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DOCK3 is specifically expressed in the central nervous system (CNS). Additionally we are shipping DOCK3 Antibodies (11) and many more products for this protein.
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Dock3 may be a therapeutic target for demyelinating disorders including optic neuritis.
Overexpression of Dock3 and pharmacological interruption of p38 (show CRK ELISA Kits) have synergistic effects for both neuroprotection and axon regeneration, thus combined application may be beneficial for the treatment of ONI.
Skeletal muscle-specific (show EIF3K ELISA Kits) miR (show MLXIP ELISA Kits)-486 overexpression in Dmdmdx-5Cv animals decreased levels of DOCK3, reduced PTEN expression, and subsequently increased levels of phosphorylated AKT (show AKT1 ELISA Kits), which resulted in an overall beneficial effect.
These results suggest that Dock3 overexpression prevents glaucomatous retinal degeneration by suppressing both NR2B (show GRIN2B ELISA Kits)-mediated glutamate (show GRIN1 ELISA Kits) neurotoxicity and oxidative stress.
The interaction between NR2D (show GRIN2D ELISA Kits) and Dock3 may have a neuroprotective effect.
MOCA (modifier of cell adhesion), which was originally identified as being a presenilin-and Rac1-binding protein, is a common downstream con (show APP ELISA Kits)stituent of neuronal death signals
Dock3 plays important roles downstream of brain-derived neurotrophic factor (BDNF (show BDNF ELISA Kits)) signaling, where it regulates cell polarity and promotes axonal outgrowth by stimulating dual pathways: actin polymerization and microtubule assembly.
Dock3 induces axonal outgrowth by stimulating membrane recruitment of the WAVE complex
MOCA may induce cytoskeletal reorganization and changes in cell adhesion by regulating the activity of Rac1.
Loss of modifier of cell adhesion reveals a pathway leading to axonal degeneration.
Inhibition of Dock3 by Dock3 shRNA impaired the severity of status epilepticus in the acute stage and decreased the spontaneous recurrent seizures times in the chronic stage of lithium-pilocarpine model and decreased the expression of rac1-GTP (show AK3 ELISA Kits).
Results supported that miR (show MLXIP ELISA Kits)-512-3p could inhibit tumor cell adhesion, migration, and invasion by regulating the RAC1 activity via DOCK3 in NSCLC A549 and H1299 cell lines.
MOCA is a key molecule of the Alzheimer disease-relevant neuronal death signals that links the presenilin-mediated death signal with the APP (show APP ELISA Kits)-mediated death signal at a point between Rac1 or Cdc42 (show CDC42 ELISA Kits) and ASK1 (show MAP3K5 ELISA Kits).
We report that MOCA modulates cell-cell adhesion and morphology by increasing the accumulation of adherens junction proteins.
MOCA is a novel Wnt (show WNT2 ELISA Kits) negative regulator and demonstrate that this screening approach can be a rapid means for isolation of new Wnt (show WNT2 ELISA Kits) regulators.
This gene is specifically expressed in the central nervous system (CNS). It encodes a member of the DOCK (dedicator of cytokinesis) family of guanine nucleotide exchange factors (GEFs). This protein, dedicator of cytokinesis 3 (DOCK3), is also known as modifier of cell adhesion (MOCA) and presenilin-binding protein (PBP). The DOCK3 and DOCK1, -2 and -4 share several conserved amino acids in their DHR-2 (DOCK homology region 2) domains that are required for GEF activity, and bind directly to WAVE proteins
dedicator of cytokinesis 3
, similar to dedicator of cytokinesis 3
, dedicator of cytokinesis protein 3-like
, dedicator of cytokinesis protein 3
, modifier of cell adhesion
, presenilin-binding protein