Vav1 GEF Protein (DHPHC1 Exchange Domain, Y174D mutant, aa168-522, 6xHis tag)

Vav1 GEF Protein (DHPHC1 Exchange Domain, Y174D mutant, aa168-522, 6xHis tag)

Catalog Number:
P001437073CYT
Mfr. No.:
CS-GE05
Price:
  • Size:
    1x100 µg
    Quantity:
    Add to Cart:
      • Overview
        • Product Uses
          Vav1 protein is a guanine exchange factor with selectivity for Rac1, which mediates Rac1 activation under a variety of conditions and has been associated with multiple diseases for example autoimmune deficiency and esophageal squamous cell carcinoma (reviewed in 1, 2, 3).
          Study inhibitors of Vav1 GTP/GDP exchange activity
          Identification of Vav1 DHPHC1 domain binding proteins
          Study of Vav1 GEF activity with different GTPases

          Material
          The DHPHC1 domain of human Vav1 protein has been produced in a bacterial expression system. It contains a mutated amino-acid that mimics tyrosine phosphorylation which is required for interaction with Rac1 (Y174D mutant). It is also 6xHis tagged at its amino terminus for purification purposes. The accession number is AAH13361. The molecular weight of GE05 is approximately 41 kDa. The Vav1 protein is supplied as a white lyophilized powder. Protein purity is determined by scanning densitometry of Coomassie Blue stained protein on a 4-20% polyacrylamide gradient gel. Vav1 DHPHC1 protein was determined to be approximately 80% pure.

          Please contact us at for specific academic pricing.

      • Properties
        • Purification
          Protein purity is determined by scanning densitometry of Coomassie blue stained protein on a 4-20% polyacrylamide gradient gel. The Vav1 protein was determined to be >80% pure.

          * For Research Use Only

    Note: If you don't receive our verification email, do the following:

    • Confirm that you entered your email address correctly.
    • Check if the email is in your spam or junk folder.
    • Or you may contact us at .
  • Copyright © Amerigo Scientific. All rights reserved.