Evidence map›Paper›PMID 25583562›Full record

ReviewBiochimica et biophysica acta2015

Pin1 dysregulation helps to explain the inverse association between cancer and Alzheimer's disease.

Jane A Driver, Xiao Zhen Zhou, Kun Ping Lu

Abstract readReview
In one paragraph

Review in Biochimica et biophysica acta, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 57 papers.

0numbers the graph read from it
0cells of the map it votes in
57citing papers in PubMed
5.6field-weighted citation impact, top 3% 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

57 citing papers in PubMed, 89 citations in OpenAlex.

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  20. The Pin1-CaMKII-AMPA Receptor Axis Regulates Epileptic Susceptibility.Cerebral cortex (New York, N.Y. : 1991) · 2021
    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

3 authors at 2 institutions in 1 country.

Jane A DriverGeriatric Research Education and Clinical Center, VA Boston Healthcare System and the Division of Aging, Department of Medicine, Brigham and Women's Hospital, Harvard Medical School, Boston, MA, USA. Electronic address: jdriver@partners.org.
Xiao Zhen ZhouCancer Research Institute, Beth Israel Deaconess Cancer Center and Department of Medicine, Beth Israel Deaconess Medical Center, Harvard Medical School, Boston, MA, USA. Electronic address: xzhou@bidmc.harvard.edu.
Kun Ping LuCancer Research Institute, Beth Israel Deaconess Cancer Center and Department of Medicine, Beth Israel Deaconess Medical Center, Harvard Medical School, Boston, MA, USA. Electronic address: klu@bidmc.harvard.edu.
Beth Israel Deaconess Medical Center · USVA Boston Healthcare System · US

Funding

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 the Phosphorylation-Specific Prolyl Isomerase Pin1R01CA167677 · NCI · BETH ISRAEL DEACONESS MEDICAL CENTER · PI LU, KUN PING · 2012 to 2016
$1.9M
The Propyl Isomerase Pin 1 and NeurodegenerationR01AG022082 · NIA · BETH ISRAEL DEACONESS MEDICAL CENTER · PI LU, KUN PING · 2003 to 2009
$1.8M
Drug Discovery against the Early, Secreted and Toxic Tau in Alzheimer's DiseaseR01AG046319 · NIA · BETH ISRAEL DEACONESS MEDICAL CENTER · PI LU, KUN PING · 2014 to 2018
$1.8M
Pin1-Catalyzed Protein Conformational Regulation in Alzheimer's DiseaseR01AG039405 · NIA · BETH ISRAEL DEACONESS MEDICAL CENTER · PI LU, KUN PING · 2011 to 2015
$1.8M
Investigating the link between cancer and neurodegenerative diseaseI01CX000934 · VA · VA BOSTON HEALTH CARE SYSTEM · PI DRIVER, JANE A · 2014 to 2017
–
CSRD VA I01 CX000934NCI NIH HHS R01 CA167677NIA NIH HHS R01 AG017870NIA NIH HHS R01 AG022082NIA NIH HHS R01 AG039405NIA NIH HHS R01 AG046319
6 · The paper itself

Abstract

backgroundPin1 is an intracellular signaling molecule which plays a critical but opposite role in the pathogenesis of Alzheimer's disease (AD) and many human cancers. SCOPE OF REVIEW: We review the structure and function of the Pin1 enzyme, the diverse roles it plays in cycling cells and neurons, the epidemiologic evidence for the inverse association between cancer and AD, and the potential therapeutic implications of Pin1-based therapies. MAJOR

conclusionsPin1 is a unique enzyme that has effects on the function of target proteins by "twisting" them into different shapes. Cycling cells use Pin1 to help coordinate cell division. It is over-expressed and/or activated by multiple mechanisms in many common human cancers, and acts on multiple signal pathways to promote tumorigenesis. Inhibition of Pin1 in animal models has profound anti-tumor effects. In contrast, Pin1 is down-regulated or inactivated by multiple mechanisms in AD brains. The absence of Pin1 impairs tau function and amyloid precursor protein processing, leading to tangle- and amyloid-related pathologies and neurodegeneration in an age-dependent manner, resembling human AD. We have developed cis and trans conformation-specific antibodies to provide the first direct evidence that tau exists in distinct cis and trans conformations and that Pin1 accelerates its cis to trans conversion, thereby protecting against tangle formation in AD. GENERAL SIGNIFICANCE: Available studies on Pin1 suggest that cancer and AD may share biological pathways that are deregulated in different directions. Pin1 biology opens exciting preventive and therapeutic horizons for both cancer and neurodegeneration. This article is part of a Special Issue entitled Proline-directed Foldases: Cell Signaling Catalysts and Drug Targets.

Indexed as

Signal TransductionAlzheimer DiseaseAmyloidAnimalsHumansNeoplasm ProteinsNeoplasmsNIMA-Interacting Peptidylprolyl IsomerasePeptidylprolyl Isomerasetau ProteinsAmyloidMAPT protein, humanNeoplasm ProteinsNIMA-Interacting Peptidylprolyl IsomerasePeptidylprolyl IsomerasePIN1 protein, humantau ProteinsAlzheimer's diseaseCancerPhosphorylation signalingPin1

Identifiers

PMID25583562
PMCPMC4499009
OpenAlexW2041521913

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.