The DOI matches its Crossref record; 45 of the 45 references it cites were found in a registry or an index.
RhoH Plays Critical Roles in FcεRI-Dependent Signal Transduction in Mast Cells
Abstract
RhoH is an atypical small G protein with defective GTPase activity that is specifically expressed in hematopoietic lineage cells. RhoH has been implicated in regulation of several physiological processes including hematopoiesis, integrin activation, and T cell differentiation and activation. In the present study, we investigated the role of RhoH in mast cells by generating RhoH knockout mice. Despite observing normal development of mast cells in vivo, passive systemic anaphylaxis and histamine release were impaired in these mice. We also observed defective degranulation and cytokine production upon FcεRI ligation in RhoH-deficient bone marrow-derived mast cells. Furthermore, FcεRI-dependent activation of Syk and phosphorylation of its downstream targets, including LAT, SLP76, PLCγ1, and PLCγ2 were impaired, however phosphorylation of the γ-subunit of FcεRI remained intact. We also found RhoH-Syk association that was greatly enhanced by active Fyn. Our results indicate that RhoH regulates FcεRI signaling in mast cells by facilitating Syk activation, possibly as an adaptor molecule for Syk.
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In the citing paper
“Nonetheless, RhoH is required for FcεRI-dependent signal transduction in mast cells and thus passive systemic anaphylaxis and histamine release are impaired in the absence of RhoH72.”
From Hematopoietic-specific Rho GTPases Rac2 and RhoH and human blood disorders (2013) · cites this paper as [72]
In the citing paper
“T-cell development is impaired”
From RhoH is a negative regulator of eosinophilopoiesis (2016) · cites this paper as [26]
In the citing paper
“mast cell development unaffected. 21,26”
From RhoH is a negative regulator of eosinophilopoiesis (2016) · cites this paper as [26]
In the citing paper
“Rhoh -/-mice have a mild myeloid phenotype (39,40); no overt myeloid phenotype was observed in our patients.”
From Human RHOH deficiency causes T cell defects and susceptibility to EV-HPV infections (2012) · cites this paper as [40]
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Metadata
- Authors
- Oda, H., Fujimoto, M., Patrick, M. S., Chida, D., Sato, Y., Azuma, Y., Aoki, H., Abe, T., Suzuki, H., & Shirai, M.
- Affiliations
- Department of Pathology, Research Institute, International Medical Center of Japan , Tokyo,
- Kanazawa University (JP)
- Yamaguchi University (JP)
- Kurume University (JP)
- RIKEN (JP)
- Corresponding author
- Oda, Hiroyo
- Chida, Dai
- Sato, Yoshinori
- Suzuki, Harumi
- Venue
- The Journal of Immunology
- Publisher
- Oxford University Press (OUP)
- Published
- 2009-01
- Volume
- 182
- Issue
- 2
- Pages
- 957-962
- ISSN
- 0022-1767 (ISSN-L)
- 1550-6606
- OpenAlex
- W1495161304
- Cited by
- 29
- References
- 45
- Citations by year
- 2024: 1 · 2022: 1 · 2021: 1 · 2020: 2 · 2018: 2 · 2017: 3 · 2016: 2 · 2015: 3 · 2014: 2 · 2013: 3 · 2012: 2
- FWCI
- 1.24
- Type
- journal article
- Language
- en
- Open access
- closed
- Locations
- The Journal of Immunology (publishedVersion)
- PubMed (publishedVersion)
- Institutional Repositories DataBase (IRDB) (submittedVersion)
- Topics
- Life Sciences › Immunology and Microbiology › Immunology › Mast cells and histamine
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Protein Kinase Regulation and GTPase Signaling
- Health Sciences › Medicine › Immunology and Allergy › Food Allergy and Anaphylaxis Research
- Keywords
- RhoH, FcεRI signaling, mast cells, Syk activation, Fyn, passive systemic anaphylaxis, histamine release, mast cell degranulation, cytokine production, LAT, SLP-76, PLCγ1, PLCγ2, adaptor molecules
- MeSH terms
- Syk Kinase, Animals, Cell Differentiation, Cells, Cultured, Enzyme Activation, Mast Cells, Mice, Inbred C57BL, Passive Cutaneous Anaphylaxis, Protein-Tyrosine Kinases, Transcription Factors, Signal Transduction, Cell Degranulation, Receptors, IgE, Mice, Knockout, rho GTP-Binding Proteins, Intracellular Signaling Peptides and Proteins, Mice
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