Evidence map›Paper›PMID 27764577›Full record

ArticleCell cycle (Georgetown, Tex.)2016

Leucine Zipper Down-regulated in Cancer-1 (LDOC1) interacts with Guanine nucleotide binding protein-like 3-like (GNL3L) to modulate Nuclear Factor-kappa B (NF-κB) signaling during cell proliferation.

Indu Jose Thoompumkal, Krishnan Rehna, Kumaraswamy Anbarasu, Sundarasamy Mahalingam

Open access · bronzeAbstract read
In one paragraph

Article in Cell cycle (Georgetown, Tex.), 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers.

0numbers the graph read from it
0cells of the map it votes in
26citing papers in PubMed
0.9field-weighted citation impact, top 26% 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, 31 citations in OpenAlex.

  1. Article
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  6. Review
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  9. Article
  10. Knockdown of GNL3L Alleviates the Progression of COPD Through Inhibiting the ATM/p53 Pathway.International journal of chronic obstructive pulmonary disease · 2023
    Article
  11. Article
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  16. LDOC1 as Negative Prognostic Marker for Vulvar Cancer Patients.International journal of molecular sciences · 2020
    Article
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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

4 authors at 1 institution in 1 country.

Indu Jose Thoompumkala Laboratory of Molecular Virology and Cell Biology, National Cancer Tissue Biobank, Bhupat and Jyoti Mehta School of Biosciences, Department of Biotechnology , Indian Institute of Technology-Madras , Chennai , India.
Krishnan Rehnaa Laboratory of Molecular Virology and Cell Biology, National Cancer Tissue Biobank, Bhupat and Jyoti Mehta School of Biosciences, Department of Biotechnology , Indian Institute of Technology-Madras , Chennai , India.
Kumaraswamy Anbarasua Laboratory of Molecular Virology and Cell Biology, National Cancer Tissue Biobank, Bhupat and Jyoti Mehta School of Biosciences, Department of Biotechnology , Indian Institute of Technology-Madras , Chennai , India.
Sundarasamy Mahalingama Laboratory of Molecular Virology and Cell Biology, National Cancer Tissue Biobank, Bhupat and Jyoti Mehta School of Biosciences, Department of Biotechnology , Indian Institute of Technology-Madras , Chennai , India.
Indian Institute of Technology Madras · IN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Guanine nucleotide binding protein-like 3-like (GNL3L) is an evolutionarily conserved putative nucleolar GTPase belonging to the HSR1-MMR1 family. In the present study, using protein-protein interaction assays, we show that Leucine Zipper Down-regulated in Cancer-1 (LDOC1) is a novel interacting partner of GNL3L. Furthermore, our results reveal that ectopic expression of LDOC1 destabilizes endogenous GNL3L levels and down modulates GNL3L-induced cell proliferation, in contrast, the knockdown of LDOC1 potentiates cell proliferation upon GNL3L expression. Interestingly, GNL3L upregulates NF-κB dependent transcriptional activity by modulating the expression of NF-κB subunit p65, which is reversed upon co-expression of LDOC1 with GNL3L. GNL3L also potentiates TNF-α mediated NF-κB activity. In addition, anti-apoptotic function of GNL3L is impaired upon p65 knockdown, suggesting its critical role in GNL3L mediated cell proliferation/survival. An inverse correlation of GNL3L and LDOC1 expression profiles in various tumor tissues from BioXpress database indicate their critical role in cancer. Collectively, our data provides evidence that GNL3L-LDOC1 interplay regulates cell proliferation through the modulation of NF-κB pathway during tumorigenesis.

Indexed as

Signal TransductionApoptosisCell Line, TumorCell ProliferationDown-RegulationGene Expression Regulation, NeoplasticGTP-Binding ProteinsHEK293 CellsHumansModels, BiologicalNF-kappa BNuclear ProteinsPhosphorylationProtein BindingProtein Interaction Domains and MotifsProtein StabilityGNL3L protein, humanGTP-Binding ProteinsLDOC1 protein, humanNF-kappa BNuclear ProteinsTranscription Factor RelATumor Suppressor ProteinsApoptosiscell signalingGNL3LLDOC1NF-κB transcription factorproliferationprotein-protein interaction

Identifiers

PMID27764577
PMCPMC5176145
OpenAlexW2538920779

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.