Dock2 in the development of inflammation and cancer
Open accessAbstract
An atypical guanine exchange factor, Dock2 is specifically expressed in hematopoietic cells and regulates activation and migration of immune cells through activating Ras‐related C3 botulinum toxin substrate (Rac). Dock2 was shown to be critical in the development of various inflammatory diseases, including allergic diseases, HIV infection, and graft rejection in organ transplantation. DOCK2 mutation in infants was recently identified to be associated with T and B cell combined immunodeficiency. Furthermore, Dock2 is involved in host protection during enteric bacterial infection and is also associated with the proliferation of cancer cells. It was also shown that patients with digestive tract cancer had high frequency mutation of DOCK2. This review summarizes the latest research progresses on the role of Dock2 for the development of various inflammatory diseases and cancers, and discusses the potential application of Dock2 modulators for patient treatment.
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DOCK2 activates RAC GTPases and is predominantly expressed in hematopoietic cells.
“DOCK2, responsible for activating RAC GTPases, is predominantly expressed in hematopoietic cells (59, 60, 61, 62).”
From RHO to the DOCK for GDP disembarking: Structural insights into the DOCK GTPase nucleotide exchange factors (2021) · cites this paper as [61]
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Haematopoietic cell-specific CDM family protein DOCK2 is essential for lymphocyte migration
Fukui, Y., Hashimoto, O., Sanui, T., Oono, T., Koga, H., Abe, M., Inayoshi, A., Noda, M., Oike, M., Shirai, T., et al. (2001) · Nature · doi:10.1038/35090591 · Cited by 449 · see citing works
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Research works printed but not linked: 2
- Hanawa-Suetsugu, K., Kukimoto-Niino, M., Mishima-Tsumagari, C., Akasaka, R., Ohsawa, N. and Sekine, S., Structural basis for mutual relief of the Rac guanine nucleotide exchange factor DOCK2 and its partner ELMO1 from their autoinhibited forms. Proc. Natl. Acad. Sci. USA 2012. 109: 3305-3310.
- C 2018 WILEY-VCH Verlag GmbH & Co. KGaA, Weinheim www.eji-journal.eu
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Thompson, A. P., Bitsina, C., Gray, J. L., von Delft, F., & Brennan, P. E. (2021) · Journal of Biological Chemistry · doi:10.1016/j.jbc.2021.100521 · Cited by 21 · see citing works
“This is illustrated in animal models, wherein genetic ablation of DOCK2 decreased the migration speed of T-cells and Bcells in lymphoid tissue (61).”
Background
- Authors
- Chen, Y., Meng, F., Wang, B., He, L., Liu, Y., & Liu, Z.
- Affiliations
- School of Basic Medicine Gannan Medical University Ganzhou Jiangxi China
- Guangdong General Hospital (CN)
- Gannan Medical University (CN)
- Corresponding author
- Liu, Zhiping
- Venue
- European Journal of Immunology
- Publisher
- Wiley
- Published
- 2018-04-11
- Volume
- 48
- Issue
- 6
- Pages
- 915-922
- ISSN
- 0014-2980 (ISSN-L)
- 1521-4141
- OpenAlex
- W2807924341
- Cited by
- 50
- References
- 1
- Citations by year
- 2026: 6 · 2025: 3 · 2024: 3 · 2023: 7 · 2022: 7 · 2021: 7 · 2020: 12 · 2019: 4 · 2018: 1
- FWCI
- 0.59
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Locations
- European Journal of Immunology (publishedVersion)
- PubMed (publishedVersion)
- Funders
- National Natural Science Foundation of China (31560260)
- Natural Science Foundation of Jiangxi Province (20151BAB205061, 20171ACB20024)
- Education Department of Jiangxi Province (Gjj150937)
- Topics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Protein Kinase Regulation and GTPase Signaling
- Life Sciences › Immunology and Microbiology › Immunology › Immunodeficiency and Autoimmune Disorders
- Health Sciences › Medicine › Oncology › Chemokine receptors and signaling
- Keywords
- DOCK2, guanine nucleotide exchange factor, Rac activation, hematopoietic cells, leukocyte migration, inflammation, allergic diseases, HIV infection, graft rejection, combined immunodeficiency, enteric bacterial infection, cancer
- MeSH terms
- Animals, Gastrointestinal Neoplasms, Graft Rejection, Humans, Hypersensitivity, Inflammation, Mutation, HIV Infections, Severe Combined Immunodeficiency, Guanine Nucleotide Exchange Factors, GTPase-Activating Proteins, Cell Proliferation, Molecular Targeted Therapy
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