Ferroptosis suppressor protein 1 (AIFM2) Antibody (FITC)

Este producto es parte de AIFM - Apoptosis inducing factor mitochondria associated
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260€ (50 µl)

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935106861
info@markelab.com
name
Ferroptosis suppressor protein 1 (AIFM2) Antibody (FITC)
category
Primary Antibodies
provider
Abbexa
reference
abx349094

Description

Ferroptosis suppressor protein 1 (AIFM2) Antibody (FITC) is a Rabbit Polyclonal antibody conjugated to FITC for the detection of Human AIFM2.

Documents del producto

Instrucciones
Data sheet
Descargar

Product specifications

Category
Primary Antibodies
Immunogen Target
Ferroptosis suppressor protein 1 (AIFM2)
Host
Rabbit
Reactivity
Human
Recommended Dilution
Optimal dilutions/concentrations should be determined by the end user.
Clonality
Polyclonal
Conjugation
FITC
Isotype
IgG
Purification
Purified by antigen affinity chromatography.
Size 1
50 µl
Size 2
100 µl
Size 3
200 µl
Size 4
1 ml
Form
Liquid
Buffer
0.01 M PBS, pH 7.4, 0.03% Proclin-300 and 50% glycerol.
Availability
Shipped within 5-10 working days.
Storage
Aliquot and store at -20°C. Avoid repeated freeze/thaw cycles.
Dry Ice
No
UniProt ID
Q9BRQ8
Gene ID
84883
OMIM
605159
Alias
AIFM2,AMID,PRG3
Background
Antibody anti-AIFM2
Status
RUO

Descripción

AIFM2, also known as AMID (apoptosis-inducing factor-homologous mitochondrion-associated inducer of death), is a flavoprotein localized in the cytosol and mitochondria, where it participates in redox signaling and apoptosis regulation. Unlike AIFM1, AIFM2 induces apoptosis through reactive oxygen species (ROS)-mediated mechanisms rather than direct DNA fragmentation. It plays a role in the cellular response to oxidative stress, linking mitochondrial dysfunction to apoptotic pathways. AIFM2 is also associated with metabolic regulation and has been reported to modulate the cellular response to hypoxia. Dysregulation of AIFM2 expression has been linked to cancer progression, with evidence suggesting its tumor suppressor function in certain contexts. The interplay between AIFM2 and oxidative stress pathways makes it a critical component of cellular homeostasis, particularly under stress conditions that compromise mitochondrial function.

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