Technical Data
A1372-32H
AIFM1 (Programmed Cell Death Protein 8, Apoptosis-inducing Factor 1, Mitochondrial, AIF, PDCD8)
Description:
Apoptosis is characterized by several morphological nuclear changes including chromatin condensation and nuclear fragmentation. These changes are triggered by the activation of members of caspase family, caspase activated DNase, and several novel proteins. A novel gene, the product of which causes chromatin condensation and DNA fragmentation, was recently identified, cloned, and designated apoptosis inducing factor (AIF). Like the critical molecules, cytochrome c and caspase-9, in apoptosis, AIF localizes in mitochondria. AIF translocates to the nucleus when apoptosis is induced and induces mitochondria to release the apoptogenic proteins cytochrome c and caspase-9. AIF induces chromatin condensation and DNA fragmentation, which are the hallmarks of apoptosis, of the isolated nucleus and the nucleus in live cells by microinjection. AIF is highly conserved between human and mouse and widely expressed.

Applications:
Suitable for use in Western Blot. and Immunocytochemistry. Other applications not tested.

Recommended Dilution:
Western Blot: 0.25-1ug/ml
Optimal dilutions to be determined by the researcher.

Positive Control:
K562 cell lysate

Storage and Stability:
May be stored at 4C for short-term only. Aliquot to avoid repeated freezing and thawing. Store at -20C. Aliquots are stable for at least 12 months. For maximum recovery of product, centrifuge the original vial after thawing and prior to removing the cap.
TypeIsotypeCloneGrade
PabIgGAffinity Purified
SizeStorageShippingSourceHost
50ug-20CBlue IceHumanRabbit
Concentration:
As reported
Immunogen:
Synthetic peptide near the C-terminus of human AIF.
Purity:
Purified by immunoaffinity chromatography.
Form
Supplied as a liquid in PBS, 0.02% sodium azide.
Specificity:
Recognizes human AIF. Species Crossreactivity: mouse and rat.
Intended for research use only. Not for use in human, therapeutic, or diagnostic applications.
1. Zamzami N. et al. Nature 401, 127 (1999). 2. Susin SA. Et al. Nature 397, 44 (1999).