Evidence map›Paper›PMID 11805292›Full record

ArticleProceedings of the National Academy of Sciences of the United States of America2002

Loss of Pin1 function in the mouse causes phenotypes resembling cyclin D1-null phenotypes.

Yih-Cherng Liou, Akihide Ryo, Han-Kuei Huang, Pei-Jung Lu, Roderick Bronson, Fumihiro Fujimori, Takafumi Uchida, Tony Hunter, Kun Ping Lu

Open access · greenAbstract read
In one paragraph

Article in Proceedings of the National Academy of Sciences of the United States of America, 2002. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 156 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
156citing papers in PubMed, 2 pooled it
5.0field-weighted citation impact, top 4% 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

156 citing papers in PubMed, 2 syntheses or guidelines pooled it, 339 citations in OpenAlex.

  1. Association of rs2233678 and rs2233679 polymorphisms in the PIN1 gene with cancer risk: a meta-analysis.Tumour biology : the journal of the International Society for Oncodevelopmental Biology and Medicine · 2014
    Pooled it
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  7. CRABP1-complexes in exosome secretion.Cell communication and signaling : CCS · 2024
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96 more citing papers are in PubMed but not listed here.

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

9 authors at 5 institutions in 3 countries.

Yih-Cherng LiouCancer Biology Program, Department of Medicine, Beth Israel Deaconess Medical Center and Harvard Medical School, Boston, MA 02215, USA.
Akihide Ryo
Han-Kuei Huang
Pei-Jung Lu
Roderick Bronson
Fumihiro Fujimori
Takafumi Uchida
Tony Hunter
Kun Ping Lu
Tufts University · USBeth Israel Deaconess Medical Center · USTokyo University of Science · JPHarvard University · USTohoku University · JP

Funding

SOMATIC CELL CYCLE REGULATION BY PHOSPHORYLATIONR01CA080100 · NCI · SALK INSTITUTE FOR BIOLOGICAL STUDIES · PI HUNTER, TONY R. · 1999 to 2018
$13.1M
Function and Regulation of the Prolyl Isomerase Pin1R01GM058556 · NIGMS · BETH ISRAEL DEACONESS MEDICAL CENTER · PI LU, KUN PING · 1999 to 2010
$3.9M
Role of the Prolyl lsomerase Pin1 in Alzheimer's DiseaseR01AG017870 · NIA · BETH ISRAEL DEACONESS MEDICAL CENTER · PI LU, KUN PING · 2001 to 2011
$2.7M
Function and Regulation of Pin2/TRF1 and PinX1R01GM056230 · NIGMS · BETH ISRAEL DEACONESS MEDICAL CENTER · PI LU, KUN PING · 1997 to 2005
$1.8M
NCI NIH HHS CA80100NCI NIH HHS R01 CA080100NIA NIH HHS AG17870NIA NIH HHS R01 AG017870NIGMS NIH HHS GM56230NIGMS NIH HHS GM58556NIGMS NIH HHS R01 GM056230NIGMS NIH HHS R01 GM058556
6 · The paper itself

Abstract

Phosphorylation of proteins on serine/threonine residues preceding proline is a key signaling mechanism. The conformation and function of a subset of these phosphorylated proteins is regulated by the prolyl isomerase Pin1 through isomerization of phosphorylated Ser/Thr-Pro bonds. Although young Pin1(-/-) mice have been previously shown to develop normally, we show here that they displayed a range of cell-proliferative abnormalities, including decreased body weight and testicular and retinal atrophies. Furthermore, in Pin1(-/-) adult females, the breast epithelial compartment failed to undergo the massive proliferative changes associated with pregnancy. Interestingly, many of these Pin1-deficient phenotypes such as retinal hypoplasia and mammary gland impairment are also the characteristic of cyclin D1-deficient mice. Cyclin D1 levels were significantly reduced in many tissues in Pin1-deficient mice, including retina and breast epithelial cells from pregnant mice. Moreover, Pin1 directly bound to cyclin D1 phosphorylated on Thr-286-Pro increased cyclin D1 in the nucleus and stabilized cyclin D1. These results indicate that Pin1 positively regulates cyclin D1 function at the transcriptional level, as demonstrated previously, and also through posttranslational stabilization, which together explain why Pin1 loss-of-function phenotypes in the mouse resemble cyclin D1-null phenotypes. Our results provide genetic evidence for an essential role of Pin1 in maintaining cell proliferation and regulating cyclin D1 function.

Indexed as

AnimalsAtrophyBody WeightCell DivisionCyclin D1FemaleMaleMammary Glands, AnimalMiceMice, KnockoutNIMA-Interacting Peptidylprolyl IsomerasePeptidylprolyl IsomerasePhenotypePhosphorylationPregnancyRetinaCyclin D1NIMA-Interacting Peptidylprolyl IsomerasePeptidylprolyl IsomerasePin1 protein, mouse

Identifiers

PMID11805292
PMCPMC122191
OpenAlexW2050000741

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.