Evidence map›Paper›PMID 30837480›Full record

ArticleScientific reports2019

Degradation of p47 by autophagy contributes to CADM1 overexpression in ATLL cells through the activation of NF-κB.

Bidhan Sarkar, Ichiro Nishikata, Shingo Nakahata, Tomonaga Ichikawa, Toshiyuki Shiraga, Hasi Rani Saha, Masahiro Fujii, Yuetsu Tanaka, Kazuya Shimoda, Kazuhiro Morishita

Open access · goldAbstract read
In one paragraph

Article in Scientific reports, 2019. 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
1.2field-weighted citation impact, top 21% 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, 16 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 4 institutions in 1 country.

Bidhan SarkarDivision of Tumor and Cellular Biochemistry, Department of Medical Sciences, Faculty of Medicine, University of Miyazaki, Miyazaki, Japan.
Ichiro NishikataDivision of Tumor and Cellular Biochemistry, Department of Medical Sciences, Faculty of Medicine, University of Miyazaki, Miyazaki, Japan.
Shingo NakahataDivision of Tumor and Cellular Biochemistry, Department of Medical Sciences, Faculty of Medicine, University of Miyazaki, Miyazaki, Japan.
Tomonaga IchikawaDivision of Tumor and Cellular Biochemistry, Department of Medical Sciences, Faculty of Medicine, University of Miyazaki, Miyazaki, Japan.
Toshiyuki ShiragaDivision of Tumor and Cellular Biochemistry, Department of Medical Sciences, Faculty of Medicine, University of Miyazaki, Miyazaki, Japan.
Hasi Rani SahaDivision of Tumor and Cellular Biochemistry, Department of Medical Sciences, Faculty of Medicine, University of Miyazaki, Miyazaki, Japan.
Masahiro FujiiDivision of Virology, Niigata University Graduate School of Medical and Dental Sciences, Niigata, Japan.
Yuetsu TanakaDepartment of Immunology, Graduate School of Medicine, University of the Ryukyus, Okinawa, Japan.
Kazuya ShimodaDivision of Gastroenterology and Hematology, Department of Internal Medicine, Faculty of Medicine, University of Miyazaki, Miyazaki, Japan.
Kazuhiro MorishitaDivision of Tumor and Cellular Biochemistry, Department of Medical Sciences, Faculty of Medicine, University of Miyazaki, Miyazaki, Japan. kmorishi@med.miyazaki-u.ac.jp.
University of Miyazaki · JPNiigata University · JPNotre Dame Seishin University · JPUniversity of the Ryukyus · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Cell adhesion molecule 1 (CADM1), a member of the immunoglobulin superfamily, is identified as a novel cell surface marker for human T-cell leukemia virus (HTLV-1)-infected T cells. Adult T-cell leukemia/lymphoma (ATLL) is developed in HTLV-1-infected T-cells after a long infection period. To examine the mechanism of CADM1 overexpression in ATLL, we first identified that CADM1 is transcriptionally up-regulated by a transcriptional enhancer element through NF-κB signaling pathway. In HTLV-1-infected T-cells, CADM1 expression is dependent on HTLV-1/Tax through activation of canonical and non-canonical NF-κB; however, in ATLL cells with frequent loss of Tax expression, the activation of canonical NF-κB only enhances the CADM1 expression. Along with active mutations in signaling molecules under T-cell recepor (TCR) signaling, degradation of p47, a negative regulator of NF-κB, was essential for activation of canonical NF-κB through stabilization of NEMO (NF-κB essential modulator). The mechanism of p47 degradation is primarily dependent on activation of lysosomal-autophagy and the autophagy is activated in most of the HTLV-infected and ATLL cells, suggesting that the p47 degradation may be a first key molecular event during HTLV-1 infection to T-cells as a connector of two important signaling pathways, NF-κB and autophagy.

Indexed as

AutophagyAdaptor Proteins, Signal TransducingBinding SitesCell Adhesion Molecule-1Cell Line, TumorDown-RegulationGene Products, taxHumansHuman T-lymphotropic virus 1Jurkat CellsLeukemia-Lymphoma, Adult T-CellLysosomesNF-kappa BPromoter Regions, GeneticSignal TransductionTranscriptional ActivationAdaptor Proteins, Signal TransducingCADM1 protein, humanCell Adhesion Molecule-1Gene Products, taxNF-kappa Bp37 protein, humantax protein, Human T-lymphotrophic virus 1

Identifiers

PMID30837480
PMCPMC6400899
OpenAlexW2918692778

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.