Key Spec Table
|Species Reactivity||Key Applications||Host||Format||Antibody Type|
|H, M, Eq, Pm||WB||Rb||Affinity Purified||Polyclonal Antibody|
|Presentation||Purified in PBS containing 0.05% NaN3.|
|Application||Anti-Dock2 Antibody is an antibody against Dock2 for use in WB.|
|Safety Information according to GHS|
|Storage and Shipping Information|
|Storage Conditions||Maintain at 2-8°C for up to 1 year from date of receipt.|
|Material Size||100 µg|
|Anti-Dock2 - 2298432||2298432|
|Anti-Dock2 - 2003022||2003022|
|Anti-Dock2 - 2905374||2905374|
|Anti-Dock2 - JBC1787316||JBC1787316|
|Anti-Dock2 - NG1584936||NG1584936|
|Anti-Dock2 - NG1842817||NG1842817|
|Anti-Dock2 - NG1941997||NG1941997|
|Reference overview||Pub Med ID|
|Addendum: defective Dock2 expression in a subset of ASC-deficient mouse lines.|
Sirish K Ippagunta,R K Subbarao Malireddi,Patrick J Shaw,Geoffrey A Neale,Lieselotte Vande Walle,Yoshinori Fukui,Douglas R Green,Mohamed Lamkanfi,Thirumala-Devi Kanneganti
Nature immunology 13 2012
|DOCK2 is a microglial specific regulator of central nervous system innate immunity found in normal and Alzheimer's disease brain.|
Cimino, PJ; Sokal, I; Leverenz, J; Fukui, Y; Montine, TJ
The American journal of pathology 175 1622-30 2009
Neuroinflammation is a hallmark of several neurodegenerative diseases, including Alzheimer's disease (AD). Strong epidemiological and experimental evidence supports the use of nonsteroidal anti-inflammatory drugs to reduce AD risk. However, poor outcome in clinical trials and toxicity in a prevention trial have shifted focus away from these cyclooxygenase (COX) inhibitors to seek additional therapeutic targets in the prostaglandin pathway. Previously, the prostaglandin E2 receptor, EP2, was shown to regulate neuroinflammation and reduce Abeta plaque burden in transgenic mice. Unfortunately, widespread EP2 distribution and a direct effect on COX2 induction make EP2 a less desirable target. In this study, we link dedicator of cytokinesis 2 (DOCK2) to the prostaglandin pathway in the brain. Additionally, we show that DOCK2 regulates microglial innate immunity independent of COX2 induction and that DOCK2+ microglia are associated with human AD pathology. Together, these results suggest DOCK2 as a COX2 expression-independent therapeutic target for neurodegenerative diseases such as AD.
|Differential requirement for DOCK2 in migration of plasmacytoid dendritic cells versus myeloid dendritic cells.|
Gotoh, Kazuhito, et al.
Blood, 111: 2973-6 (2008) 2008
|A central role for DOCK2 during interstitial lymphocyte motility and sphingosine-1-phosphate-mediated egress.|
Nombela-Arrieta, César, et al.
J. Exp. Med., 204: 497-510 (2007) 2007
|Non-adherent cell-specific expression of DOCK2, a member of the human CDM-family proteins.|
Nishihara, H, et al.
Biochim. Biophys. Acta, 1452: 179-87 (1999) 1999