|Tested species reactivity||Human, Mouse|
|Published species reactivity||Human|
|Host / Isotype||Mouse / IgG2b, kappa|
|Immunogen||Synthetic peptide corresponding to a region containing the Fas-induced cleavage site of human D4-GDI.|
|Storage buffer||PBS with 0.05% BSA|
|Contains||0.05% sodium azide|
|Storage Conditions||Store at 4°C short term. For long term storage, store at -20°C, avoiding freeze/thaw cycles.|
|Tested Applications||Dilution *|
|Flow Cytometry (Flow)||0.5-1 µg/10^6 cells|
|Immunohistochemistry (Paraffin) (IHC (P))||1:10-1:500|
|Immunoprecipitation (IP)||1-2 µg/ml|
|Western Blot (WB)||2 µg/ml|
* Suggested working dilutions are given as a guide only. It is recommended that the user titrate the product for use in their own experiment using appropriate negative and positive controls.
|Immunohistochemistry (IHC)||See 1 publications below|
Suggested positive control: anti-Fas treated Jurkat (10 ng/ml), antigen standard for ARHGDIB (transient overexpression lysate).
D4-GDI (GDP dissociation inhibitor) is a negative regulator of the ras-related Rho family of GTPases. Since the Rho GTPases promote cytoskeletal and membrane changes associated with apoptotic cell death, the removal of the D4-GDI block through its cleavage is important for inducing apoptosis. Caspase-3 cleaves the 28 kD mature form of D4-GDI to give a 23 kD and 5 kD size fragment. The 23 kD fragment then translocates to the nucleus. The mechanisms involving cleavage of D4-GDI with apoptosis are not presently known. Activation of the Jun N-terminal kinase, a regulator of apoptosis, may be one of the mechanisms.
For Research Use Only. Not for use in diagnostic procedures. Not for resale without express authorization.
Association of D4-GDI expression with breast cancer progression.
MA1-41085 was used in immunohistochemistry to study the relationship between D4-GDI expression and breast cancer progression
|Rivera Rosado LA,Rodriguez-Canales J,Zhang B||Cancer biomarkers : section A of Disease markers (10:163)||2012|