Evidence map›Paper›PMID 33999958›Full record

ArticlePloS one2021

Altering mammalian transcription networking with ADAADi: An inhibitor of ATP-dependent chromatin remodeling.

Radhakrishnan Rakesh, Upasana Bedi Chanana, Saddam Hussain, Soni Sharma, Kaveri Goel, Deepa Bisht, Ketki Patne, Pynskhem Bok Swer, Joel W Hockensmith, Rohini Muthuswami

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.

0numbers the graph read from it
0cells of the map it votes in
8citing papers in PubMed
0.5field-weighted citation impact, top 39% 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

8 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 2 institutions in 2 countries.

Radhakrishnan RakeshChromatin Remodeling Laboratory, School of Life Sciences, JNU, New Delhi, India.
Upasana Bedi ChananaChromatin Remodeling Laboratory, School of Life Sciences, JNU, New Delhi, India.
Saddam HussainChromatin Remodeling Laboratory, School of Life Sciences, JNU, New Delhi, India.
Soni SharmaChromatin Remodeling Laboratory, School of Life Sciences, JNU, New Delhi, India.
Kaveri GoelChromatin Remodeling Laboratory, School of Life Sciences, JNU, New Delhi, India.
Deepa BishtChromatin Remodeling Laboratory, School of Life Sciences, JNU, New Delhi, India.
Ketki PatneChromatin Remodeling Laboratory, School of Life Sciences, JNU, New Delhi, India.
Pynskhem Bok SwerChromatin Remodeling Laboratory, School of Life Sciences, JNU, New Delhi, India.
Joel W HockensmithDepartment of Biochemistry and Molecular Genetics, University of Virginia, Charlottesville, Virginia, United States of America.
Rohini MuthuswamiChromatin Remodeling Laboratory, School of Life Sciences, JNU, New Delhi, India.ORCID 0000-0002-0559-9484
Jawaharlal Nehru University · INUniversity of Virginia · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Active DNA-dependent ATPase A Domain inhibitor (ADAADi) is the only known inhibitor of ATP-dependent chromatin remodeling proteins that targets the ATPase domain of these proteins. The molecule is synthesized by aminoglycoside phosphotransferase enzyme in the presence of aminoglycosides. ADAADi interacts with ATP-dependent chromatin remodeling proteins through motif Ia present in the conserved helicase domain, and thus, can potentially inhibit all members of this family of proteins. We show that mammalian cells are sensitive to ADAADi but with variable responses in different cell lines. ADAADi can be generated from a wide variety of aminoglycosides; however, cells showed differential response to ADAADi generated from various aminoglycosides. Using HeLa and DU145 cells as model system we have explored the effect of ADAADi on cellular functions. We show that the transcriptional network of a cell type is altered when treated with sub-lethal concentration of ADAADi. Although ADAADi has no known effects on DNA chemical and structural integrity, expression of DNA-damage response genes was altered. The transcripts encoding for the pro-apoptotic proteins were found to be upregulated while the anti-apoptotic genes were found to be downregulated. This was accompanied by increased apoptosis leading us to hypothesize that the ADAADi treatment promotes apoptotic-type of cell death by upregulating the transcription of pro-apoptotic genes. ADAADi also inhibited migration of cells as well as their colony forming ability leading us to conclude that the compound has effective anti-tumor properties.

Indexed as

Adenosine TriphosphatasesAdenosine TriphosphateAminoglycosidesAnimalsCell Line, TumorChromatinChromatin Assembly and DisassemblyDNADNA HelicasesGene Regulatory NetworksHeLa CellsHumansMammalsProtein DomainsAdenosine TriphosphatasesAdenosine TriphosphateAminoglycosidesChromatinDNADNA Helicases

Identifiers

PMID33999958
PMCPMC8128233
OpenAlexW3162681070

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.