Evidence map›Paper›PMID 31664887›Full record

ArticleMolecular biology of the cell2019

Nopp140-mediated concentration of telomerase in Cajal bodies regulates telomere length.

Jonathan Bizarro, Amit Bhardwaj, Susan Smith, U Thomas Meier

Abstract read
In one paragraph

Article in Molecular biology of the cell, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.

0numbers the graph read from it
0cells of the map it votes in
19citing papers in PubMed
1.6field-weighted citation impact, top 16% 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

19 citing papers in PubMed, 32 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

4 authors at 2 institutions in 1 country.

Jonathan BizarroDepartment of Anatomy and Structural Biology, Albert Einstein College of Medicine, Bronx, NY 10461.
Amit BhardwajDepartment of Pathology, Kimmel Center for Biology and Medicine at the Skirball Institute, New York University School of Medicine, New York, NY 10016.
Susan SmithDepartment of Pathology, Kimmel Center for Biology and Medicine at the Skirball Institute, New York University School of Medicine, New York, NY 10016.
U Thomas MeierDepartment of Anatomy and Structural Biology, Albert Einstein College of Medicine, Bronx, NY 10461.ORCID 0000-0001-6677-2677
Albert Einstein College of Medicine · USNew York University · US

Funding

WORD PROCESSORP30CA013330 · NCI · YESHIVA UNIVERSITY · PI THOMAS E ROHAN · 1985 to 2026
$111.2M
Mechanisms of Sister Telomere Cohesion and ResolutionR01CA116352 · NCI · NEW YORK UNIVERSITY SCHOOL OF MEDICINE · PI SMITH, SUSAN · 2007 to 2016
$3.1M
Cellular impact of X-linked dyskeratosis congenitaR01HL136662 · NHLBI · ALBERT EINSTEIN COLLEGE OF MEDICINE, INC · PI MEIER, U THOMAS · 2017 to 2020
$2.4M
MOLECULAR MECHANISM OF DYSKERATOSIS CONGENITAR01HL079566 · NHLBI · ALBERT EINSTEIN COL OF MED YESHIVA UNIV · PI MEIER, U THOMAS · 2004 to 2008
$2.0M
Regulation of telomere recombination in ALT cancer cellsR01CA200751 · NCI · NEW YORK UNIVERSITY SCHOOL OF MEDICINE · PI SMITH, SUSAN · 2016 to 2020
$2.0M
120kV Transmission Electron Microscope for a Multi-user Microscopy FacilityS10OD016214 · OD · ALBERT EINSTEIN COLLEGE OF MEDICINE, INC · PI CONDEELIS, JOHN S · 2014 to 2014
$459k
NCI NIH HHS P30 CA013330NCI NIH HHS R01 CA116352NCI NIH HHS R01 CA200751NHLBI NIH HHS R01 HL079566NHLBI NIH HHS R01 HL136662NIH HHS S10 OD016214
6 · The paper itself

Abstract

Cajal bodies (CBs) are nuclear organelles concentrating two kinds of RNA--protein complexes (RNPs), spliceosomal small nuclear (sn), and small CB-specific (sca)RNPs. Whereas the CB marker protein coilin is responsible for retaining snRNPs, the tether for scaRNPs is not known. Here we show that Nopp140, an intrinsically disordered CB phosphoprotein, is required to recruit and retain all scaRNPs in CBs. Knockdown (KD) of Nopp140 releases all scaRNPs leading to an unprecedented reduction in size of CB granules, hallmarks of CB ultrastructure. The CB-localizing protein WDR79 (aka TCAB1), which is mutated in the inherited bone marrow failure syndrome dyskeratosis congenita, is a specific component of all scaRNPs, including telomerase. Whereas mislocalization of telomerase by mutation of WDR79 leads to critically shortened telomeres, mislocalization of telomerase by Nopp140 KD leads to gradual extension of telomeres. Our studies suggest that the dynamic distribution of telomerase between CBs and nucleoplasm uniquely impacts telomere length maintenance and identify Nopp140 as a novel player in telomere biology.

Indexed as

Cell Line, TumorCoiled BodiesDyskeratosis CongenitaHeLa CellsHumansMolecular ChaperonesNuclear ProteinsPhosphoproteinsRNA InterferenceRNA, Small InterferingTelomeraseTelomereTelomere HomeostasisMolecular ChaperonesNOLC1 protein, humanNuclear ProteinsPhosphoproteinsRNA, Small InterferingTelomeraseWRAP53 protein, human

Identifiers

PMID31664887
PMCPMC6938241
OpenAlexW2982661801

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-SA
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.