Evidence map›Paper›PMID 26869315›Full record

ReviewGene2016

Structure, expression and functions of MTA genes.

Rakesh Kumar, Rui-An Wang

Open access · greenAbstract readReview
In one paragraph

Review in Gene, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 51 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
51citing papers in PubMed, 1 pooled it
4.9field-weighted citation impact, top 5% 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

51 citing papers in PubMed, 1 synthesis or guideline pooled it, 91 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

2 authors at 2 institutions in 3 countries.

Rakesh KumarDepartment of Biochemistry and Molecular Medicine, School of Medicine and Health Sciences, 530 Ross Hall, 2300 Eye Street, N.W., George Washington University, Washington, DC 20037, USA; Cancer Biology Program, Rajiv Gandhi Center of Biotechnology, Thiruvananthapuram 695014, India. Electronic address: bcmrxk@gwu.edu.
Rui-An WangState Key Laboratory of Cancer Biology, Xijing Hospital, Fourth Military Medical University, Xi'an 710032, China; Department of Pathology, Xijing Hospital, Fourth Military Medical University, Xi'an 710032, China. Electronic address: Wangra@fmmu.edu.cn.
Air Force Medical University · CNGeorge Washington University · US

Funding

The Gene Wiki: Community intelligence applied to gene annotationR01GM089820 · NIGMS · SCRIPPS RESEARCH INSTITUTE, THE · PI SU, ANDREW I · 2010 to 2021
$5.2M
Pak1 Signaling and Targets in Breast Cancer ProgressionR01CA090970 · NCI · UNIVERSITY OF TX MD ANDERSON CAN CTR · PI KUMAR, RAKESH · 2001 to 2014
$3.5M
Role of Metastatic Tumor Antigen-1 in Mammary GlandR01CA098823 · NCI · UNIVERSITY OF TX MD ANDERSON CAN CTR · PI KUMAR, RAKESH · 2003 to 2013
$3.1M
NCI NIH HHS CA090970NCI NIH HHS CA98823NCI NIH HHS R01 CA090970NCI NIH HHS R01 CA098823NIGMS NIH HHS GM089820NIGMS NIH HHS R01 GM089820
6 · The paper itself

Abstract

Metastatic associated proteins (MTA) are integrators of upstream regulatory signals with the ability to act as master coregulators for modifying gene transcriptional activity. The MTA family includes three genes and multiple alternatively spliced variants. The MTA proteins neither have their own enzymatic activity nor have been shown to directly interact with DNA. However, MTA proteins interact with a variety of chromatin remodeling factors and complexes with enzymatic activities for modulating the plasticity of nucleosomes, leading to the repression or derepression of target genes or other extra-nuclear and nucleosome remodeling and histone deacetylase (NuRD)-complex independent activities. The functions of MTA family members are driven by the steady state levels and subcellular localization of MTA proteins, the dynamic nature of modifying signals and enzymes, the structural features and post-translational modification of protein domains, interactions with binding proteins, and the nature of the engaged and resulting features of nucleosomes in the proximity of target genes. In general, MTA1 and MTA2 are the most upregulated genes in human cancer and correlate well with aggressive phenotypes, therapeutic resistance, poor prognosis and ultimately, unfavorable survival of cancer patients. Here we will discuss the structure, expression and functions of the MTA family of genes in the context of cancer cells.

Indexed as

Gene Expression Regulation, NeoplasticAlternative SplicingAnimalsHumansMultigene FamilyMutationNM23 Nucleoside Diphosphate KinasesProtein Structure, TertiaryNM23 Nucleoside Diphosphate KinasesCancerChromatin remodelingCoregulatorsMetastasisMTA1MTA2MTA3

Identifiers

PMID26869315
PMCPMC4785049
OpenAlexW2258047954

What OpenQuestion holds

Textmetadata
LicenceTDM
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.