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Key Documents

AB16501

Sigma-Aldrich

Anti-AIF Antibody, internal domain

Chemicon®, from rabbit

Synonym(s):

Apoptosis Inducing Factor

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About This Item

UNSPSC Code:
12352203
eCl@ss:
32160702
NACRES:
NA.41

biological source

rabbit

Quality Level

antibody form

purified immunoglobulin

antibody product type

primary antibodies

clone

polyclonal

species reactivity

human, mouse, rat

manufacturer/tradename

Chemicon®

technique(s)

immunohistochemistry: suitable (paraffin)
western blot: suitable

UniProt accession no.

shipped in

wet ice

target post-translational modification

unmodified

Gene Information

human ... AIFM1(9131)

General 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 the caspase family, caspase activated DNase, and several novel proteins (Zamzami et al., 1999). A novel gene, the product of which causes chromatin condensation and DNA fragmentation, was recently identified, cloned, and designated apoptosis inducing factor (AIF) (Susin et al., 1999). 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 (Susin et al., 1999).

Specificity

Apoptosis is characterized by several morphological nuclear changes including chromatin condensation and nuclear fragmentation. These changes are triggered by the activation of members of the caspase family, caspase activated DNase, and several novel proteins (Zamzami & Kroemer 1999). A novel gene, the product of which causes chromatin condensation and DNA fragmentation, was recently identified, cloned, and designated apoptosis inducing factor (AIF) (Susin et al. 1999). 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 (Susin et al. 1999).

Immunogen

Epitope: internal domain
Rabbit anti-AIF (Internal region) polyclonal antibody was raised against a peptide corresponding to amino acids 517 to 531 of human AIF (Susin et al. 1999). This sequence is identical to those of mouse and rat AIF (Susin et al. 1999).

Application

Anti-AIF Antibody, internal domain is an antibody against AIF for use in IH(P) & WB.
Research Category
Apoptosis & Cancer
Research Sub Category
Apoptosis - Additional
Western blot: 0.25 to 1 μg/mL.

K562 cell lysate can be used as a positive control and a 67 kDa band should be detected.

Immunohistochemistry on formalin fixed, paraffin sections: 5-20 μg/ml, with antigen retrieval; see website protocol for details and photographs.

Optimal working dilutions must be determined by end user.

Target description

67 kDa

Linkage

Replaces: 04-430

Physical form

Ammonium sulfate precipitation and DEAE-cellulose chromatography
Format: Purified
Purified IgG in PBS containing 0.02% sodium azide.

Storage and Stability

Maintain for 1 year at 2–8°C from date of shipment. For maximum recovery of product, centrifuge the original vial after thawing and prior to removing the cap.

Analysis Note

Control
Widely expressed

Other Notes

Concentration: Please refer to the Certificate of Analysis for the lot-specific concentration.

Legal Information

CHEMICON is a registered trademark of Merck KGaA, Darmstadt, Germany

Disclaimer

Unless otherwise stated in our catalog or other company documentation accompanying the product(s), our products are intended for research use only and are not to be used for any other purpose, which includes but is not limited to, unauthorized commercial uses, in vitro diagnostic uses, ex vivo or in vivo therapeutic uses or any type of consumption or application to humans or animals.

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Storage Class Code

10 - Combustible liquids

WGK

WGK 2

Flash Point(F)

Not applicable

Flash Point(C)

Not applicable


Certificates of Analysis (COA)

Search for Certificates of Analysis (COA) by entering the products Lot/Batch Number. Lot and Batch Numbers can be found on a product’s label following the words ‘Lot’ or ‘Batch’.

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Carlo Rinaldi et al.
American journal of human genetics, 91(6), 1095-1102 (2012-12-12)
Cowchock syndrome (CMTX4) is a slowly progressive X-linked recessive disorder with axonal neuropathy, deafness, and cognitive impairment. The disease locus was previously mapped to an 11 cM region at chromosome X: q24-q26. Exome sequencing of an affected individual from the
Alfredo Criollo et al.
Apoptosis : an international journal on programmed cell death, 12(1), 3-18 (2006-11-03)
HeLa and HCT116 cells respond differentially to sorbitol, an osmolyte able to induce hypertonic stress. In these models, sorbitol promoted the phenotypic manifestations of early apoptosis followed by complete loss of viability in a time-, dose-, and cell type-specific fashion
Loss of Aif function causes cell death in the mouse embryo, but the temporal progression of patterning is normal.
Brown, D; Yu, BD; Joza, N; Benit, P; Meneses, J; Firpo, M; Rustin, P; Penninger, JM; Martin, GR
Proceedings of the National Academy of Sciences of the USA null
P2X7 receptor differentially modulates astroglial apoptosis and clasmatodendrosis in the rat brain following status epilepticus.
Ji-Eun Kim,Hea Jin Ryu,Seong-Il Yeo,Tae-Cheon Kang
Hippocampus null
Acyl coenzyme A-binding protein augments bid-induced mitochondrial damage and cell death by activating mu-calpain.
Shulga, N; Pastorino, JG
The Journal of Biological Chemistry null

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