Dock2 in the development of inflammation and cancer.
Yayun ChenFan MengBingyu WangLiangmei HeYangbin LiuZhiping LiuPublished in: European journal of immunology (2018)
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.
Keyphrases
- wild type
- high frequency
- oxidative stress
- papillary thyroid
- botulinum toxin
- signaling pathway
- transcranial magnetic stimulation
- induced apoptosis
- squamous cell carcinoma
- small molecule
- case report
- stem cells
- risk assessment
- bone marrow
- human health
- childhood cancer
- antiretroviral therapy
- climate change
- lymph node metastasis
- smoking cessation
- amino acid
- cell migration