Evidence map›Paper›PMID 21398516›Full record

ArticleThe Journal of biological chemistry2011

Mechanistic control of carcinoembryonic antigen-related cell adhesion molecule-1 (CEACAM1) splice isoforms by the heterogeneous nuclear ribonuclear proteins hnRNP L, hnRNP A1, and hnRNP M.

Kenneth J Dery, Shikha Gaur, Marieta Gencheva, Yun Yen, John E Shively, Rajesh K Gaur

Open access · hybridAbstract read
In one paragraph

Article in The Journal of biological chemistry, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 41 papers.

0numbers the graph read from it
0cells of the map it votes in
41citing papers in PubMed
4.7field-weighted citation impact, top 6% 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

41 citing papers in PubMed, 59 citations in OpenAlex.

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  5. Structural basis for immune cell binding ofProceedings of the National Academy of Sciences of the United States of America · 2025
    Article
  6. Mechanism and function of CEACAM1 splice isoforms.European journal of clinical investigation · 2024
    Review
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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

6 authors at 3 institutions in 2 countries.

Kenneth J DeryDepartment of Immunology, Beckman Research Institute of the City of Hope, Duarte, California 91010, USA.
Shikha Gaur
Marieta Gencheva
Yun Yen
John E Shively
Rajesh K Gaur
Institute of Immunology · HRBeckman Research InstituteCity of Hope · US

Funding

Role of CEACAM1 in Epithelial Cell PolarizationR01CA084202 · NCI · CITY OF HOPE/BECKMAN RESEARCH INSTITUTE · PI SHIVELY, JOHN ERNEST · 2000 to 2010
$4.1M
NCI NIH HHS CA84202NCI NIH HHS R01 CA084202
6 · The paper itself

Abstract

Carcinoembryonic antigen-related cell adhesion molecule-1 (CEACAM1) is expressed in a variety of cell types and is implicated in carcinogenesis. Alternative splicing of CEACAM1 pre-mRNA generates two cytoplasmic domain splice variants characterized by the inclusion (L-isoform) or exclusion (S-isoform) of exon 7. Here we show that the alternative splicing of CEACAM1 pre-mRNA is regulated by novel cis elements residing in exon 7. We report the presence of three exon regulatory elements that lead to the inclusion or exclusion of exon 7 CEACAM1 mRNA in ZR75 breast cancer cells. Heterologous splicing reporter assays demonstrated that the maintenance of authentic alternative splicing mechanisms were independent of the CEACAM1 intron sequence context. We show that forced expression of these exon regulatory elements could alter CEACAM1 splicing in HEK-293 cells. Using RNA affinity chromatography, three members of the heterogeneous nuclear ribonucleoprotein family (hnRNP L, hnRNP A1, and hnRNP M) were identified. RNA immunoprecipitation of hnRNP L and hnRNP A1 revealed a binding motif located central and 3' to exon 7, respectively. Depletion of hnRNP A1 or L by RNAi in HEK-293 cells promoted exon 7 inclusion, whereas overexpression led to exclusion of the variable exon. By contrast, overexpression of hnRNP M showed exon 7 inclusion and production of CEACAM1-L mRNA. Finally, stress-induced cytoplasmic accumulation of hnRNP A1 in MDA-MB-468 cells dynamically alters the CEACAM1-S:CEACAM1:L ratio in favor of the l-isoform. Thus, we have elucidated the molecular factors that control the mechanism of splice-site recognition in the alternative splicing regulation of CEACAM1.

Indexed as

Alternative SplicingAntigens, CDCell Adhesion MoleculesExonsHEK293 CellsHeLa CellsHeterogeneous Nuclear Ribonucleoprotein A1Heterogeneous-Nuclear Ribonucleoprotein Group A-BHeterogeneous-Nuclear Ribonucleoprotein Group MHeterogeneous-Nuclear Ribonucleoprotein LHumansIntronsProtein IsoformsRNA, MessengerAntigens, CDCD66 antigensCell Adhesion MoleculesHeterogeneous Nuclear Ribonucleoprotein A1Heterogeneous-Nuclear Ribonucleoprotein Group A-BHeterogeneous-Nuclear Ribonucleoprotein Group MHeterogeneous-Nuclear Ribonucleoprotein LProtein IsoformsRNA, Messenger

Identifiers

PMID21398516
PMCPMC3091213
OpenAlexW1998243827

What OpenQuestion holds

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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.