Evidence map›Paper›PMID 26757802›Full record

ArticlePhysiological genomics2016

Peptide affinity analysis of proteins that bind to an unstructured NH2-terminal region of the osmoprotective transcription factor NFAT5.

Jenna F DuMond, Kevin Ramkissoon, Xue Zhang, Yuichiro Izumi, Xujing Wang, Koji Eguchi, Shouguo Gao, Masashi Mukoyama, Maurice B Burg, Joan D Ferraris

Open access · bronzeAbstract read
In one paragraph

Article in Physiological genomics, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.

0numbers the graph read from it
0cells of the map it votes in
6citing papers in PubMed
0.6field-weighted citation impact, top 32% 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

6 citing papers in PubMed, 9 citations in OpenAlex.

  1. Article
  2. Article
  3. NFAT5, which protects against hypertonicity, is activated by that stress via structuring of its intrinsically disordered domain.Proceedings of the National Academy of Sciences of the United States of America · 2020
    Article
  4. Article
  5. 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

10 authors at 2 institutions in 2 countries.

Jenna F DuMondSystems Biology Center, Division of Intramural Research, National Heart, Lung and Blood Institute, Bethesda Maryland; and.
Kevin RamkissoonSystems Biology Center, Division of Intramural Research, National Heart, Lung and Blood Institute, Bethesda Maryland; and.
Xue ZhangSystems Biology Center, Division of Intramural Research, National Heart, Lung and Blood Institute, Bethesda Maryland; and.
Yuichiro IzumiSystems Biology Center, Division of Intramural Research, National Heart, Lung and Blood Institute, Bethesda Maryland; and Department of Nephrology, Kumamoto University Graduate School of Medical Sciences, Kumamoto, Japan.
Xujing WangSystems Biology Center, Division of Intramural Research, National Heart, Lung and Blood Institute, Bethesda Maryland; and.
Koji EguchiDepartment of Nephrology, Kumamoto University Graduate School of Medical Sciences, Kumamoto, Japan.
Shouguo GaoSystems Biology Center, Division of Intramural Research, National Heart, Lung and Blood Institute, Bethesda Maryland; and.
Masashi MukoyamaDepartment of Nephrology, Kumamoto University Graduate School of Medical Sciences, Kumamoto, Japan.
Maurice B BurgSystems Biology Center, Division of Intramural Research, National Heart, Lung and Blood Institute, Bethesda Maryland; and Maurice_burg@nih.gov.
Joan D FerrarisSystems Biology Center, Division of Intramural Research, National Heart, Lung and Blood Institute, Bethesda Maryland; and.
National Heart Lung and Blood Institute · USKumamoto University · JP

Funding

Systems Biology CoreZIAHL006192 · NHLBI · NATIONAL HEART, LUNG, AND BLOOD INSTITUTE · PI WANG, XUJING · 2014 to 2016
$4.6M
6 · The paper itself

Abstract

NFAT5 is an osmoregulated transcription factor that particularly increases expression of genes involved in protection against hypertonicity. Transcription factors often contain unstructured regions that bind co-regulatory proteins that are crucial for their function. The NH2-terminal region of NFAT5 contains regions predicted to be intrinsically disordered. We used peptide aptamer-based affinity chromatography coupled with mass spectrometry to identify protein preys pulled down by one or more overlapping 20 amino acid peptide baits within a predicted NH2-terminal unstructured region of NFAT5. We identify a total of 467 unique protein preys that associate with at least one NH2-terminal peptide bait from NFAT5 in either cytoplasmic or nuclear extracts from HEK293 cells treated with elevated, normal, or reduced NaCl concentrations. Different sets of proteins are pulled down from nuclear vs. cytoplasmic extracts. We used GeneCards to ascertain known functions of the protein preys. The protein preys include many that were previously known, but also many novel ones. Consideration of the novel ones suggests many aspects of NFAT5 regulation, interaction and function that were not previously appreciated, for example, hypertonicity inhibits NFAT5 by sumoylating it and the NFAT5 protein preys include components of the CHTOP complex that desumoylate proteins, an action that should contribute to activation of NFAT5.

Indexed as

Cell NucleusChromatography, AffinityCytoplasmHEK293 CellsHumansNuclear Pore Complex ProteinsNuclear ProteinsPeptidesProtein Interaction MappingProteinsTandem Mass SpectrometryTranscription FactorsCHTOP protein, humanNFAT5 protein, humanNuclear Pore Complex ProteinsNuclear ProteinsNUP160 protein, humanNup205 protein, humanPeptidesProteinsTranscription Factorsintrinsic disorderosmolalityproteomics

Identifiers

PMID26757802
PMCPMC4824150
OpenAlexW2288496836

What OpenQuestion holds

Textmetadata
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.