Evidence map›Paper›PMID 33852859›Full record

ArticleCell reports2021

Functional analyses of human LUC7-like proteins involved in splicing regulation and myeloid neoplasms.

Noah J Daniels, Courtney E Hershberger, Xiaorong Gu, Caroline Schueger, William M DiPasquale, Jonathan Brick, Yogen Saunthararajah, Jaroslaw P Maciejewski, Richard A Padgett

Open access · goldAbstract read
In one paragraph

Article in Cell reports, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 35 papers.

0numbers the graph read from it
0cells of the map it votes in
35citing papers in PubMed
3.1field-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

35 citing papers in PubMed, 62 citations in OpenAlex.

  1. Role of alternative splicing in cancer progression.Irish journal of medical science · 2026
    Review
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  7. Sustainable integrative cell biology: CENP-C is guilty by association.Chromosome research : an international journal on the molecular, supramolecular and evolutionary aspects of chromosome biology · 2025
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4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

9 authors at 2 institutions in 1 country.

Noah J DanielsDepartment of Molecular Medicine, Cleveland Clinic Lerner College of Medicine, School of Medicine, Case Western Reserve University, Cleveland, OH, USA; Department of Cardiovascular and Metabolic Sciences, Lerner Research Institute, Cleveland Clinic, Cleveland, OH, USA.
Courtney E HershbergerDepartment of Molecular Medicine, Cleveland Clinic Lerner College of Medicine, School of Medicine, Case Western Reserve University, Cleveland, OH, USA; Department of Cardiovascular and Metabolic Sciences, Lerner Research Institute, Cleveland Clinic, Cleveland, OH, USA.
Xiaorong GuDepartment of Translational Hematology and Oncology Research, Taussig Cancer Institute, Cleveland Clinic, Cleveland, OH, USA.
Caroline SchuegerDepartment of Molecular Medicine, Cleveland Clinic Lerner College of Medicine, School of Medicine, Case Western Reserve University, Cleveland, OH, USA; Department of Translational Hematology and Oncology Research, Taussig Cancer Institute, Cleveland Clinic, Cleveland, OH, USA.
William M DiPasqualeDepartment of Cardiovascular and Metabolic Sciences, Lerner Research Institute, Cleveland Clinic, Cleveland, OH, USA.
Jonathan BrickDepartment of Cardiovascular and Metabolic Sciences, Lerner Research Institute, Cleveland Clinic, Cleveland, OH, USA.
Yogen SaunthararajahDepartment of Translational Hematology and Oncology Research, Taussig Cancer Institute, Cleveland Clinic, Cleveland, OH, USA.
Jaroslaw P MaciejewskiDepartment of Translational Hematology and Oncology Research, Taussig Cancer Institute, Cleveland Clinic, Cleveland, OH, USA.
Richard A PadgettDepartment of Molecular Medicine, Cleveland Clinic Lerner College of Medicine, School of Medicine, Case Western Reserve University, Cleveland, OH, USA; Department of Cardiovascular and Metabolic Sciences, Lerner Research Institute, Cleveland Clinic, Cleveland, OH, USA. Electronic address: padgetr@ccf.org.
Cleveland Clinic Lerner College of Medicine · USCleveland Clinic · US

Funding

TUMOR METABOLISM PROGRAMP30CA043703 · NCI · CASE WESTERN RESERVE UNIVERSITY · PI Amar Desai · 1987 to 2026
$142.3M
Targeting Enzymatic Regulation of Fetal Hemoglobin RepressionP01HL146372 · NHLBI · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI LAVELLE, DONALD · 2019 to 2023
$10.9M
Therapeutic Implications of Molecular Defects in Bone Marrow FailureR35HL135795 · NHLBI · CLEVELAND CLINIC LERNER COM-CWRU · PI MACIEJEWSKI, JAROSLAW P. · 2017 to 2023
$5.7M
Novel Spliceosomal Defects in Myelodysplastic SyndromesR01HL132071 · NHLBI · CLEVELAND CLINIC LERNER COM-CWRU · PI MACIEJEWSKI, JAROSLAW P., PADGETT, RICHARD A · 2016 to 2019
$2.4M
Imaging Liver Cancer ProliferationR01CA204373 · NCI · CASE WESTERN RESERVE UNIVERSITY · PI LEE, ZHENGHONG, SAUNTHARARAJAH, YOGEN · 2016 to 2021
$1.8M
The effects of LUC7L2 on alternative splicing in myelodysplastic syndromesF31HL131140 · NHLBI · CLEVELAND CLINIC LERNER COM-CWRU · PI HERSHBERGER, COURTNEY ELIZABETH · 2016 to 2018
$106k
NCI NIH HHS P30 CA043703NCI NIH HHS R01 CA204373NHLBI NIH HHS F31 HL131140NHLBI NIH HHS P01 HL146372NHLBI NIH HHS R01 HL132071NHLBI NIH HHS R35 HL135795
6 · The paper itself

Abstract

Vertebrates have evolved three paralogs, termed LUC7L, LUC7L2, and LUC7L3, of the essential yeast U1 small nuclear RNA (snRNA)-associated splicing factor Luc7p. We investigated the mechanistic and regulatory functions of these putative splicing factors, of which one (LUC7L2) is mutated or deleted in myeloid neoplasms. Protein interaction data show that all three proteins bind similar core but distinct regulatory splicing factors, probably mediated through their divergent arginine-serine-rich domains, which are not present in Luc7p. Knockdown of each factor reveals mostly unique sets of significantly dysregulated alternative splicing events dependent on their binding locations, which are largely non-overlapping. Notably, knockdown of LUC7L2 alone significantly upregulates the expression of multiple spliceosomal factors and downregulates glycolysis genes, possibly contributing to disease pathogenesis. RNA binding studies reveal that LUC7L2 and LUC7L3 crosslink to weak 5' splice sites and to the 5' end of U1 snRNA, establishing an evolutionarily conserved role in 5' splice site selection.

Indexed as

RNA SplicingBase SequenceExonsGene Expression ProfilingGene Expression Regulation, NeoplasticHumansIntronsLeukemia, MyeloidMutationMyelodysplastic SyndromesNuclear ProteinsRibonucleoprotein, U1 Small NuclearRNA-Binding ProteinsRNA, Small NuclearSaccharomyces cerevisiaeSaccharomyces cerevisiae ProteinsLUC7L2 protein, humanLUC7L3 protein, humanLUC7L protein, humanLuc7 protein, S cerevisiaeNuclear ProteinsRibonucleoprotein, U1 Small NuclearRNA-Binding ProteinsRNA, Small NuclearSaccharomyces cerevisiae ProteinsSNRNP70 protein, humanU1 small nuclear RNA5′ splice sitealternative splicingLUC7LLUC7L2LUC7L3myeloid neoplasms

Identifiers

PMID33852859
PMCPMC8078730
OpenAlexW3153565341

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
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.