Evidence map›Paper›PMID 21651512›Full record

ReviewClinical genetics2011

Rab GTPases as regulators of endocytosis, targets of disease and therapeutic opportunities.

J O Agola, P A Jim, H H Ward, S Basuray, A Wandinger-Ness

Open access · bronzeAbstract readReview
In one paragraph

Review in Clinical genetics, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 75 papers.

0numbers the graph read from it
0cells of the map it votes in
75citing papers in PubMed
5.7field-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

75 citing papers in PubMed, 139 citations in OpenAlex.

  1. Article
  2. BAG3 modulates clathrin-mediated endocytosis and tau uptake in astrocytes.American journal of physiology. Cell physiology · 2026
    Article
  3. Article
  4. Review
  5. Article
  6. Article
  7. Article
  8. Article
  9. Review
  10. Virus infection and vesicle trafficking.Frontiers in immunology · 2025
    Review
  11. Article
  12. Article
  13. Article
  14. Article
  15. Cryo-EM structure of the Mon1-Ccz1-RMC1 complex reveals molecular basis of metazoan RAB7A activation.Proceedings of the National Academy of Sciences of the United States of America · 2023
    Article
  16. Review
  17. Article
  18. Article
  19. Review
  20. Review

15 more citing papers are in PubMed but not listed here.

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

5 authors at 1 institution in 1 country.

J O AgolaDepartment of Pathology Cancer Center, University of New Mexico School of Medicine, Albuquerque, NM 87131, USA.
P A Jim
H H Ward
S Basuray
A Wandinger-Ness
University of New Mexico · US

Funding

UNM PREP (Post-baccalaureate Research Education ProgramR25GM075149 · NIGMS · UNIVERSITY OF NEW MEXICO · PI Kelly Miller · 2005 to 2026
$7.3M
Misregulation of the TDP-43 RNA target, Sortilin, in neurodegenerationR01NS077402 · NINDS · MAYO CLINIC JACKSONVILLE · PI PETRUCELLI, LEONARD · 2011 to 2015
$1.7M
HTS to identify small molecules that disrupt Rab GTPase activator and effector prR21NS066435 · NINDS · UNIVERSITY OF NEW MEXICO · PI WANDINGER-NESS, ANGELA · 2009 to 2009
$149k
HTS to Identify Specific Small Molecule Inhibitors and Activators of Ras and Ras-R03MH081231 · NIMH · UNIVERSITY OF NEW MEXICO · PI WANDINGER-NESS, ANGELA · 2007 to 2007
$25k
NIGMS NIH HHS 5R25GM075149NIGMS NIH HHS R25 GM075149NIMH NIH HHS R03 MH081231NIMH NIH HHS R03MH081231NINDS NIH HHS R21 NS066435NINDS NIH HHS R21NS7740241
6 · The paper itself

Abstract

Rab GTPases are well-recognized targets in human disease, although are underexplored therapeutically. Elucidation of how mutant or dysregulated Rab GTPases and accessory proteins contribute to organ specific and systemic disease remains an area of intensive study and an essential foundation for effective drug targeting. Mutation of Rab GTPases or associated regulatory proteins causes numerous human genetic diseases. Cancer, neurodegeneration and diabetes represent examples of acquired human diseases resulting from the up- or downregulation or aberrant function of Rab GTPases. The broad range of physiologic processes and organ systems affected by altered Rab GTPase activity is based on pivotal roles in responding to cell signaling and metabolic demand through the coordinated regulation of membrane trafficking. The Rab-regulated processes of cargo sorting, cytoskeletal translocation of vesicles and appropriate fusion with the target membranes control cell metabolism, viability, growth and differentiation. In this review, we focus on Rab GTPase roles in endocytosis to illustrate normal function and the consequences of dysregulation resulting in human disease. Selected examples are designed to illustrate how defects in Rab GTPase cascades alter endocytic trafficking that underlie neurologic, lipid storage, and metabolic bone disorders as well as cancer. Perspectives on potential therapeutic modulation of GTPase activity through small molecule interventions are provided.

Indexed as

AnimalsAutophagyBiological TransportCell MembraneEndocytosisHumansrab GTP-Binding ProteinsSignal Transductionrab GTP-Binding Proteins

Identifiers

PMID21651512
PMCPMC3187864
OpenAlexW2061033339

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.