graph read from it
0cells of the map it votes in
13citing papers in PubMed
2.3field-weighted citation impact, top 12% 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

13 citing papers in PubMed, 37 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

5 authors at 1 institution in 1 country.

Vinay K BariCSIR-Institute of Microbial Technology, Sector 39-A, Chandigarh - 160036, India.
Sushma SharmaCSIR-Institute of Microbial Technology, Sector 39-A, Chandigarh - 160036, India.
Md AlfatahCSIR-Institute of Microbial Technology, Sector 39-A, Chandigarh - 160036, India.
Alok K MondalCSIR-Institute of Microbial Technology, Sector 39-A, Chandigarh - 160036, India.
K GanesanCSIR-Institute of Microbial Technology, Sector 39-A, Chandigarh - 160036, India.
Institute of Microbial Technology · IN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Invasive opportunistic fungal infections of humans are common among those suffering from impaired immunity, and are difficult to treat resulting in high mortality. Amphotericin B (AmB) is one of the few antifungals available to treat such infections. The AmB resistance mechanisms reported so far mainly involve decrease in ergosterol content or alterations in cell wall. In contrast, depletion of sphingolipids sensitizes cells to AmB. Recently, overexpression of PMP3 gene, encoding plasma membrane proteolipid 3 protein, was shown to increase and its deletion to decrease, AmB resistance. Here we have explored the mechanistic basis of PMP3 effect on AmB resistance. It was found that ergosterol content and cell wall integrity are not related to modulation of AmB resistance by PMP3. A few prominent phenotypes of PMP3 delete strain, namely, defective actin polarity, impaired salt tolerance, and reduced rate of endocytosis are also not related to its AmB-sensitivity. However, PMP3 overexpression mediated increase in AmB resistance requires a functional sphingolipid pathway. Moreover, AmB sensitivity of strains deleted in PMP3 can be suppressed by the addition of phytosphingosine, a sphingolipid pathway intermediate, confirming the importance of this pathway in modulation of AmB resistance by PMP3.

Indexed as

Amphotericin BDrug Resistance, FungalCandidaCell MembraneProteolipidsSaccharomyces cerevisiaeSaccharomyces cerevisiae ProteinsSphingolipidsAmphotericin BProteolipidsSaccharomyces cerevisiae ProteinsSphingolipids

Identifiers

PMID25965669
PMCPMC4428271
OpenAlexW591011915

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Registered trials

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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.