Evidence map›Paper›PMID 27764768›Full record

ArticlePhysiological genomics2016

Peptide affinity analysis of proteins that bind to an unstructured region containing the transactivating domain of the osmoprotective transcription factor NFAT5.

Jenna F Dumond, Xue Zhang, Yuichiro Izumi, Kevin Ramkissoon, Guanghui Wang, Marjan Gucek, Xujing Wang, 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 1 paper.

0numbers the graph read from it
0cells of the map it votes in
1citing papers in PubMed
–field-weighted citation impact, top 90% 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

1 citing paper in PubMed, 2 citations in OpenAlex.

  1. 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 · 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

9 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.
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.
Kevin RamkissoonSystems Biology Center, Division of Intramural Research, National Heart, Lung and Blood Institute, Bethesda, Maryland; and.
Guanghui WangSystems Biology Center, Division of Intramural Research, National Heart, Lung and Blood Institute, Bethesda, Maryland; and.
Marjan GucekSystems Biology Center, Division of Intramural Research, National Heart, Lung and Blood Institute, Bethesda, Maryland; and.
Xujing WangSystems Biology Center, Division of Intramural Research, National Heart, Lung and Blood Institute, Bethesda, Maryland; and.
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

Proteomics CoreZICHL005903 · NHLBI · NATIONAL HEART, LUNG, AND BLOOD INSTITUTE · PI GUCEK, MARJAN · 2009 to 2022
$23.3M
6 · The paper itself

Abstract

NFAT5 is a transcription factor originally identified because it is activated by hypertonicity and that activation increases expression of genes that protect against the adverse effects of the hypertonicity. However, its targets also include genes not obviously related to tonicity. The transactivating domain of NFAT5 is contained in its COOH-terminal region, which is predicted to be unstructured. Unstructured regions are common in transcription factors particularly in transactivating domains where they can bind co-regulatory proteins essential to their function. To identify potential binding partners of NFAT5 from either cytoplasmic or nuclear HEK293 cell extracts, we used peptide affinity chromatography followed by mass spectrometry. Peptide aptamer-baits consisted of overlapping 20 amino acid peptides within the predicted COOH-terminal unstructured region of NFAT5. We identify a total of 351 unique protein preys that associate with at least one COOH-terminal peptide bait from NFAT5 in either cytoplasmic or nuclear extracts from cells incubated at various tonicities (NaCl varied). In addition to finding many proteins already known to associate with NFAT5, we found many new ones whose function suggest novel aspects of NFAT5 regulation, interaction, and function. Relatively few of the proteins pulled down by peptide baits from NFAT5 are generally involved in transcription, and most, therefore, are likely to be specifically related to the regulation of NFAT5 or its function. The novel associated proteins are involved with cancer, effects of hypertonicity on chromatin, development, splicing of mRNA, transcription, and vesicle trafficking.

Indexed as

Amino Acid SequenceCell ExtractsChromatography, AffinityHEK293 CellsHumansNFATC Transcription FactorsOsmosisPeptidesProtein BindingProtein DomainsProtein Interaction MapsProtein IsoformsSodium ChlorideCell ExtractsNFATC Transcription FactorsPeptidesProtein IsoformsSodium ChloridedisorderhypertonicityNFAT5peptide affinityproteomics

Identifiers

PMID27764768
PMCPMC6223574
OpenAlexW2528948968

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.