Evidence map›Paper›PMID 23810987›Full record

ReviewExperimental cell research2013

Evidence for defective Rab GTPase-dependent cargo traffic in immune disorders.

Konrad Krzewski, Andrew R Cullinane

Open access · greenAbstract readReview
In one paragraph

Review in Experimental cell research, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.

0numbers the graph read from it
0cells of the map it votes in
18citing papers in PubMed
1.6field-weighted citation impact, top 18% 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

18 citing papers in PubMed, 30 citations in OpenAlex.

  1. Endosomal Mechanisms in Heart Failure Pathophysiology.Current heart failure reports · 2025
    Review
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  14. Review
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  17. New Insights into How Trafficking Regulates T Cell Receptor Signaling.Frontiers in cell and developmental biology · 2016
    Review
  18. The role of the small GTPase Rab31 in cancer.Journal of cellular and molecular medicine · 2015
    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

2 authors at 1 institution in 1 country.

Konrad KrzewskiReceptor Cell Biology Section, Laboratory of Immunogenetics, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Rockville, MD 20852, USA.
Andrew R Cullinane
National Institutes of Health · US

Funding

Human Biochemical GeneticsZIAHG000215 · NHGRI · NATIONAL HUMAN GENOME RESEARCH INSTITUTE · PI GAHL, WILLIAM · 2009 to 2025
$72.6M
Cell Biology of Metabolic DisordersZIAHG200322 · NHGRI · NATIONAL HUMAN GENOME RESEARCH INSTITUTE · PI GAHL, WILLIAM · 2009 to 2014
$3.1M
Intramural NIH HHS Z99 HG999999Intramural NIH HHS Z99 HL999999Intramural NIH HHS Z99 MH999999Intramural NIH HHS ZIA HG000215Intramural NIH HHS ZIA HG200322
6 · The paper itself

Abstract

A fully functional immune system is essential to protect the body against pathogens and other diseases, including cancer. Vesicular trafficking provides the correct localization of proteins within all cell types, but this process is most exquisitely controlled and coordinated in immune cells because of their specialized organelles and their requirement to respond to selected stimuli. More than 60 Rab GTPases play important roles in protein trafficking, but only five Rab-encoding genes have been associated with inherited human disorders, and only one of these (Rab27a) causes an immune defect. Mutations in RAB27A cause Griscelli Syndrome type 2 (GS2), an autosomal recessive disorder of pigmentation and severe immune deficiency. In lymphocytes, Munc13-4 is an effector of Rab27a, and mutations in the gene encoding this protein (UNC13D) cause Familial Hemophagocytic Lymphohistiocytosis Type 3 (FHL3). The immunological features of GS2 and FHL3 include neutropenia, thrombocytopenia, and immunodeficiency due to impaired function of cytotoxic lymphocytes. The small number of disorders caused by mutations in genes encoding Rabs could be due to their essential functions, where defects in these genes could be lethal. However, with the increasing use of next generation sequencing technologies, more mutations in genes encoding Rabs may be identified in the near future.

Indexed as

Chediak-Higashi SyndromeCrohn DiseaseGene Expression RegulationHermanski-Pudlak SyndromeHumansImmunologic Deficiency SyndromesLymphohistiocytosis, HemophagocyticMembrane ProteinsMutationPiebaldismPrimary Immunodeficiency DiseasesProtein Transportrab27 GTP-Binding Proteinsrab GTP-Binding ProteinsSignal TransductionT-Lymphocytes, CytotoxicMembrane ProteinsRAB27A protein, humanrab27 GTP-Binding Proteinsrab GTP-Binding ProteinsUNC13D protein, humanFamilial Hemophagocytic Lymphohistiocytosis Type 3Griscelli Syndrome Type 2ImmunodeficienciesMuc13-4Rab27aRab GTPases

Identifiers

PMID23810987
PMCPMC3759575
OpenAlexW1995278825

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.