Evidence map›Paper›PMID 21147240›Full record

ReviewSeminars in cell & developmental biology2011

Rab GTPases implicated in inherited and acquired disorders.

Shreya Mitra, Kwai W Cheng, Gordon B Mills

Abstract readReview
In one paragraph

Review in Seminars in cell & developmental biology, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 52 papers.

0numbers the graph read from it
0cells of the map it votes in
52citing papers in PubMed
4.0field-weighted citation impact, top 6% 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

52 citing papers in PubMed, 89 citations in OpenAlex.

  1. Article
  2. Review
  3. Article
  4. Rab44 Deficiency Induces Impaired Immune Responses to Nickel Allergy.International journal of molecular sciences · 2023
    Article
  5. Article
  6. Article
  7. Review
  8. Role of Rab GTPases in Hepatocellular Carcinoma.Journal of hepatocellular carcinoma · 2021
    Review
  9. Review
  10. Article
  11. Article
  12. Review
  13. Article
  14. Article
  15. Review
  16. Probing the druggability of membrane-bound Rab5 by molecular dynamics simulations.Journal of enzyme inhibition and medicinal chemistry · 2017
    Article
  17. Article
  18. Article
  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

3 authors at 2 institutions in 1 country.

Shreya MitraDepartment of Systems Biology, The University of Texas, MD Anderson Cancer Center, Houston, TX 77054-1942, USA. smitra@mdanderson.org
Kwai W Cheng
Gordon B Mills
The University of Texas MD Anderson Cancer Center · USCenter for Systems Biology · US

Funding

Tumor Evolution and Metastasis ProgramP30CA016672 · NCI · UNIVERSITY OF TX MD ANDERSON CAN CTR · PI Scott Kopetz · 1985 to 2026
$290.8M
Targeting the PI3K Signaling Pathway in Endometrial CarcinomaP50CA098258 · NCI · UNIVERSITY OF TX MD ANDERSON CAN CTR · PI BODURKA, DIANE · 2003 to 2020
$32.0M
Tyrosine Kinase-Dependant and - Independent Pathways of EGFR in Breast Cancer ProP01CA099031 · NCI · UNIVERSITY OF TX MD ANDERSON CAN CTR · PI HUNG, MIEN-CHIE · 2003 to 2014
$11.6M
NCI NIH HHS P01 CA099031NCI NIH HHS P01CA099031NCI NIH HHS P30 CA016672NCI NIH HHS P30CA16672NCI NIH HHS P50 CA098258
6 · The paper itself

Abstract

The endocytotic machinery imports, transports and exports receptors and associated molecules between the plasma membrane and various cytoplasmic chambers resulting in selective recycling, degradation, or secretion of molecules and signaling complexes. Trafficking of receptors, growth factors, nutrients, cytokines, integrins as well as pathogens dictates the kinetics and magnitude of signal transduction cascades. Understandably, alterations in the 'fate' of such cargo complexes have profound physiologic and pathophysiologic implications. Rab GTPases regulate endocytosis by decorating intracellular vesicles and targeting these vesicles along with their cargoes to appropriate subcellular compartments. In the last decade, the number of genetic diseases driven by germline mutations in Rab GTPases or their interacting proteins, has increased and there is growing evidence of aberrant Rab GTPase function in acquired pathophysiologies such as immune deficiency, infection, obesity, diabetes and cancer.

Indexed as

Genetic Predisposition to DiseaseAnimalsBiological TransportEndocytosisHumansMutationrab GTP-Binding ProteinsTransport Vesiclesrab GTP-Binding Proteins

Identifiers

PMID21147240
PMCPMC3395236
OpenAlexW2020918761

What OpenQuestion 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 OpenQuestion graph.