|Tested species reactivity||Mouse, Rat|
|Host / Isotype||Rabbit / IgG|
|Immunogen||Synthetic peptide: C-TGEEDTSEKDEL, corresponding to amino acids 643-654 of Rat GRP78 BiP.|
|Purification||Antigen affinity chromatography|
|Storage buffer||PBS with 30% glycerol|
|Contains||0.05% sodium azide|
|Storage Conditions||-20°C or -80°C if preferred|
|Tested Applications||Dilution *|
|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.
This antibody does not react with human or COS samples.
Within the ER misfolded proteins are detected by Bip(GPR78). In the presence of misfolded proteins, Bip disscociates from PERK, allowing it to homodimerize and autophosphoyate. In its dimerized, phosphorylated form PERK phosphorylates eIF2. The phosphorylation of eIF2 blocks the majority of translation to prevent the continued accumulation of protein in the ER. Bip also is binds to IRE1 and ATF6 under normal ER conditions, but dissociates upon accumulation of misfolded proteins. Unbound ATF6 is translocated to the gogli where it is converted into a cleaved, active form. The cleaved form of ATF6 is then able to up regulated transcription of UPR genes including XBP1. Activated IRE1 acts as an endoribonuclease to an intron from XBP1 transcripts. The XBP1 splice variant codes for an active transcription factor which activates transcription of P58IPK. P58IPK is a HSP40 protein which binds to and inhibits PERK. Thus, if the accumulated, misfolded proteins have been removed, P58IPK acts to shut down the UPR by removing the block to translation.
For Research Use Only. Not for use in diagnostic procedures. Not for resale without express authorization.