Evidence map›Paper›PMID 26283729›Full record

ArticleMolecular and cellular biology2015

Role of the Exocyst Complex Component Sec6/8 in Genomic Stability.

Michael J Torres, Raj K Pandita, Ozlem Kulak, Rakesh Kumar, Etienne Formstecher, Nobuo Horikoshi, Kalpana Mujoo, Clayton R Hunt, Yingming Zhao, Lawrence Lum and 4 more

Open access · bronzeAbstract read
In one paragraph

Article in Molecular and cellular biology, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.

0numbers the graph read from it
0cells of the map it votes in
11citing papers in PubMed
1.4field-weighted citation impact, top 20% 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

11 citing papers in PubMed, 16 citations in OpenAlex.

  1. Article
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  9. Article
  10. The Exocyst Complex in Health and Disease.Frontiers in cell and developmental biology · 2016
    Review
  11. 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

14 authors at 5 institutions in 2 countries.

Michael J TorresDepartment of Cell Biology, University of Texas Southwestern Medical Center, Dallas, Texas, USA.
Raj K PanditaDepartment of Radiation Oncology, University of Texas Southwestern Medical Center, Dallas, Texas, USA The Houston Methodist Research Institute, Houston, Texas, USA.
Ozlem KulakDepartment of Cell Biology, University of Texas Southwestern Medical Center, Dallas, Texas, USA.
Rakesh KumarDepartment of Radiation Oncology, University of Texas Southwestern Medical Center, Dallas, Texas, USA.
Etienne FormstecherHybrigenics, Inc., Paris, France.
Nobuo HorikoshiThe Houston Methodist Research Institute, Houston, Texas, USA.
Kalpana MujooThe Houston Methodist Research Institute, Houston, Texas, USA.
Clayton R HuntThe Houston Methodist Research Institute, Houston, Texas, USA.
Yingming ZhaoBen May Department for Cancer Research, The University of Chicago, Chicago, Illinois, USA.
Lawrence LumDepartment of Cell Biology, University of Texas Southwestern Medical Center, Dallas, Texas, USA.
Aubhishek ZamanDepartment of Cell Biology, University of Texas Southwestern Medical Center, Dallas, Texas, USA.
Charles YeamanDepartment of Anatomy and Cell Biology, University of Iowa, Iowa City, Iowa, USA.
Michael A WhiteDepartment of Cell Biology, University of Texas Southwestern Medical Center, Dallas, Texas, USA Michael.White@UTSouthwestern.edu tpandita@houstonmethodist.org.
Tej K PanditaDepartment of Radiation Oncology, University of Texas Southwestern Medical Center, Dallas, Texas, USA The Houston Methodist Research Institute, Houston, Texas, USA Michael.White@UTSouthwestern.edu tpandita@houstonmethodist.org.
The University of Texas Southwestern Medical Center · USHouston Methodist · USHybrigenics (France) · FRUniversity of Chicago · USUniversity of Iowa · US

Funding

UT Southwestern Medical Center Simmons Comprehensive Cancer CenterP30CA142543 · NCI · UT SOUTHWESTERN MEDICAL CENTER · PI Sandi Leigh Pruitt · 2010 to 2026
$53.7M
COMPONENTS OF RAS-MEDIATED GROWTH CONTROLR01CA071443 · NCI · UT SOUTHWESTERN MEDICAL CENTER · PI WHITE, MICHAEL A. · 1996 to 2015
$4.8M
CHROMATIN MODIFYING FACTORS CONTROL RADIATION RESPONSE AND GENOMIC STABILITYR01CA129537 · NCI · WASHINGTON UNIVERSITY · PI PANDITA, TEJ K · 2008 to 2018
$3.3M
Tumor-cell-specific targets for combined hyperthermia and radiation effectsR01CA154320 · NCI · UT SOUTHWESTERN MEDICAL CENTER · PI PANDITA, TEJ K · 2010 to 2014
$1.6M
The RaLGTPase Regulatory NetworkR01CA129451 · NCI · UT SOUTHWESTERN MEDICAL CENTER · PI WHITE, MICHAEL A. · 2007 to 2011
$1.3M
Role of Heterochromatin protein 1 Beta in Genome Maintenance and OncogenesisR01GM109768 · NIGMS · METHODIST HOSPITAL RESEARCH INSTITUTE · PI PANDITA, TEJ K · 2014 to 2017
$1.2M
Targeting Mechanistic Subtypes of Neoplastic DiseaseR35CA197717 · NCI · UT SOUTHWESTERN MEDICAL CENTER · PI WHITE, MICHAEL A. · 2015 to 2015
$725k
NCI NIH HHS CA129451NCI NIH HHS CA129537NCI NIH HHS CA154320NCI NIH HHS CA71443NCI NIH HHS P30 CA142543NCI NIH HHS R01 CA071443NCI NIH HHS R01 CA129451NCI NIH HHS R01 CA129537NCI NIH HHS R01 CA154320NCI NIH HHS R35 CA197717NIGMS NIH HHS GM109768NIGMS NIH HHS R01 GM109768
6 · The paper itself

Abstract

The exocyst is a heterooctomeric complex well appreciated for its role in the dynamic assembly of specialized membrane domains. Accumulating evidence indicates that this macromolecular machine also serves as a physical platform that coordinates regulatory cascades supporting biological systems such as host defense signaling, cell fate, and energy homeostasis. The isolation of multiple components of the DNA damage response (DDR) as exocyst-interacting proteins, together with the identification of Sec8 as a suppressor of the p53 response, suggested functional interactions between the exocyst and the DDR. We found that exocyst perturbation resulted in resistance to ionizing radiation (IR) and accelerated resolution of DNA damage. This occurred at the expense of genomic integrity, as enhanced recombination frequencies correlated with the accumulation of aberrant chromatid exchanges. Sec8 perturbation resulted in the accumulation of ATF2 and RNF20 and the promiscuous accumulation of DDR-associated chromatin marks and Rad51 repairosomes. Thus, the exocyst supports DNA repair fidelity by limiting the formation of repair chromatin in the absence of DNA damage.

Indexed as

DNA RepairGenomic InstabilityActivating Transcription Factor 2Apoptosis Regulatory ProteinsAutophagyBeclin-1Cell Line, TumorExocytosisGene DeletionHumansIntracellular Signaling Peptides and ProteinsMembrane ProteinsTumor Suppressor p53-Binding Protein 1Ubiquitin-Protein LigasesVesicular Transport ProteinsActivating Transcription Factor 2Apoptosis Regulatory ProteinsATF2 protein, humanBeclin-1BECN1 protein, humanEXOC3 protein, humanEXOC4 protein, humanIntracellular Signaling Peptides and ProteinsMembrane ProteinsRNF20 protein, humanTP53BP1 protein, humanTumor Suppressor p53-Binding Protein 1Ubiquitin-Protein LigasesVesicular Transport Proteins

Identifiers

PMID26283729
PMCPMC4589602
OpenAlexW1766223589

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.