Evidence map›Paper›PMID 27872149›Full record

ArticleMolecular and cellular biology2017

Endogenous Telomerase Reverse Transcriptase N-Terminal Tagging Affects Human Telomerase Function at Telomeres In Vivo.

Kunitoshi Chiba, Jacob M Vogan, Robert A Wu, Manraj S Gill, Xiaozhu Zhang, Kathleen Collins, Dirk Hockemeyer

Open access · bronzeAbstract read
In one paragraph

Article in Molecular and cellular biology, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.

0numbers the graph read from it
0cells of the map it votes in
10citing papers in PubMed
1.4field-weighted citation impact, top 18% 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

10 citing papers in PubMed, 18 citations in OpenAlex.

  1. Review
  2. Review
  3. Review
  4. Genome-wide screens identify specific drivers of mutantProceedings of the National Academy of Sciences of the United States of America · 2022
    Article
  5. Article
  6. Article
  7. Article
  8. Review
  9. Article
  10. Mutations in the promoter of the telomerase geneScience (New York, N.Y.) · 2017
    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

7 authors at 1 institution in 1 country.

Kunitoshi ChibaDepartment of Molecular and Cell Biology, University of California, Berkeley, Berkeley, California, USA.
Jacob M VoganDepartment of Molecular and Cell Biology, University of California, Berkeley, Berkeley, California, USA.
Robert A WuDepartment of Molecular and Cell Biology, University of California, Berkeley, Berkeley, California, USA.
Manraj S GillDepartment of Molecular and Cell Biology, University of California, Berkeley, Berkeley, California, USA.
Xiaozhu ZhangDepartment of Molecular and Cell Biology, University of California, Berkeley, Berkeley, California, USA.
Kathleen CollinsDepartment of Molecular and Cell Biology, University of California, Berkeley, Berkeley, California, USA.
Dirk HockemeyerDepartment of Molecular and Cell Biology, University of California, Berkeley, Berkeley, California, USA hockemeyer@berkeley.edu.
University of California, Berkeley · US

Funding

STRUCTURE AND FUNCTION OF TELOMERASER01GM054198 · NIGMS · UNIVERSITY OF CALIFORNIA BERKELEY · PI COLLINS, KATHLEEN · 1996 to 2018
$5.4M
Molecular Mechanism of X-linked Dyskeratosis CongenitaR01HL079585 · NHLBI · UNIVERSITY OF CALIFORNIA BERKELEY · PI COLLINS, KATHLEEN · 2004 to 2017
$4.1M
Telomerase function in human tumor and stem cell biologyR01CA196884 · NCI · UNIVERSITY OF CALIFORNIA BERKELEY · PI HOCKEMEYER, DIRK · 2015 to 2019
$1.7M
NCI NIH HHS R01 CA196884NHLBI NIH HHS R01 HL079585NIGMS NIH HHS R01 GM054198
6 · The paper itself

Abstract

Telomerase action at telomeres is essential for the immortal phenotype of stem cells and the aberrant proliferative potential of cancer cells. Insufficient telomere maintenance can cause stem cell and tissue failure syndromes, while increased telomerase levels are associated with tumorigenesis. Both pathologies can arise from only small perturbation of telomerase function. To analyze telomerase at its low endogenous expression level, we genetically engineered human pluripotent stem cells (hPSCs) to express various N-terminal fusion proteins of the telomerase reverse transcriptase from its endogenous locus. Using this approach, we found that these modifications can perturb telomerase function in hPSCs and cancer cells, resulting in telomere length defects. Biochemical analysis suggests that this defect is multileveled, including changes in expression and activity. These findings highlight the unknown complexity of telomerase structural requirements for expression and function in vivo.

Indexed as

Blotting, SouthernEpitopesGene EditingGenotypeHuman Embryonic Stem CellsHumansPhenotypeRepetitive Sequences, Nucleic AcidTelomeraseTelomereTelomere HomeostasisEpitopesTelomeraseCRISPR/Cas9embryonic stem cellsgenome editingpluripotent stem cellstelomerasetelomeres

Identifiers

PMID27872149
PMCPMC5247607
OpenAlexW2550040363

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.