Product Description
DOK2 Antibody | 63-148 | ProSci
Host: Rabbit
Reactivity: Human
Homology: N/A
Immunogen: This DOK2 antibody is generated from rabbits immunized with a KLH conjugated synthetic peptide between 380-412 amino acids from the C-terminal region of human DOK2.
Research Area: Cancer, Signal Transduction
Tested Application: WB, IHC-P
Application: For WB starting dilution is: 1:1000
For IHC-P starting dilution is: 1:50~100
Specificiy: N/A
Positive Control 1: N/A
Positive Control 2: N/A
Positive Control 3: N/A
Positive Control 4: N/A
Positive Control 5: N/A
Positive Control 6: N/A
Molecular Weight: 45 kDa
Validation: N/A
Isoform: N/A
Purification: This antibody is prepared by Saturated Ammonium Sulfate (SAS) precipitation followed by dialysis
Clonality: Polyclonal
Clone: N/A
Isotype: Rabbit Ig
Conjugate: Unconjugated
Physical State: Liquid
Buffer: Supplied in PBS with 0.09% (W/V) sodium azide.
Concentration: batch dependent
Storage Condition: Store at 4˚C for three months and -20˚C, stable for up to one year. As with all antibodies care should be taken to avoid repeated freeze thaw cycles. Antibodies should not be exposed to prolonged high temperatures.
Alternate Name: Docking protein 2, Downstream of tyrosine kinase 2, p56 (dok-2) , DOK2
User Note: Optimal dilutions for each application to be determined by the researcher.
BACKGROUND: Docking proteins interact with receptor tyrosine kinases and mediate particular biological responses using signal transduction. Dok-2 acts as a multiple docking protein downstream of receptor or non-receptor tyrosine kinases. By this mechanism it acts to negatively regulate signal transduction and cell proliferation controlled by cytokines in a feedback loop. Dok-2 is highly expressed in cells and tissues of hematopoietic origin as well as in lung. Expression of bcr/abl induces additional tyrosine phosphorylation of the Dok1 and Dok2 proteins and their association with Ras-GAP. Thus, it is suspected that DOK association regulates GAP activity toward Ras and that the Dok proteins serve as mediators of bcr-abl signaling. The role of Dok proteins in bcr-abl regulation may also be implicated in chronic myelogenous leukemia (CML) , which is characterized by a Philadelphia chromosome translocation t (9;22) . Such a mutation would result in a p210-bcr/abl chimeric protein-tyrosine kinase which has been found in many CML cases.