Evidence map›Paper›PMID 26645974›Full record

ArticlePLoS neglected tropical diseases2015

Cloning and Characterization of Two Potent Kunitz Type Protease Inhibitors from Echinococcus granulosus.

Shiwanthi L Ranasinghe, Katja Fischer, Wenbao Zhang, Geoffrey N Gobert, Donald P McManus

Open access · goldAbstract read
In one paragraph

Article in PLoS neglected tropical diseases, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
26citing papers in PubMed, 1 pooled it
1.8field-weighted citation impact, top 16% 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

26 citing papers in PubMed, 1 synthesis or guideline pooled it, 66 citations in OpenAlex.

  1. Pooled it
  2. Article
  3. Review
  4. Review
  5. Review
  6. Parasites revive hope for cancer therapy.European journal of medical research · 2024
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  12. Parasites as potential targets for cancer immunotherapy.Journal of cancer research and clinical oncology · 2023
    Review
  13. Article
  14. Review
  15. Article
  16. Article
  17. Article
  18. Article
  19. Echinococcosis: Advances in the 21st Century.Clinical microbiology reviews · 2019
    Review
  20. 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

5 authors at 2 institutions in 2 countries.

Shiwanthi L RanasingheMolecular Parasitology Laboratory, QIMR Berghofer Medical Research Institute, Herston, Queensland, Australia.
Katja FischerMolecular Parasitology Laboratory, QIMR Berghofer Medical Research Institute, Herston, Queensland, Australia.
Wenbao ZhangMolecular Parasitology Laboratory, QIMR Berghofer Medical Research Institute, Herston, Queensland, Australia.
Geoffrey N GobertMolecular Parasitology Laboratory, QIMR Berghofer Medical Research Institute, Herston, Queensland, Australia.
Donald P McManusMolecular Parasitology Laboratory, QIMR Berghofer Medical Research Institute, Herston, Queensland, Australia.
QIMR Berghofer Medical Research Institute · AUFirst Affiliated Hospital of Xinjiang Medical University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The tapeworm Echinococcus granulosus is responsible for cystic echinococcosis (CE), a cosmopolitan disease which imposes a significant burden on the health and economy of affected communities. Little is known about the molecular mechanisms whereby E. granulosus is able to survive in the hostile mammalian host environment, avoiding attack by host enzymes and evading immune responses, but protease inhibitors released by the parasite are likely implicated. We identified two nucleotide sequences corresponding to secreted single domain Kunitz type protease inhibitors (EgKIs) in the E. granulosus genome, and their cDNAs were cloned, bacterially expressed and purified. EgKI-1 is highly expressed in the oncosphere (egg) stage and is a potent chymotrypsin and neutrophil elastase inhibitor that binds calcium and reduced neutrophil infiltration in a local inflammation model. EgKI-2 is highly expressed in adult worms and is a potent inhibitor of trypsin. As powerful inhibitors of mammalian intestinal proteases, the EgKIs may play a pivotal protective role in preventing proteolytic enzyme attack thereby ensuring survival of E. granulosus within its mammalian hosts. EgKI-1 may also be involved in the oncosphere in host immune evasion by inhibiting neutrophil elastase and cathepsin G once this stage is exposed to the mammalian blood system. In light of their key roles in protecting E. granulosus from host enzymatic attack, the EgKI proteins represent potential intervention targets to control CE. This is important as new public health measures against CE are required, given the inefficiencies of available drugs and the current difficulties in its treatment and control. In addition, being a small sized highly potent serine protease inhibitor, and an inhibitor of neutrophil chemotaxis, EgKI-1 may have clinical potential as a novel anti-inflammatory therapeutic.

Indexed as

AnimalsCloning, MolecularEchinococcus granulosusGene ExpressionHumansMiceProtease InhibitorsRecombinant ProteinsSubstrate SpecificityProtease InhibitorsRecombinant Proteins

Identifiers

PMID26645974
PMCPMC4672886
OpenAlexW2192963623

What OpenQuestion holds

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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.