(800) 943-6396

150 Essex St, Millburn, NJ 07041, USA

©2020 by Bon Opus Biosciences, LLC.

KDEL Recombinant Rabbit monoclonal Antibody IgG

SKU: BA112555-100µl
$279.00Price

Fig1: Western blot analysis of KDEL on different lysates using anti-KDEL antibody at 1/1,000 dilution.

 Positive control:

 Lane 1: Rat testis tissue

 Lane 2: Human placenta tissue

 Lane 3: Mouse testis tissue

 Lane 4: 293

 

Fig2: ICC staining KDEL in A549 cells (green). The nuclear counter stain is DAPI (blue). Cells were fixed in paraformaldehyde, permeabilised with 0.25% Triton X100/PBS.

Fig3: ICC staining KDEL in HepG2 cells (green). The nuclear counter stain is DAPI (blue). Cells were fixed in paraformaldehyde, permeabilised with 0.25% Triton X100/PBS.

Bon Opus Cat. #BA112555
Size
  • Host Species; Species Reactivity

    Rabbit; Human, Mouse, Rat
  • Immunogen

    Recombinant protein
  • Application Summary

    WB,ICC,IF,IHC,FC
  • Purification; Formulation

    ProA affinity purified; 1*TBS (pH7.4), 1%BSA, 40%Glycerol. Preservative: 0.05% Sodium Azide.; Liquid form.
  • ALTnames

    ER lumen protein-retaining receptor 1, KDEL endoplasmic reticulum protein retention receptor 1, Putative MAPK-activating protein PM23
  • Background

    Soluble proteins in the endoplasmic reticulum (ER) contain a specific carboxy terminal sequence KDEL (Lys-Asp-Glu-Leu), and include the coat proteins required for vesicle budding from the ER, proteins that form retrograde vesicles on post-ER compartments, and integral membrane proteins that target vesicles to their correct destination. The retention of these soluble proteins in the ER depends on the interaction of the KDEL sequence with the corresponding KDEL receptor, also designated ERD2, in the Golgi apparatus. When KDEL proteins reach the Golgi complex, they are recognized by the KDEL receptor and transported retrograde in COPI-coated vesicles back to the ER. The small GTPase ADP-ribosylation factor 1 (ARF1), a regulator of vesicle transport, interacts with the KDEL receptor. Subsequently, this interaction allows the KDEL receptor to recruit a GTPase-activating protein (GAP) from the cytosol to membranes, which inactivates ARF1.(ET7107-86)