Evidence map›Paper›PMID 27248179›Full record

ArticleOncotarget2016

β2-spectrin depletion impairs DNA damage repair.

Nobuo Horikoshi, Raj K Pandita, Kalpana Mujoo, Shashank Hambarde, Dharmendra Sharma, Abid R Mattoo, Sharmistha Chakraborty, Vijaya Charaka, Clayton R Hunt, Tej K Pandita

Open access · diamondAbstract read
In one paragraph

Article in Oncotarget, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.

0numbers the graph read from it
0cells of the map it votes in
15citing papers in PubMed
1.7field-weighted citation impact, top 15% 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

15 citing papers in PubMed, 25 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Article
  5. Article
  6. Article
  7. Article
  8. Review
  9. Article
  10. Article
  11. Spectrin and its interacting partners in nuclear structure and function.Experimental biology and medicine (Maywood, N.J.) · 2018
    Review
  12. Article
  13. Article
  14. Article
  15. 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

10 authors at 2 institutions in 1 country.

Nobuo Horikoshi
Raj K Pandita
Kalpana Mujoo
Shashank Hambarde
Dharmendra Sharma
Abid R Mattoo
Sharmistha Chakraborty
Vijaya Charaka
Clayton R Hunt
Tej K Pandita
Houston Methodist · USThe University of Texas Southwestern Medical Center · US

Funding

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
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
NCI NIH HHS R01 CA129537NCI NIH HHS R01 CA154320NIGMS NIH HHS R01 GM109768
6 · The paper itself

Abstract

β2-Spectrin (β2SP/SPTBN1, gene SPTBN1) is a key TGF-β/SMAD3/4 adaptor and transcriptional cofactor that regulates TGF-β signaling and can contribute to liver cancer development. Here we report that cells deficient in β2-Spectrin (β2SP) are moderately sensitive to ionizing radiation (IR) and extremely sensitive to agents that cause interstrand cross-links (ICLs) or replication stress. In response to treatment with IR or ICL agents (formaldehyde, cisplatin, camptothecin, mitomycin), β2SP deficient cells displayed a higher frequency of cells with delayed γ-H2AX removal and a higher frequency of residual chromosome aberrations. Following hydroxyurea (HU)-induced replication stress, β2SP-deficient cells displayed delayed disappearance of γ-H2AX foci along with defective repair factor recruitment (MRE11, CtIP, RAD51, RPA, and FANCD2) as well as defective restart of stalled replication forks. Repair factor recruitment is a prerequisite for initiation of DNA damage repair by the homologous recombination (HR) pathway, which was also defective in β2SP deficient cells. We propose that β2SP is required for maintaining genomic stability following replication fork stalling, whether induced by either ICL damage or replicative stress, by facilitating fork regression as well as DNA damage repair by homologous recombination.

Indexed as

AnimalsCell Line, TumorDNA DamageDNA RepairGenomic InstabilityHumansMiceSpectrinSpectrinDNA repairgenotoxicityβ2-spectrin

Identifiers

PMID27248179
PMCPMC5085102
OpenAlexW2405239438

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.