ArticleThe Journal of clinical investigation2002
Functional redundancy of Rab27 proteins and the pathogenesis of Griscelli syndrome.
Article in The Journal of clinical investigation, 2002. 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 68 papers.
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Who cites it
68 citing papers in PubMed, 159 citations in OpenAlex.
- Secreted exosomes induce filopodia formation.eLife · 2026Article
- Immune cell infiltration into brain tumor microenvironment is mediated by Rab27-regulated vascular wall integrity.Science advances · 2025Article
- Melanophilin regulates dendritogenesis in melanocytes for feather pigmentation.Communications biology · 2024Article
- Targeting TYK2 alleviates Rab27A-induced malignant progression of non-small cell lung cancer via disrupting IFNα-TYK2-STAT-HSPA5 axis.NPJ precision oncology · 2024Article
- Vesicular Trafficking, a Mechanism Controlled by Cascade Activation of Rab Proteins: Focus on Rab27.Biology · 2023Review
- RAB27B controls palmitoylation-dependent NRAS trafficking and signaling in myeloid leukemia.The Journal of clinical investigation · 2023Article
- Article
- GDP/GTP exchange factor MADD drives activation and recruitment of secretory Rab GTPases to Weibel-Palade bodies.Blood advances · 2021Article
- Article
- Rab27a Contributes to Cathepsin S Secretion in Lacrimal Gland Acinar Cells.International journal of molecular sciences · 2021Article
- Rab27a deletion impairs the therapeutic potential of endothelial progenitor cells for myocardial infarction.Molecular and cellular biochemistry · 2021Article
- Treating primary immunodeficiencies with defects in NK cells: from stem cell therapy to gene editing.Stem cell research & therapy · 2020Review
- Article
- KIBRA controls exosome secretion via inhibiting the proteasomal degradation of Rab27a.Nature communications · 2019Article
- Small GTPases in platelet membrane trafficking.Platelets · 2019Review
- Dynamins 2 and 3 control the migration of human megakaryocytes by regulating CXCR4 surface expression and ITGB1 activity.Blood advances · 2018Article
- Functional implications of Rab27 GTPases in Cancer.Cell communication and signaling : CCS · 2018Review
- Consequences of Rab GTPase dysfunction in genetic or acquired human diseases.Small GTPases · 2018Review
- MST1-dependent vesicle trafficking regulates neutrophil transmigration through the vascular basement membrane.The Journal of clinical investigation · 2016Article
- Molecular mechanisms regulating secretory organelles and endosomes in neutrophils and their implications for inflammation.Immunological reviews · 2016Review
8 more citing papers are in PubMed but not listed here.
Corrections and comments
- Erratum issued
Authors and funding
10 authors at 3 institutions in 3 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Griscelli syndrome (GS) patients and the corresponding mouse model ashen exhibit defects mainly in two types of lysosome-related organelles, melanosomes in melanocytes and lytic granules in CTLs. This disease is caused by loss-of-function mutations in RAB27A, which encodes 1 of the 60 known Rab GTPases, critical regulators of vesicular transport. Here we present evidence that Rab27a function can be compensated by a closely related protein, Rab27b. Rab27b is expressed in platelets and other tissues but not in melanocytes or CTLs. Morphological and functional tests in platelets derived from ashen mice are all within normal limits. Both Rab27a and Rab27b are found associated with the limiting membrane of platelet-dense granules and to a lesser degree with alpha-granules. Ubiquitous transgenic expression of Rab27a or Rab27b rescues ashen coat color, and melanocytes derived from transgenic mice exhibit widespread peripheral distribution of melanosomes instead of the perinuclear clumping observed in ashen melanocytes. Finally, transient expression in ashen melanocytes of Rab27a or Rab27b, but not other Rab's, restores peripheral distribution of melanosomes. Our data suggest that Rab27b is functionally redundant with Rab27a and that the pathogenesis of GS is determined by the relative expression of Rab27a and Rab27b in specialized cell types.
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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.