Evidence map›Paper›PMID 38281682›Full record

ArticleProgress in neurobiology2024

The Reelin receptor ApoER2 is a cargo for the adaptor protein complex AP-4: Implications for Hereditary Spastic Paraplegia.

Mario O Caracci, Héctor Pizarro, Carlos Alarcón-Godoy, Luz M Fuentealba, Pamela Farfán, Raffaella De Pace, Natacha Santibañez, Viviana A Cavieres, Tammy P Pástor, Juan S Bonifacino and 2 more

Erratum issuedOpen access · greenAbstract read
In one paragraph

Article in Progress in neurobiology, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 7 papers.

0numbers the graph read from it
0cells of the map it votes in
7citing papers in PubMed
4.5field-weighted citation impact, top 5% 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

7 citing papers in PubMed, 11 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Uncovering cargo clients and accessory factors of AP-1 and AP-4 through vesicle proteomics.Proceedings of the National Academy of Sciences of the United States of America · 2025
    Article
  5. Article
  6. Review
  7. Article
4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

12 authors at 5 institutions in 2 countries.

Mario O CaracciDepartamento de Biología Celular y Molecular, Facultad de Ciencias Biológicas, P. Universidad Católica de Chile, Santiago, Chile.
Héctor PizarroDepartamento de Biología Celular y Molecular, Facultad de Ciencias Biológicas, P. Universidad Católica de Chile, Santiago, Chile.
Carlos Alarcón-GodoyDepartamento de Biología Celular y Molecular, Facultad de Ciencias Biológicas, P. Universidad Católica de Chile, Santiago, Chile.
Luz M FuentealbaDepartamento de Biología Celular y Molecular, Facultad de Ciencias Biológicas, P. Universidad Católica de Chile, Santiago, Chile.
Pamela FarfánDepartamento de Biología Celular y Molecular, Facultad de Ciencias Biológicas, P. Universidad Católica de Chile, Santiago, Chile.
Raffaella De PaceNeurosciences and Cellular and Structural Biology Division, Eunice Kennedy Shriver National Institute of Child Health and Human Development, National Institutes of Health, Bethesda, MD, USA.
Natacha SantibañezInstituto de Patología Animal, Facultad de Ciencias Veterinarias, Universidad Austral de Chile, Valdivia, Chile.
Viviana A CavieresDepartamento de Ciencias Biológicas y Químicas, Fac. Med y Ciencia, USS, Santiago, Chile.
Tammy P PástorEscuela de Medicina, Facultad de Medicina y Ciencia, Universidad San Sebastián, Valdivia, Chile.
Juan S BonifacinoNeurosciences and Cellular and Structural Biology Division, Eunice Kennedy Shriver National Institute of Child Health and Human Development, National Institutes of Health, Bethesda, MD, USA.
Gonzalo A MardonesEscuela de Medicina, Facultad de Medicina y Ciencia, Universidad San Sebastián, Valdivia, Chile.
María-Paz MarzoloDepartamento de Biología Celular y Molecular, Facultad de Ciencias Biológicas, P. Universidad Católica de Chile, Santiago, Chile. Electronic address: mmarzolo@bio.puc.cl.
Pontificia Universidad Católica de Chile · CLSan Sebastián University · CLAustral University of Chile · CLEunice Kennedy Shriver National Institute of Child Health and Human Development · USNational Institutes of Health · US

Funding

Protein Trafficking In The Endosomal-Lysosomal SystemZIAHD001607 · NICHD · EUNICE KENNEDY SHRIVER NATIONAL INSTITUTE OF CHILD HEALTH & HUMAN DEVELOPMENT · PI BONIFACINO, JUAN · 2009 to 2025
$48.3M
REGULATION OF THE FATE OF NEWLY SYNTHESIZED PROTEINSZ01HD001607 · NICHD · EUNICE KENNEDY SHRIVER NATIONAL INSTITUTE OF CHILD HEALTH & HUMAN DEVELOPMENT · PI BONIFACINO, JUAN · 1991 to 2008
$4.4M
Intramural NIH HHS Z01 HD001607Intramural NIH HHS ZIA HD001607
6 · The paper itself

Abstract

Adaptor protein complex 4 (AP-4) is a heterotetrameric complex that promotes export of selected cargo proteins from the trans-Golgi network. Mutations in each of the AP-4 subunits cause a complicated form of Hereditary Spastic Paraplegia (HSP). Herein, we report that ApoER2, a receptor in the Reelin signaling pathway, is a cargo of the AP-4 complex. We identify the motif ISSF/Y within the ApoER2 cytosolic domain as necessary for interaction with the canonical signal-binding pocket of the µ4 (AP4M1) subunit of AP-4. AP4E1- knock-out (KO) HeLa cells and hippocampal neurons from Ap4e1-KO mice display increased co-localization of ApoER2 with Golgi markers. Furthermore, hippocampal neurons from Ap4e1-KO mice and AP4M1-KO human iPSC-derived cortical i3Neurons exhibit reduced ApoER2 protein expression. Analyses of biosynthetic transport of ApoER2 reveal differential post-Golgi trafficking of the receptor, with lower axonal distribution in KO compared to wild-type neurons, indicating a role of AP-4 and the ISSF/Y motif in the axonal localization of ApoER2. Finally, analyses of Reelin signaling in mouse hippocampal and human cortical KO neurons show that AP4 deficiency causes no changes in Reelin-dependent activation of the AKT pathway and only mild changes in Reelin-induced dendritic arborization, but reduces Reelin-induced ERK phosphorylation, CREB activation, and Golgi deployment. This work thus establishes ApoER2 as a novel cargo of the AP-4 complex, suggesting that defects in the trafficking of this receptor and in the Reelin signaling pathway could contribute to the pathogenesis of HSP caused by mutations in AP-4 subunits.

Indexed as

Adaptor Protein Complex 4LDL-Receptor Related ProteinsSpastic Paraplegia, HereditaryAnimalsHeLa CellsHumansMiceReceptors, Cell SurfaceAdaptor Protein Complex 4LDL-Receptor Related Proteinslow density lipoprotein receptor-related protein 8Receptors, Cell Surfacereelin receptorAP-4ApoER2GolgiHereditary Spastic ParaplegiaNeuronReelin

Identifiers

PMID38281682
PMCPMC10979513
OpenAlexW4391247869

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.