Evidence map›Paper›PMID 30915713›Full record

ReviewMolecular neurobiology2019

Dysregulation of CRMP2 Post-Translational Modifications Drive Its Pathological Functions.

Aubin Moutal, Katherine A White, Aude Chefdeville, Rachel N Laufmann, Peter F Vitiello, Douglas Feinstein, Jill M Weimer, Rajesh Khanna

Open access · greenAbstract readReview
In one paragraph

Review in Molecular neurobiology, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 44 papers.

0numbers the graph read from it
0cells of the map it votes in
44citing papers in PubMed
5.8field-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

44 citing papers in PubMed, 84 citations in OpenAlex.

  1. Semaphorins and Their Role in Neuropathic Pain.Life (Basel, Switzerland) · 2026
    Review
  2. Article
  3. Article
  4. Article
  5. Article
  6. Review
  7. Review
  8. Article
  9. Review
  10. Article
  11. Article
  12. A peptidomimetic modulator of the CaProceedings of the National Academy of Sciences of the United States of America · 2023
    Article
  13. Article
  14. Article
  15. Article
  16. Article
  17. Article
  18. Review
  19. Article
  20. 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

8 authors at 4 institutions in 1 country.

Aubin MoutalDepartment of Pharmacology, College of Medicine, University of Arizona, 1501 North Campbell Drive, P.O. Box 245050, Tucson, AZ, 85724, USA.
Katherine A WhitePediatrics and Rare Diseases Group, Sanford Research, 2301 E 60th St N, Sioux Falls, SD, 57104, USA.
Aude ChefdevilleDepartment of Pharmacology, College of Medicine, University of Arizona, 1501 North Campbell Drive, P.O. Box 245050, Tucson, AZ, 85724, USA.
Rachel N LaufmannPediatrics and Rare Diseases Group, Sanford Research, 2301 E 60th St N, Sioux Falls, SD, 57104, USA.
Peter F VitielloDepartment of Pharmacology, College of Medicine, University of Arizona, 1501 North Campbell Drive, P.O. Box 245050, Tucson, AZ, 85724, USA.
Douglas FeinsteinDepartment of Veterans Affairs, Jesse Brown VA Medical Center, University of Illinois at Chicago, Chicago, IL, USA.
Jill M WeimerDepartment of Pharmacology, College of Medicine, University of Arizona, 1501 North Campbell Drive, P.O. Box 245050, Tucson, AZ, 85724, USA. Jill.Weimer@SanfordHealth.org.
Rajesh KhannaDepartment of Pharmacology, College of Medicine, University of Arizona, 1501 North Campbell Drive, P.O. Box 245050, Tucson, AZ, 85724, USA. rkhanna@email.arizona.edu.ORCID http://orcid.org/0000-0002-9066-2969
University of Arizona · USSanford Research · USSanford Health · USUniversity of Illinois Chicago · US

Funding

NATIONAL ALZHEIMERS COORDINATING CENTER (NACC)U01AG016976 · NIA · UNIVERSITY OF WASHINGTON · PI KUKULL, WALTER ANTHONY · 1999 to 2020
$72.8M
National Alzheimer's Coordinating CenterU24AG072122 · NIA · UNIVERSITY OF WASHINGTON · PI STEPHENS, KARI A · 2021 to 2025
$45.8M
CRMP2, mitochondria, and Huntington’s diseaseR01NS098772 · NINDS · INDIANA UNIVERSITY INDIANAPOLIS · PI BRUSTOVETSKY, NICKOLAY, KHANNA, RAJESH · 2017 to 2021
$2.8M
Green Light Therapy for Chronic PainR01AT009716 · NCCIH · UNIVERSITY OF ARIZONA · PI IBRAHIM, MOHAB M · 2018 to 2022
$2.1M
Hyperoxic Modulation of Thioredoxin SignalingR01HL135112 · NHLBI · UNIVERSITY OF OKLAHOMA HLTH SCIENCES CTR · PI VITIELLO, PETER · 2017 to 2021
$2.0M
CRMP2, Nav1.7 sodium channel, and chronic painR01DA042852 · NIDA · UNIVERSITY OF ARIZONA · PI KHANNA, RAJESH · 2017 to 2021
$1.9M
Novel mechanisms for distal transport in developing and mature neuronsR01NS082283 · NINDS · SANFORD RESEARCH/USD · PI WEIMER, JILL M · 2014 to 2018
$1.9M
NCCIH NIH HHS R01 AT009716NHLBI NIH HHS R01 HL135112NIA NIH HHS U01 AG016976NIA NIH HHS U24 AG072122NIDA NIH HHS 1R01DA042852NIDA NIH HHS R01 DA042852NINDS NIH HHS 1R01NS098772NINDS NIH HHS R01 NS082283NINDS NIH HHS R01 NS098772
6 · The paper itself

Abstract

Collapsin response mediator proteins (CRMPs) are a family of ubiquitously expressed, homologous phosphoproteins best known for coordinating cytoskeletal formation and regulating cellular division, migration, polarity, and synaptic connection. CRMP2, the most studied of the five family members, is best known for its affinity for tubulin heterodimers and function in regulating the microtubule network. These functions are tightly regulated by post-translational modifications including phosphorylation, SUMOylation, oxidation, and O-GlcNAcylation. While CRMP2's physiological functions rely mostly on its non-phosphorylated state, dysregulation of CRMP2 phosphorylation and SUMOylation has been reported to be involved in the pathophysiology of multiple diseases including cancer, chronic pain, spinal cord injury, neurofibromatosis type 1, and others. Here, we provide a consolidated update on what is known about CRMP2 signaling and function, first focusing on axonal growth and neuronal polarity, then illustrating the link between dysregulated CRMP2 post-translational modifications and diseases. We additionally discuss the roles of CRMP2 in non-neuronal cells, both in the CNS and regions of the periphery. Finally, we offer thoughts on the therapeutic implications of modulating CRMP2 function in a variety of diseases.

Indexed as

Protein Processing, Post-TranslationalAnimalsCell PolarityCentral Nervous SystemHumansIntercellular Signaling Peptides and ProteinsModels, BiologicalNerve Tissue ProteinsNeuronscollapsin response mediator protein-2Intercellular Signaling Peptides and ProteinsNerve Tissue ProteinsAlzheimer’s diseaseCancerChronic painCRMP2Human diseaseInteractomeMultiple sclerosisNeurite outgrowthNon-neuronal cellsPost-translational modificationsStrokeTherapeutics

Identifiers

PMID30915713
PMCPMC6728212
OpenAlexW2924069622

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.