Evidence map›Paper›PMID 37013192›Full record

ArticleiScience2023

TZAP overexpression induces telomere dysfunction and ALT-like activity in ATRX/DAXX-deficient cells.

Sara Priego Moreno, Javier Miralles Fusté, Melanie Kaiser, Julia Su Zhou Li, Joe Nassour, Candy Haggblom, Eros Lazzerini Denchi, Jan Karlseder

Open access · goldAbstract read
In one paragraph

Article in iScience, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.

0numbers the graph read from it
0cells of the map it votes in
6citing papers in PubMed
1.4field-weighted citation impact, top 19% 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

6 citing papers in PubMed, 8 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

8 authors at 3 institutions in 1 country.

Sara Priego MorenoThe Salk Institute for Biological Studies, Molecular and Cell Biology Department, 10010 N. Torrey pines Road, La Jolla, CA 92037, USA.
Javier Miralles FustéThe Salk Institute for Biological Studies, Molecular and Cell Biology Department, 10010 N. Torrey pines Road, La Jolla, CA 92037, USA.
Melanie KaiserThe Salk Institute for Biological Studies, Molecular and Cell Biology Department, 10010 N. Torrey pines Road, La Jolla, CA 92037, USA.
Julia Su Zhou LiThe Ludwig Institute for Cancer Research, University of California San Diego, 9500 Gilman Drive, La Jolla, CA 92093, USA.
Joe NassourThe Salk Institute for Biological Studies, Molecular and Cell Biology Department, 10010 N. Torrey pines Road, La Jolla, CA 92037, USA.
Candy HaggblomThe Salk Institute for Biological Studies, Molecular and Cell Biology Department, 10010 N. Torrey pines Road, La Jolla, CA 92037, USA.
Eros Lazzerini DenchiLaboratory for Genome Integrity, National Cancer Institute, Building 37, Room 2144B, Bethesda, MD 20892, USA.
Jan KarlsederThe Salk Institute for Biological Studies, Molecular and Cell Biology Department, 10010 N. Torrey pines Road, La Jolla, CA 92037, USA.
Salk Institute for Biological Studies · USNational Cancer Institute · USUniversity of California San Diego · US

Funding

Viral Vector Core (VVC)P30CA014195 · NCI · SALK INSTITUTE FOR BIOLOGICAL STUDIES · PI Reuben Shaw · 1985 to 2026
$82.8M
Understanding the role of autophagy-regulated cell death in the escape from replicative crisisR01CA234047 · NCI · SALK INSTITUTE FOR BIOLOGICAL STUDIES · PI KARLSEDER, JAN, SHAW, REUBEN · 2020 to 2024
$3.1M
A nucleus-to-mitochondria nucleic acid-sensing pathway prevents bypass of age-associated proliferative boundariesR01AG077324 · NIA · SALK INSTITUTE FOR BIOLOGICAL STUDIES · PI Jan Karlseder · 2022 to 2026
$3.0M
Mitochondria-to-Nucleus Signaling in Colorectal CancerR01CA228211 · NCI · SALK INSTITUTE FOR BIOLOGICAL STUDIES · PI HARGREAVES, DIANA CLARE, SHADEL, GERALD · 2020 to 2024
$2.6M
Understanding DNA break repair pathway choice regulation by the cNHEJ inhibitor CYRENR01CA227934 · NCI · SALK INSTITUTE FOR BIOLOGICAL STUDIES · PI KARLSEDER, JAN · 2018 to 2022
$2.2M
The role of autophagy in the escape from replicative crisis and tumorigenesisK99CA252447 · NCI · SALK INSTITUTE FOR BIOLOGICAL STUDIES · PI NASSOUR, JOE · 2020 to 2021
$326k
NCI NIH HHS K99 CA252447NCI NIH HHS P30 CA014195NCI NIH HHS R01 CA227934NCI NIH HHS R01 CA228211NCI NIH HHS R01 CA234047NIA NIH HHS R01 AG077324
6 · The paper itself

Abstract

The appropriate regulation of telomere length homeostasis is crucial for the maintenance of genome integrity. The telomere-binding protein TZAP has been suggested to regulate telomere length by promoting t-circle and c-circle excisions through telomere trimming, yet the molecular mechanisms by which TZAP functions at telomeres are not understood. Using a system based on TZAP overexpression, we show that efficient TZAP recruitment to telomeres occurs in the context of open telomeric chromatin caused by loss of ATRX/DAXX independently of H3.3 deposition. Moreover, our data indicate that TZAP binding to telomeres induces telomere dysfunction and ALT-like activity, resulting in the generation of t-circles and c-circles in a Bloom-Topoisomerase IIIα-RMI1-RMI2 (BTR)-dependent manner.

Indexed as

Chromosome organizationMolecular biology experimental approachMolecular interaction

Identifiers

PMID37013192
PMCPMC10066556
OpenAlexW4324031139

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.