Evidence map›Paper›PMID 26597983›Full record

ArticleInfection and immunity2016

ALL2, a Homologue of ALL1, Has a Distinct Role in Regulating pH Homeostasis in the Pathogen Cryptococcus neoformans.

Neena Jain, Tejas Bouklas, Anjali Gupta, Avanish K Varshney, Erika P Orner, Bettina C Fries

Open access · bronzeAbstract read
In one paragraph

Article in Infection and immunity, 2016. 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, top 91% 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

2 citing papers in PubMed, 4 citations in OpenAlex.

  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

6 authors at 2 institutions in 1 country.

Neena JainDepartment of Medicine (Infectious Diseases), Albert Einstein College of Medicine, Bronx, New York, USA.
Tejas BouklasDepartment of Medicine (Infectious Diseases), Stony Brook University, Stony Brook, New York, USA.
Anjali GuptaDepartment of Medicine (Infectious Diseases), Albert Einstein College of Medicine, Bronx, New York, USA.
Avanish K VarshneyDepartment of Medicine (Infectious Diseases), Stony Brook University, Stony Brook, New York, USA.
Erika P OrnerDepartment of Microbiology and Molecular Genetics, Stony Brook University, Stony Brook, New York, USA.
Bettina C FriesDepartment of Medicine (Infectious Diseases), Stony Brook University, Stony Brook, New York, USA Department of Microbiology and Molecular Genetics, Stony Brook University, Stony Brook, New York, USA bettina.fries@stonybrookmedicine.edu.
Stony Brook University · USAlbert Einstein College of Medicine · US

Funding

Training in HIV/AIDS Pathogenesis; Basic and Translational ResearchT32AI007501 · NIAID · YESHIVA UNIVERSITY · PI PRASAD, VINAYAKA R. · 1995 to 2024
$6.6M
response to phenotypic switch variants to C. neoformansR01AI059681 · NIAID · STATE UNIVERSITY NEW YORK STONY BROOK · PI FRIES, BETTINA · 2004 to 2014
$3.6M
Consequences of replicative aging in Cryptococcus neoformansR21AI087564 · NIAID · ALBERT EINSTEIN COLLEGE OF MEDICINE · PI FRIES, BETTINA · 2010 to 2011
$454k
NIAID NIH HHS R01 AI059681NIAID NIH HHS R01AI059681NIAID NIH HHS R21 AI087564NIAID NIH HHS T32 AI007501PHS HHS R21A1087564
6 · The paper itself

Abstract

Cryptococcus neoformans is a facultative intracellular fungal pathogen that has a polysaccharide capsule and causes life-threatening meningoencephalitis. Its capsule, as well as its ability to survive in the acidic environment of the phagolysosome, contributes to the pathogen's resilience in the host environment. Previously, we reported that downregulation of allergen 1 (ALL1) results in the secretion of a shorter, more viscous exopolysaccharide with less branching and structural complexity, as well as altered iron homeostasis. Now, we report on a homologous coregulated gene, allergen 2 (ALL2). ALL2's function was characterized by generating null mutants in C. neoformans. In contrast to ALL1, loss of ALL2 attenuated virulence in the pulmonary infection model. The all2Δ mutant shed a less viscous exopolysaccharide and exhibited higher sensitivity to hydrogen peroxide than the wild type, and as a result, the all2Δ mutant was more resistant to macrophage-mediated killing. Transcriptome analysis further supported the distinct function of these two genes. Unlike ALL1's involvement in iron homeostasis, we now present data on ALL2's unique function in maintaining intracellular pH in low-pH conditions. Thus, our data highlight that C. neoformans, a human-pathogenic basidiomycete, has evolved a unique set of virulence-associated genes that contributes to its resilience in the human niche.

Indexed as

HomeostasisAllergensAnimalsCryptococcosisCryptococcus neoformansDisease Models, AnimalFungal ProteinsHumansHydrogen-Ion ConcentrationHydrogen PeroxideLungMice, Inbred BALB CMicroarray AnalysisMolecular Sequence DataMutationPhenotypeAllergensFungal ProteinsHydrogen PeroxideVirulence Factors

Identifiers

PMID26597983
PMCPMC4730584
OpenAlexW2174558210

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.