Evidence map›Paper›PMID 32093146›Full record

ArticleCells2020

An Alternative Splice Variant of HIPK2 with Intron Retention Contributes to Cytokinesis.

Veronica Gatti, Manuela Ferrara, Ilaria Virdia, Silvia Matteoni, Laura Monteonofrio, Simona di Martino, Maria Grazia Diodoro, Giuliana Di Rocco, Cinzia Rinaldo, Silvia Soddu

Open access · goldAbstract read
In one paragraph

Article in Cells, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.

0numbers the graph read from it
0cells of the map it votes in
7citing papers in PubMed
0.7field-weighted citation impact, top 33% 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

7 citing papers in PubMed, 12 citations in OpenAlex.

  1. Article
  2. Article
  3. Inactivation of HIPK2 attenuates KRASJournal of experimental & clinical cancer research : CR · 2024
    Article
  4. Review
  5. HIPK2 in the physiology of nervous system and its implications in neurological disorders.Biochimica et biophysica acta. Molecular cell research · 2023
    Review
  6. Article
  7. Article
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

10 authors at 4 institutions in 2 countries.

Veronica GattiUnit of Cellular Networks and Molecular Therapeutic Targets; IRCCS-Regina Elena National Cancer Institute, 00144 Rome, Italy.
Manuela FerraraInstitute of Molecular Biology and Pathology (IBPM), National Research Council (CNR), c/o Sapienza University, 00185 Rome, Italy.
Ilaria VirdiaUnit of Cellular Networks and Molecular Therapeutic Targets; IRCCS-Regina Elena National Cancer Institute, 00144 Rome, Italy.
Silvia MatteoniUnit of Cellular Networks and Molecular Therapeutic Targets; IRCCS-Regina Elena National Cancer Institute, 00144 Rome, Italy.ORCID 0000-0001-6926-6593
Laura MonteonofrioUnit of Cellular Networks and Molecular Therapeutic Targets; IRCCS-Regina Elena National Cancer Institute, 00144 Rome, Italy.ORCID 0000-0003-3981-942X
Simona di MartinoPathology Unit, IRCCS-Regina Elena National Cancer Institute, 00144 Rome, Italy.
Maria Grazia DiodoroPathology Unit, IRCCS-Regina Elena National Cancer Institute, 00144 Rome, Italy.
Giuliana Di RoccoUnit of Cellular Networks and Molecular Therapeutic Targets; IRCCS-Regina Elena National Cancer Institute, 00144 Rome, Italy.
Cinzia RinaldoUnit of Cellular Networks and Molecular Therapeutic Targets; IRCCS-Regina Elena National Cancer Institute, 00144 Rome, Italy.ORCID 0000-0001-6124-762X
Silvia SodduUnit of Cellular Networks and Molecular Therapeutic Targets; IRCCS-Regina Elena National Cancer Institute, 00144 Rome, Italy.ORCID 0000-0001-8526-0044
Target (United States) · USIstituti di Ricovero e Cura a Carattere Scientifico · ITInstitute of Molecular Biology and Pathology · ITRoma Tre University · IT

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

HIPK2 is a DYRK-like kinase involved in cellular stress response pathways, development, and cell division. Two alternative splice variants of HIPK2, HIPK2-FL and HIPK2-Δe8, have been previously identified as having different protein stability but similar functional activity in the stress response. Here, we describe one additional HIPK2 splice variant with a distinct subcellular distribution and functional activity in cytokinesis. This novel splice variant lacks the last two exons and retains intron13 with a stop codon after 89 bp of the intron, generating a short isoform, HIPK2-S, that is detectable by 2D Western blots. RT-PCR analyses of tissue arrays and tumor samples show that HIPK2-FL and HIPK2-S are expressed in normal human tissues in a tissue-dependent manner and differentially expressed in human colorectal and pancreatic cancers. Gain- and loss-of-function experiments showed that in contrast to HIPK2-FL, HIPK2-S has a diffuse, non-speckled distribution and is not involved in the DNA damage response. Rather, we found that HIPK2-S, but not HIPK2-FL, localizes at the intercellular bridge, where it phosphorylates histone H2B and spastin, both required for faithful cell division. Altogether, these data show that distinct human HIPK2 splice variants are involved in distinct HIPK2-regulated functions like stress response and cytokinesis.

Indexed as

IntronsAlternative SplicingCarrier ProteinsCodon, TerminatorCytokinesisExonsHCT116 CellsHeLa CellsHistonesHumansIsoenzymesPhosphorylationProtein Serine-Threonine KinasesRNA InterferenceSpastinTransfectionCarrier ProteinsCodon, TerminatorHIPK2 protein, humanHistonesIsoenzymesProtein Serine-Threonine KinasesSpastinSPAST protein, humanabscissionalternative splicingcolorectal cancerfaithful cytokinesisHIPK2 isoformspancreatic cancer

Identifiers

PMID32093146
PMCPMC7072727
OpenAlexW3008312130

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.