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DOCK8 encodes a member of the DOCK180 family of guanine nucleotide exchange factors. Additionally we are shipping and many more products for this protein.
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Human Polyclonal DOCK8 Primary Antibody for ICC, IF - ABIN4304781
Jabara, McDonald, Janssen, Massaad, Ramesh, Borzutzky, Rauter, Benson, Schneider, Baxi, Recher, Notarangelo, Wakim, Dbaibo, Dasouki, Al-Herz, Barlan, Baris, Kutukculer, Ochs, Plebani, Kanariou et al.: DOCK8 functions as an adaptor that links TLR-MyD88 signaling to B cell activation. ... in Nature immunology 2012
Show all 2 references for ABIN4304781
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
mutations in Chinese patients with hyper-IgE syndrome
Letter/Case Report: DOCK8 homozygous mutation leading to primary immune deficiency.
DOCK8 deficiency is likely in patients with severe viral infections, allergies, and/or low IgM levels.
CD147 has a role in promoting Src (show SRC Antibodies)-dependent activation of Rac1 signaling through STAT3 (show STAT3 Antibodies)/DOCK8 during the motility of hepatocellular carcinoma cells
DOCK8-regulated shape integrity of lymphocytes prevents cytothripsis and promotes antiviral immunity in the skin.
Dedicator of cytokinesis 8-deficient patients have a breakdown in peripheral B-cell tolerance and defective regulatory T cells
Mutations of DOCK8 in three children, two of whom developed sclerosing cholangitis, are reported.
Hyper-IgE syndromes and atopic dermatitis patients showed different sensitization pattern of serum IgE corresponding to the allergic disease manifestations and Th-cell subset data, suggesting a key role of DOCK8 in the development of food allergy
This is a case of systemic lupus erythematosus with hyper-immunoglobulin E syndrome documented as DOCK8 deficiency.
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 (show CD4 Antibodies)(+) 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 is required for the development and survival of mature NKT (show CTSL1 Antibodies) cells.
DOCK8 regulates interstitial DC migration by controlling Cdc42 (show CDC42 Antibodies) activity spatially.
Characterisation of the DOCK8-deficient mouse revealed T-cell lymphopenia, with increased T-cell turnover and decreased survival.
These findings highlight a key role for DOCK8 in the survival and function of human and mouse CD8 (show CD8A Antibodies) T cells.
Mutation of the DOCK8 protein in mice has profound effects on humoral immunity with a failure to sustain the antibody response and failure of germinal center B cell persistence. (Review)
Humoral immunodeficiency due to Dock8 mutation provides evidence that organization of the immunological synapse is critical for signaling the survival of B cell subsets required for long-lasting immunity.
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