Evidence map›Paper›PMID 10713173›Full record

ArticleMolecular and cellular biology2000

Expression and functional analysis of Uch-L3 during mouse development.

L J Kurihara, E Semenova, J M Levorse, S M Tilghman

Open access · greenAbstract read
In one paragraph

Article in Molecular and cellular biology, 2000. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 31 papers.

0numbers the graph read from it
0cells of the map it votes in
31citing papers in PubMed
1.1field-weighted citation impact, top 24% 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

31 citing papers in PubMed, 69 citations in OpenAlex.

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  14. Protein neddylation: beyond cullin-RING ligases.Nature reviews. Molecular cell biology · 2015
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  18. The NEDD8 modification pathway in plants.Frontiers in plant science · 2014
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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.

L J KuriharaHoward Hughes Medical Institute and Department of Molecular Biology, Princeton University, Princeton, New Jersey 08544, USA.
E Semenova
J M Levorse
S M Tilghman
Princeton University · USHoward Hughes Medical Institute · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Mice homozygous for the s(1Acrg) deletion at the Ednrb locus arrest at embryonic day 8.5. To determine the molecular basis of this defect, we initiated positional cloning of the s(1Acrg) minimal region. The mouse Uch-L3 (ubiquitin C-terminal hydrolase L3) gene was mapped within the s(1Acrg) minimal region. Because Uch-L3 transcripts were present in embryonic structures relevant to the s(1Acrg) phenotype, we created a targeted mutation in Uch-L3 to address its role during development and its possible contribution to the s(1Acrg) phenotype. Mice homozygous for the mutation Uch-L3(Delta3-7) were viable, with no obvious developmental or histological abnormalities. Although high levels of Uch-L3 RNA were detected in testes and thymus, Uch-L3(Delta3-7) homozygotes were fertile, and no defect in intrathymic T-cell differentiation was detected. We conclude that the s(1Acrg) phenotype is either complex and multigenic or due to the loss of another gene within the region. We propose that Uch-L3 may be functionally redundant with its homologue Uch-L1.

Indexed as

Amino Acid SequenceAnimalsBase SequenceCell DifferentiationCloning, MolecularGene Expression Regulation, DevelopmentalGene TargetingGestational AgeHomozygoteIn Situ HybridizationMajor Histocompatibility ComplexMiceMice, KnockoutMolecular Sequence DataMutationPhenotypeRNA, MessengerThiolester HydrolasesUbiquitin Thiolesterase

Identifiers

PMID10713173
PMCPMC85452
OpenAlexW2009092091

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.