Evidence map›Paper›PMID 33189799›Full record

ReviewGene2021

KALRN: A central regulator of synaptic function and synaptopathies.

Euan Parnell, Lauren P Shapiro, Roos A Voorn, Marc P Forrest, Hiba A Jalloul, Daniel D Loizzo, Peter Penzes

Open access · greenAbstract readReview
In one paragraph

Review in Gene, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers.

0numbers the graph read from it
0cells of the map it votes in
29citing papers in PubMed
2.4field-weighted citation impact, top 11% 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

29 citing papers in PubMed, 44 citations in OpenAlex.

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  13. The genetic landscape of early-onset Alzheimer's disease in China.Alzheimer's & dementia : the journal of the Alzheimer's Association · 2025
    Article
  14. Review
  15. Are Methylation Patterns in theInternational journal of molecular sciences · 2024
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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

7 authors at 1 institution in 1 country.

Euan ParnellDepartment of Physiology, Northwestern University Feinberg School of Medicine, Chicago, 60611 IL, USA.
Lauren P ShapiroDepartment of Physiology, Northwestern University Feinberg School of Medicine, Chicago, 60611 IL, USA.
Roos A VoornDepartment of Physiology, Northwestern University Feinberg School of Medicine, Chicago, 60611 IL, USA.
Marc P ForrestDepartment of Physiology, Northwestern University Feinberg School of Medicine, Chicago, 60611 IL, USA.
Hiba A JalloulDepartment of Physiology, Northwestern University Feinberg School of Medicine, Chicago, 60611 IL, USA.
Daniel D LoizzoDepartment of Physiology, Northwestern University Feinberg School of Medicine, Chicago, 60611 IL, USA.
Peter PenzesDepartment of Physiology, Northwestern University Feinberg School of Medicine, Chicago, 60611 IL, USA; Department of Psychiatry and Behavioral Sciences, Northwestern University Feinberg School of Medicine, Chicago, 60611 IL, USA; Northwestern University Center for Autism and Neurodevelopment, Chicago, IL 60611, USA. Electronic address: p-penzes@northwestern.edu.
Northwestern University · US

Funding

Small GTPase signaling in spinesR01MH071316 · NIMH · NORTHWESTERN UNIVERSITY AT CHICAGO · PI BARBOLINA, MARIA V., PENZES, PETER · 2005 to 2025
$7.1M
The Gene Wiki: Community intelligence applied to gene annotationR01GM089820 · NIGMS · SCRIPPS RESEARCH INSTITUTE, THE · PI SU, ANDREW I · 2010 to 2021
$5.2M
Small GTPase signaling in dendrites and spinesR56MH071316 · NIMH · NORTHWESTERN UNIVERSITY AT CHICAGO · PI PENZES, PETER · 2020 to 2020
$782k
NIGMS NIH HHS R01 GM089820NIMH NIH HHS R01 MH071316NIMH NIH HHS R56 MH071316Wellcome Trust
6 · The paper itself

Abstract

The synaptic regulator, kalirin, plays a key role in synaptic plasticity and formation of dendritic arbors and spines. Dysregulation of the KALRN gene has been linked to various neurological disorders, including autism spectrum disorder, Alzheimer's disease, schizophrenia, addiction and intellectual disabilities. Both genetic and molecular studies highlight the importance of normal KALRN expression for healthy neurodevelopment and function. This review aims to give an in-depth analysis of the structure and molecular mechanisms of kalirin function, particularly within the brain. These data are correlated to genetic evidence of patient mutations within KALRN and animal models of Kalrn that together give insight into the manner in which this gene may be involved in neurodevelopment and the etiology of disease. The emerging links to human disease from post-mortem, genome wide association (GWAS) and exome sequencing studies are examined to highlight the disease relevance of kalirin, particularly in neurodevelopmental diseases. Finally, we will discuss efforts to pharmacologically regulate kalirin protein activity and the implications of such endeavors for the treatment of human disease. As multiple disease states arise from deregulated synapse formation and altered KALRN expression and function, therapeutics may be developed to provide control over KALRN activity and thus synapse dysregulation. As such, a detailed understanding of how kalirin regulates neuronal development, and the manner in which kalirin dysfunction promotes neurological disease, may support KALRN as a valuable therapeutic avenue for future pharmacological intervention.

Indexed as

AnimalsGenome-Wide Association StudyGuanine Nucleotide Exchange FactorsHumansNeuronal PlasticityProtein Serine-Threonine KinasesSynapsesGuanine Nucleotide Exchange FactorsProtein Serine-Threonine KinasesAlzheimer’s diseaseAutism spectrum disorderDendritic spineDevelopmental delayKalirinKALRNNeurodegenerationNeurodevelopmentSchizophreniaSynaptic plasticity

Identifiers

PMID33189799
PMCPMC7803032
OpenAlexW3101526080

What Socratic 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 Socratic graph.