Immunofluorescent analysis of Bax inhibitor 1 in HeLa cells. Cells were fixed for 10 minutes using 10% formalin and then permeabilized for 5 minutes using 1X TBS + 0.5% Triton-X100. The cells were incubated with anti Bax inhibitor 1 (20F248) Antibody (Product # MA1-41678) at a 1:200 dilution overnight at 4C and detected with an anti-mouse IgM Dylight 488 (Green) at a 1:500 dilution. Actin was detected with Phalloidin (Red) at a 1:200 dilution. Nuclei wre counterstained with DAPI (Blue). Cells were imaged using a 40X objective.
|Tested species reactivity||Human|
|Host / Isotype||Mouse / IgM|
|Immunogen||A mixture of three synthetic peptides corresponding to the N-terminal, internal and C-terminal regions of human Bax inhibitor 1.|
|Contains||0.05% sodium azide|
|Storage Conditions||-20° C, Avoid Freeze/Thaw Cycles|
|Tested Applications||Dilution *|
|Flow Cytometry (Flow)||1:200|
|Western Blot (WB)||1:500-1:1000|
* 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.
MA1-41678 is derived from a mixture of three synthetic peptides corresponding to the N-terminal, internal and C-terminal regions of human B1. 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.