Immunohistochemical analysis of formalin-fixed, paraffin-embedded tissue sections stained for Bi-1 expression using a Bi-1 monoclonal antibody (Product # MA1-41108) at 5 ug/ml. A: normal human lung alveoli with positive lung macrophages. B: normal mouse cartilage with positive chondrocytes. Hematoxylin-eosin counterstain.
|Tested species reactivity||Human, Mouse, Rat|
|Published species reactivity||Not Applicable|
|Host / Isotype||Mouse / IgG2b, kappa|
|Immunogen||Synthetic peptides corresponding to the N-terminal, internal, and C-terminal regions of human B1.|
|Storage buffer||PBS with 0.2% gelatin|
|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 *|
|Immunohistochemistry (Paraffin) (IHC (P))||5-10 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 (Paraffin) (IHC (P))||See 1 publications below|
Epitope mapping indicates that the antibody recognizes an epitope in the N-terminal region of Bi-1.
BI-1 (Bax Inhibitor 1) is in anti-apoptotic protein that has been linked to protection from apoptosis induced endoplasmic reticulum (ER) stress (reviewed in Bailley-Maitre et al, 2007). BI-1 contains several transmembrane domains, localizes to ER membranes, and has cytoprotective functions that are conserved in both animals and plants. BI-1 suppresses apoptosis induced by ectopic expression of the proapoptotic protein Bax as well as other types of stimuli. Cells from BI-1 knockout (KO) mice are hypersensitivite to apoptosis induced by ER stress–causing chemical agents (thapsigargin, tunicamycin, and brefeldin A) or by ischemia-reperfusion (IR) injury. Conversely, overexpression of BI-1 protects against apoptosis induced by ER stress and IR. The mechanism by which BI-1 protects cells from ER-stress induced apoptosis remains to be fully elucidated, it is thought to involve regulation of Ca2+ handling by the ER.
For Research Use Only. Not for use in diagnostic procedures. Not for resale without express authorization.
|Not Applicable||1 µg/ml||
Selective A3 adenosine receptor agonist protects against doxorubicin-induced cardiotoxicity.
MA1-41108 was used in immunohistochemistry - paraffin section to elucidate the function of selective A3 adenosine receptor agonist against doxorubicin-induced cardiotoxicity
|Galal A,El-Bakly WM,Al Haleem EN,El-Demerdash E||Cancer chemotherapy and pharmacology (77:309)||2016|