Evidence map›Paper›PMID 26921396›Full record

ArticleDisease models & mechanisms2016

Stem-cell-specific endocytic degradation defects lead to intestinal dysplasia in Drosophila.

Péter Nagy, Laura Kovács, Gyöngyvér O Sándor, Gábor Juhász

Open access · goldAbstract read
In one paragraph

Article in Disease models & mechanisms, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.

0numbers the graph read from it
0cells of the map it votes in
14citing papers in PubMed
1.7field-weighted citation impact, top 17% 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

14 citing papers in PubMed, 24 citations in OpenAlex.

  1. Article
  2. Review
  3. Article
  4. Article
  5. Article
  6. Article
  7. Lysosomes at the Crossroads of Cell Metabolism, Cell Cycle, and Stemness.International journal of molecular sciences · 2022
    Review
  8. Article
  9. Article
  10. On the Fly: Recent Progress on Autophagy and Aging in Drosophila.Frontiers in cell and developmental biology · 2019
    Review
  11. Autophagy and Tumorigenesis in Drosophila.Advances in experimental medicine and biology · 2019
    Review
  12. Review
  13. Article
  14. 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

4 authors at 1 institution in 1 country.

Péter NagyDepartment of Anatomy, Cell and Developmental Biology, Eötvös Loránd University, Pázmány s. 1/C, Budapest H-1117, Hungary.
Laura KovácsDepartment of Anatomy, Cell and Developmental Biology, Eötvös Loránd University, Pázmány s. 1/C, Budapest H-1117, Hungary.
Gyöngyvér O SándorDepartment of Anatomy, Cell and Developmental Biology, Eötvös Loránd University, Pázmány s. 1/C, Budapest H-1117, Hungary.
Gábor JuhászDepartment of Anatomy, Cell and Developmental Biology, Eötvös Loránd University, Pázmány s. 1/C, Budapest H-1117, Hungary Institute of Genetics, Biological Research Centre of the Hungarian Academy of Sciences, Temesvári krt. 62, Szeged H-6726, Hungary szmrt@elte.hu.ORCID 0000-0001-8548-8874
Eötvös Loránd University · HU

Funding

Wellcome Trust 087518
6 · The paper itself

Abstract

UV radiation resistance-associated gene (UVRAG) is a tumor suppressor involved in autophagy, endocytosis and DNA damage repair, but how its loss contributes to colorectal cancer is poorly understood. Here, we show that UVRAG deficiency in Drosophila intestinal stem cells leads to uncontrolled proliferation and impaired differentiation without preventing autophagy. As a result, affected animals suffer from gut dysfunction and short lifespan. Dysplasia upon loss of UVRAG is characterized by the accumulation of endocytosed ligands and sustained activation of STAT and JNK signaling, and attenuation of these pathways suppresses stem cell hyperproliferation. Importantly, the inhibition of early (dynamin-dependent) or late (Rab7-dependent) steps of endocytosis in intestinal stem cells also induces hyperproliferation and dysplasia. Our data raise the possibility that endocytic, but not autophagic, defects contribute to UVRAG-deficient colorectal cancer development in humans.

Indexed as

EndocytosisProteolysisAnimalsAutophagyCell DifferentiationCell ProliferationCell ShapeDrosophila melanogasterDrosophila ProteinsEndosomesHumansIntestinesModels, BiologicalReceptors, NotchSignal TransductionSTAT Transcription FactorsDrosophila ProteinsReceptors, NotchSTAT Transcription FactorsTumor Suppressor ProteinsUVRAG protein, DrosophilaAutophagyDrosophilaEndocytosisUVRAG

Identifiers

PMID26921396
PMCPMC4892661
OpenAlexW2287787864

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.