Evidence map›Paper›PMID 26993302›Full record

ReviewMolecular neurobiology2017

Insulin-Like Growth Factor-II/Cation-Independent Mannose 6-Phosphate Receptor in Neurodegenerative Diseases.

Y Wang, R G MacDonald, G Thinakaran, S Kar

Open access · greenAbstract readReview
In one paragraph

Review in Molecular neurobiology, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 42 papers.

0numbers the graph read from it
0cells of the map it votes in
42citing papers in PubMed
2.1field-weighted citation impact, top 13% 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

42 citing papers in PubMed, 61 citations in OpenAlex.

  1. Article
  2. Insulin-like growth factor receptor signaling in physiology and disease.Signal transduction and targeted therapy · 2026
    Review
  3. Article
  4. Review
  5. Article
  6. Article
  7. Article
  8. Review
  9. The Immune Microenvironment in Liver Cancer: From Analysis to Targeting.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025
    Review
  10. Article
  11. Article
  12. Article
  13. Targeting Neurological Aspects of Mucopolysaccharidosis Type II: Enzyme Replacement Therapy and Beyond.BioDrugs : clinical immunotherapeutics, biopharmaceuticals and gene therapy · 2024
    Review
  14. Article
  15. Article
  16. Review
  17. Article
  18. Review
  19. Article
  20. Review
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 3 institutions in 2 countries.

Y WangDepartment of Psychiatry, University of Alberta, Edmonton, AB, T6G 2M8, Canada.
R G MacDonaldDepartment of Biochemistry and Molecular Biology, University of Nebraska Medical Center, Omaha, NE, 68198, USA.
G ThinakaranDepartments of Neurobiology, Neurology, and Pathology, The University of Chicago, Chicago, IL, 60637, USA.
S KarDepartment of Psychiatry, University of Alberta, Edmonton, AB, T6G 2M8, Canada. skar@ualberta.ca.ORCID 0000-0003-0167-3808
University of Alberta · CAUniversity of Chicago · USUniversity of Nebraska Medical Center · US

Funding

STRUCTURAL AND FUNCTIONAL ANALYSIS OF PRESENILINSR01AG019070 · NIA · UNIVERSITY OF CHICAGO · PI THINAKARAN, GOPAL · 2001 to 2015
$4.9M
Molecular Dissection of IGF2R Growth Suppressor ActivityR01CA091885 · NCI · UNIVERSITY OF NEBRASKA MEDICAL CENTER · PI MACDONALD, RICHARD G. · 2001 to 2004
$659k
CIHR MOP-84480NCI NIH HHS R01 CA091885NIA NIH HHS R01 AG019070
6 · The paper itself

Abstract

The insulin-like growth factor II/mannose 6-phosphate (IGF-II/M6P) receptor is a multifunctional single transmembrane glycoprotein. Recent studies have advanced our understanding of the structure, ligand-binding properties, and trafficking of the IGF-II/M6P receptor. This receptor has been implicated in a variety of important cellular processes including growth and development, clearance of IGF-II, proteolytic activation of enzymes, and growth factor precursors, in addition to its well-known role in the delivery of lysosomal enzymes. The IGF-II/M6P receptor, distributed widely in the central nervous system, has additional roles in mediating neurotransmitter release and memory enhancement/consolidation, possibly through activating IGF-II-related intracellular signaling pathways. Recent studies suggest that overexpression of the IGF-II/M6P receptor may have an important role in regulating the levels of transcripts and proteins involved in the development of Alzheimer's disease (AD)-the prevalent cause of dementia affecting the elderly population in our society. It is reported that IGF-II/M6P receptor overexpression can increase the levels/processing of amyloid precursor protein leading to the generation of β-amyloid peptide, which is associated with degeneration of neurons and subsequent development of AD pathology. Given the significance of the receptor in mediating the transport and functioning of the lysosomal enzymes, it is being considered for therapeutic delivery of enzymes to the lysosomes to treat lysosomal storage disorders. Notwithstanding these results, additional studies are required to validate and fully characterize the function of the IGF-II/M6P receptor in the normal brain and its involvement in various neurodegenerative disorders including AD. It is also critical to understand the interaction between the IGF-II/M6P receptor and lysosomal enzymes in neurodegenerative processes, which may shed some light on developing approaches to detect and prevent neurodegeneration through the dysfunction of the receptor and the endosomal-lysosomal system.

Indexed as

Alzheimer DiseaseAnimalsCationsHumansInsulin-Like Growth Factor IILysosomesNeurodegenerative DiseasesReceptor, IGF Type 2CationsInsulin-Like Growth Factor IIReceptor, IGF Type 2Alzheimer’s diseaseEndosomal-lysosomal systemInsulin-like growth factor II receptorMannose 6-phosphate receptorNeurodegenerative diseases

Identifiers

PMID26993302
PMCPMC5901910
OpenAlexW2306294932

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.