Evidence map›Paper›PMID 28955502›Full record

ArticleCell discovery2017

Systematic analysis of human telomeric dysfunction using inducible telosome/shelterin CRISPR/Cas9 knockout cells.

Hyeung Kim, Feng Li, Quanyuan He, Tingting Deng, Jun Xu, Feng Jin, Cristian Coarfa, Nagireddy Putluri, Dan Liu, Zhou Songyang

Open access · goldAbstract read
In one paragraph

Article in Cell discovery, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 39 papers.

0numbers the graph read from it
0cells of the map it votes in
39citing papers in PubMed
3.2field-weighted citation impact, top 7% 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

39 citing papers in PubMed, 53 citations in OpenAlex.

  1. Article
  2. How telomere attrition protects against cancer.Nature reviews. Genetics · 2026
    Review
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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.

Hyeung KimVerna and Marrs McLean Department of Biochemistry and Molecular Biology, Baylor College of Medicine, Houston, TX, USA.
Feng LiKey Laboratory of Gene Engineering of the Ministry of Education and State Key Laboratory for Biocontrol, School of Life Sciences, Sun Yat-sen University, Guangzhou, China.
Quanyuan HeVerna and Marrs McLean Department of Biochemistry and Molecular Biology, Baylor College of Medicine, Houston, TX, USA.
Tingting DengKey Laboratory of Gene Engineering of the Ministry of Education and State Key Laboratory for Biocontrol, School of Life Sciences, Sun Yat-sen University, Guangzhou, China.
Jun XuCell-Based Assay Screening Service Core, Baylor College of Medicine, Houston, TX, USA.
Feng JinDepartment of Molecular and Cellular Biology and Advanced Technology Core, Baylor College of Medicine, Houston, TX, USA.
Cristian CoarfaDepartment of Molecular and Cellular Biology and Advanced Technology Core, Baylor College of Medicine, Houston, TX, USA.
Nagireddy PutluriDepartment of Molecular and Cellular Biology and Advanced Technology Core, Baylor College of Medicine, Houston, TX, USA.
Dan LiuVerna and Marrs McLean Department of Biochemistry and Molecular Biology, Baylor College of Medicine, Houston, TX, USA.
Zhou SongyangVerna and Marrs McLean Department of Biochemistry and Molecular Biology, Baylor College of Medicine, Houston, TX, USA.
Baylor College of Medicine · USSun Yat-sen University · CN

Funding

Tumor BiologyP30CA125123 · NCI · BAYLOR COLLEGE OF MEDICINE · PI DAVID R ROWLEY · 2007 to 2026
$73.9M
Molecular Genetics of the Telomere Biology DisordersR01HL131744 · NHLBI · BAYLOR COLLEGE OF MEDICINE · PI BERTUCH, ALISON A, HOCKEMEYER, DIRK · 2016 to 2025
$4.5M
THE ROLE OF TELOMERASE REGULATORS IN TELOMERE MAINTENANCE AND GENOMIC INSTABILITYR01CA211653 · NCI · BAYLOR COLLEGE OF MEDICINE · PI BERTUCH, ALISON A · 2017 to 2022
$1.8M
Defining the human telomere signaling networks and their implication in cancerR01GM095599 · NIGMS · BAYLOR COLLEGE OF MEDICINE · PI SONGYANG, ZHOU · 2011 to 2014
$1.2M
NCI NIH HHS P30 CA125123NCI NIH HHS R01 CA211653NHLBI NIH HHS R01 HL131744NIGMS NIH HHS R01 GM095599
6 · The paper itself

Abstract

CRISPR/Cas9 technology enables efficient loss-of-function analysis of human genes using somatic cells. Studies of essential genes, however, require conditional knockout (KO) cells. Here, we describe the generation of inducible CRISPR KO human cell lines for the subunits of the telosome/shelterin complex, TRF1, TRF2, RAP1, TIN2, TPP1 and POT1, which directly interact with telomeres or can bind to telomeres through association with other subunits. Homozygous inactivation of several subunits is lethal in mice, and most loss-of-function studies of human telomere regulators have relied on RNA interference-mediated gene knockdown, which suffers its own limitations. Our inducible CRISPR approach has allowed us to more expediently obtain large numbers of KO cells in which essential telomere regulators have been inactivated for biochemical and molecular studies. Our systematic analysis revealed functional differences between human and mouse telomeric proteins in DNA damage responses, telomere length and metabolic control, providing new insights into how human telomeres are maintained.

Indexed as

CRISPR/Cas9inducible knockoutmetabolismPOT1 isoformtelomeretelosome/shelterin

Identifiers

PMID28955502
PMCPMC5613224
OpenAlexW2757243315

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.