DOK3 overexpression 293T lysate (whole cell) (ab94169)

Overview

  • Product nameDOK3 overexpression 293T lysate (whole cell)
  • Description
    DOK3 overexpression lysate
  • General notesab94169 is a 293T cell transfected lysate in which Human DOK3 has been transiently over-expressed using a pCMV-DOK3 plasmid. The lysate is provided in 1X Sample Buffer. Note: For more detailed about how the transfected lysate was prepared view preparation notes
  • Tested applicationsSuitable for: WBmore details

Properties

  • BackgroundFunction: DOK proteins are enzymatically inert adaptor or scaffolding proteins. They provide a docking platform for the assembly of multimolecular signaling complexes. DOK3 is a negative regulator of JNK signaling in B-cells through interaction with INPP5D/SHIP1. May modulate Abl function. Tissue specificity: Expressed in spleen. Similarity: Belongs to the DOK family. Type A subfamily. Contains 1 IRS-type PTB domain. Contains 1 PH domain. Domain: PTB domain mediates receptor interaction. PTM: Constitutively tyrosine-phosphorylated. On IL2 stimulation, phosphorylated on C-terminal tyrosine residues possibly by Src kinases. Can also be phosphorylated by ABL kinase.

Associated products

Applications

Our Abpromise guarantee covers the use of ab94169 in the following tested applications.

The application notes include recommended starting dilutions; optimal dilutions/concentrations should be determined by the end user.

Application Abreviews Notes
WB Use at an assay dependent dilution.

DOK3 overexpression 293T lysate (whole cell) images

  • ab94169 at 15µg/lane on an SDS-PAGE gel.
  • All lanes : Anti-DOK3 antibody (ab89327) at 1/500 dilution

    Lane 1 : DOK3 overexpression 293T lysate (whole cell) (ab94169)
    Lane 2 : 293T non-transfected lysate

    Lysates/proteins at 25 µg per lane.

    Secondary
    Goat Anti-mouse IgG (H and L) HRP conjugate at 1/2500 dilution

References for DOK3 overexpression 293T lysate (whole cell) (ab94169)

ab94169 has not yet been referenced specifically in any publications.

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