Use your antibodies-online credentials, if available.
DOCK8 encodes a member of the DOCK180 family of guanine nucleotide exchange factors. 再加上，我们可以发 和 和数多这个蛋白质的别的产品。
Showing 10 out of 42 products:
EPAS1 (显示 EPAS1 抗体) links DOCK8 deficiency to atopic skin inflammation via IL-31 (显示 IL31 抗体) induction in CD4thorn T cells.
A novel DOCK8 sequence insertion caused primary immunodeficiency in two siblings from a consanguineous family.
DOCK8 deficiency may present severe immune dysregulation with features that may overlap with those of immune dysregulation, polyendocrinopathy, enteropathy, X-linked (IPEX (显示 FOXP3 抗体)) and other IPEX (显示 FOXP3 抗体)-like disorders
Recent advances in the understanding of DOCK8 function are summarized, paying particular attention to an emerging role as a signaling intermediate to promote immune responses to diverse external stimuli. [Review]
In severe atopic eczema the dermatologist should initially suspect and document a mutation of DOCK8.
Our results suggest that decreased expression of DOCK8 in response to CRH (显示 CRH 抗体) might disturb the immunosuppressive function of Tregs and contribute to stress-induced aggravation of AD symptoms.
Sequence analysis identified two copies of missense mutation, c.4346C > T, in the coding region of the DOCK8 gene in a family with 3 patients with autosomal recessive Hyper-IgE syndrome.
Our results showed that DOCK8-deficient patients have a profound defect in TH17 differentiation related to decreased STAT3 (显示 STAT3 抗体) phosphorylation, translocation to the nucleus, and transcriptional activity
The CD4 (显示 CD4 抗体)+ T-cell compartment is greatly altered in the absence of DOCK8. Specifically, DOCK8-deficient patients have increased TH2 cells and defects in TH1 (显示 TH1L 抗体) and TH17 cell differentiation
comparative study provides a long-term observation of DOCK8- and STAT3-hyper-IgE syndrome patients with regard to clinical and laboratory findings, and assesses the activation and cytokine secretion of lymphocytes after in vitro stimulation
DOCK8 and WASp are in the same signaling pathway that links T-cell receptors (TCRs) to the actin cytoskeleton in TCR-driven actin assembly.
LRCH1 (显示 LRCH1 抗体) as a novel effector to restrain PKCalpha (显示 PKCa 抗体)-DOCK8-Cdc42 (显示 CDC42 抗体) module-induced T cell migration and ameliorate experimental autoimmune encephalomyelitis (EAE).
found that DOCK8 associated with LRAP35a, an adaptor molecule that binds to the Cdc42 effector myotonic dystrophy kinase-related Cdc42-binding kinase, and facilitated its activity to phosphorylate myosin II regulatory light chain
DOCK8-deficient mice have poor control of primary cutaneous herpes simplex lesions and this is associated with increased virus loads. Furthermore, DOCK8-deficient mice showed a lack of CD4 (显示 CD4 抗体)(+) T-cell infiltration into HSV-infected skin.
DOCK8 expression in the haematopoietic compartment is required for protective immunity and its deficiency results in drastic reduction of RORgammat+ innate lymphoid cells in the GI tract
conclude that DOCK8 is an important regulator of DC migration during an immune response and is prone to mutations that disrupt its crucial function
DOCK8-regulated shape integrity of lymphocytes prevents cytothripsis and promotes antiviral immunity in the skin.
DOCK8 is required for the development and survival of mature NKT (显示 CTSL1 抗体) cells.
DOCK8 regulates interstitial DC migration by controlling Cdc42 (显示 CDC42 抗体) activity spatially.
Characterisation of the DOCK8-deficient mouse revealed T-cell lymphopenia, with increased T-cell turnover and decreased survival.
This gene encodes a member of the DOCK180 family of guanine nucleotide exchange factors. Guanine nucleotide exchange factors interact with Rho GTPases and are components of intracellular signaling networks. Mutations in this gene result in the autosomal recessive form of the hyper-IgE syndrome. Alternatively spliced transcript variants encoding different isoforms have been described.
dedicator of cytokinesis 8
, dedicator of cytokinesis protein 8-like
, dedicator of cytokinesis protein 8