Evidence map›Paper›PMID 18942145›Full record

ArticleDevelopmental dynamics : an official publication of the American Association of Anatomists2008

Characterization of two Mst1-deficient mouse models.

Montserrat C Anguera, Matthew Liu, Joseph Avruch, Jeannie T Lee

Open access · bronzeAbstract read
In one paragraph

Article in Developmental dynamics : an official publication of the American Association of Anatomists, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
5citing papers in PubMed, 1 pooled it
0.3field-weighted citation impact, top 44% 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

5 citing papers in PubMed, 1 synthesis or guideline pooled it, 9 citations in OpenAlex.

  1. Pooled it
  2. Article
  3. Article
  4. Review
  5. Hippo signaling is a potent in vivo growth and tumor suppressor pathway in the mammalian liver.Proceedings of the National Academy of Sciences of the United States of America · 2010
    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

4 authors at 2 institutions in 1 country.

Montserrat C AngueraHoward Hughes Medical Institute, Department of Molecular Biology, Massachusetts General Hospital, Department of Genetics, Harvard Medical School, Boston, Massachusetts 02114, USA.
Matthew Liu
Joseph Avruch
Jeannie T Lee
Harvard University · USMassachusetts General Hospital · US

Funding

ROLE OF DIETARY CONSTITUENTS ON GENE EXPRESSION IN INTESTINAL EPITHELIUMP30DK040561 · NIDDK · MASSACHUSETTS GENERAL HOSPITAL · PI ALEXANDER A SOUKAS · 1994 to 2026
$31.6M
PHOSPHOPEPTIDE METABOLISM IN ADIPOCYTESR37DK017776 · NIDDK · MASSACHUSETTS GENERAL HOSPITAL · PI AVRUCH, JOSEPH · 1999 to 2018
$9.3M
Transcriptional Silencing of the X-chromosomeF32GM076955 · NIGMS · MASSACHUSETTS GENERAL HOSPITAL · PI ANGUERA, MONTSERRAT C · 2006 to 2007
$95k
PHOSPHOPEPTIDE METABOLISM IN ADIPOCYTESR01DK017776 · NIDDK · MASSACHUSETTS GENERAL HOSPITAL · PI AVRUCH, JOSEPH · 1986 to 1998
–
Howard Hughes Medical InstituteNIDDK NIH HHS DK17776NIDDK NIH HHS P30 DK040561NIDDK NIH HHS R37 DK017776NIGMS NIH HHS F32 GM076955NIGMS NIH HHS F32-GM076955
6 · The paper itself

Abstract

Mammalian sterile 20-like kinase 1 (Mst1) is a ubiquitously expressed serine/threonine kinase belonging to the family of Sterile 20-like kinases. MST1 has been inferred to play important roles in apoptosis and in the inhibition of proliferation in mammalian cells. Here, we describe the genetic characterization of Mst1-deficient mice produced by two distinct gene-trap insertions. Animals generated from clone RRT293 exhibit transmission ratio distortion favoring the mutated allele which is amplified with each generation. Inexplicably, while the mutated allele is favored for transmission, its homozygosity is embryonic lethal. By contrast, animals generated from the second Mst1 gene-trap clone, AJ0315, do not show any gross abnormalities. We find that the discrepancy in phenotype is most likely attributable to a second insertion in the RRT293 clone. Thus, a mutation in Mst1 alone does not affect survival. Our results set the stage for identification of the lethal second-site mutation that is paradoxically favored for transmission.

Indexed as

AllelesCell ProliferationModels, BiologicalAnimalsApoptosisEmbryo LossHippo KinasesHomozygoteMiceMice, KnockoutProtein Serine-Threonine KinasesHippo KinasesProtein Serine-Threonine KinasesStk4 protein, mouse

Identifiers

PMID18942145
PMCPMC2596583
OpenAlexW1996475519

What OpenQuestion holds

Textmetadata
LicenceTDM
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.