Evidence map›Paper›PMID 25836674›Full record

ArticleBiology open2015

The Drosophila TIPE family member Sigmar interacts with the Ste20-like kinase Misshapen and modulates JNK signaling, cytoskeletal remodeling and autophagy.

Suganthi Chittaranjan, Jing Xu, Michael Kuzyk, Harpreet K Dullat, James Wilton, Lindsay DeVorkin, Chandra Lebovitz, Gregg B Morin, Marco A Marra, Sharon M Gorski

Open access · goldAbstract read
In one paragraph

Article in Biology open, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.

0numbers the graph read from it
0cells of the map it votes in
9citing papers in PubMed
0.9field-weighted citation impact, top 27% 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

9 citing papers in PubMed, 13 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

10 authors at 3 institutions in 1 country.

Suganthi ChittaranjanThe Genome Sciences Centre, BC Cancer Agency, 675 West 10 Avenue, Vancouver, BC V5Z 1L3, Canada.
Jing XuThe Genome Sciences Centre, BC Cancer Agency, 675 West 10 Avenue, Vancouver, BC V5Z 1L3, Canada Department of Molecular Biology and Biochemistry, Simon Fraser University, Burnaby, BC V5A 1S6, Canada.
Michael KuzykThe Genome Sciences Centre, BC Cancer Agency, 675 West 10 Avenue, Vancouver, BC V5Z 1L3, Canada.
Harpreet K DullatThe Genome Sciences Centre, BC Cancer Agency, 675 West 10 Avenue, Vancouver, BC V5Z 1L3, Canada.
James WiltonThe Genome Sciences Centre, BC Cancer Agency, 675 West 10 Avenue, Vancouver, BC V5Z 1L3, Canada.
Lindsay DeVorkinThe Genome Sciences Centre, BC Cancer Agency, 675 West 10 Avenue, Vancouver, BC V5Z 1L3, Canada Department of Molecular Biology and Biochemistry, Simon Fraser University, Burnaby, BC V5A 1S6, Canada.
Chandra LebovitzThe Genome Sciences Centre, BC Cancer Agency, 675 West 10 Avenue, Vancouver, BC V5Z 1L3, Canada Department of Molecular Biology and Biochemistry, Simon Fraser University, Burnaby, BC V5A 1S6, Canada.
Gregg B MorinThe Genome Sciences Centre, BC Cancer Agency, 675 West 10 Avenue, Vancouver, BC V5Z 1L3, Canada Department of Medical Genetics, The University of British Columbia, Vancouver, BC V6T 1Z3, Canada.
Marco A MarraThe Genome Sciences Centre, BC Cancer Agency, 675 West 10 Avenue, Vancouver, BC V5Z 1L3, Canada.
Sharon M GorskiThe Genome Sciences Centre, BC Cancer Agency, 675 West 10 Avenue, Vancouver, BC V5Z 1L3, Canada Department of Molecular Biology and Biochemistry, Simon Fraser University, Burnaby, BC V5A 1S6, Canada sgorski@bcgsc.ca.
BC Cancer Agency · CASimon Fraser University · CAUniversity of British Columbia · CA

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

TNFAIP8 and other mammalian TIPE family proteins have attracted increased interest due to their associations with disease-related processes including oncogenic transformation, metastasis, and inflammation. The molecular and cellular functions of TIPE family proteins are still not well understood. Here we report the molecular and genetic characterization of the Drosophila TNFAIP8 homolog, CG4091/sigmar. Previous gene expression studies revealed dynamic expression of sigmar in larval salivary glands prior to histolysis. Here we demonstrate that in sigmar loss-of-function mutants, the salivary glands are morphologically abnormal with defects in the tubulin network and decreased autophagic flux. Sigmar localizes subcellularly to microtubule-containing projections in Drosophila S2 cells, and co-immunoprecipitates with the Ste20-like kinase Misshapen, a regulator of the JNK pathway. Further, the Drosophila TNF ligand Eiger can induce sigmar expression, and sigmar loss-of-function leads to altered localization of pDJNK in salivary glands. Together, these findings link Sigmar to the JNK pathway, cytoskeletal remodeling and autophagy activity during salivary gland development, and provide new insights into TIPE family member function.

Indexed as

AutophagyCytoskeletonEigerMsnTIPETNFAIP8

Identifiers

PMID25836674
PMCPMC4434819
OpenAlexW2115793439

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.