AIFM2 Antibody - #DF8636

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Product: AIFM2 Antibody
Catalog: DF8636
Description: Rabbit polyclonal antibody to AIFM2
Application: WB IHC IF/ICC
Reactivity: Human, Mouse, Rat
Prediction: Bovine, Horse, Sheep, Rabbit, Dog, Chicken, Xenopus
Mol.Wt.: 40 kDa; 41kD(Calculated).
Uniprot: Q9BRQ8
RRID: AB_2841840

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 100ul $280 In stock
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Related Downloads
MSDS
Data Sheet
COA
Protocols
WB Handbook
IHC Protocol
IF/ICC Protocol

Product Info

Source:
Rabbit
Application:
IHC 1:50-1:200, WB 1:1000-3000, IF/ICC 1:100-1:500
*The optimal dilutions should be determined by the end user.
*Tips:

WB: For western blot detection of denatured protein samples. IHC: For immunohistochemical detection of paraffin sections (IHC-p) or frozen sections (IHC-f) of tissue samples. IF/ICC: For immunofluorescence detection of cell samples. ELISA(peptide): For ELISA detection of antigenic peptide.

Reactivity:
Human,Mouse,Rat
Prediction:
Bovine(88%), Horse(88%), Sheep(88%), Rabbit(86%), Dog(88%), Chicken(83%), Xenopus(88%)
Clonality:
Polyclonal
Specificity:
AIFM2 Antibody detects endogenous levels of total AIFM2.
RRID:
AB_2841840
Cite Format: Affinity Biosciences Cat# DF8636, RRID:AB_2841840.
Conjugate:
Unconjugated.
Purification:
The antiserum was purified by peptide affinity chromatography using SulfoLink™ Coupling Resin (Thermo Fisher Scientific).
Storage:
Rabbit IgG in phosphate buffered saline , pH 7.4, 150mM NaCl, 0.02% sodium azide and 50% glycerol. Store at -20 °C. Stable for 12 months from date of receipt.
Alias:

Fold/Unfold

5430437E11Rik; aifm2; AIFM2_HUMAN; AMID; Apoptosis inducing factor (AIF) homologous mitochondrion associated inducer of death; Apoptosis inducing factor (AIF) like mitochondrion associated inducer of death; Apoptosis inducing factor mitochondrion associated 2; Apoptosis-inducing factor 2; Apoptosis-inducing factor homologous mitochondrion-associated inducer of death; Apoptosis-inducing factor-like mitochondrion-associated inducer of death; Cys51Stop; HGNC11998; p53 responsive gene 3; p53 tumor suppressor; p53-responsive gene 3 protein; PRG3; TRP53; Tumor protein p53;

Immunogens

Immunogen:
Uniprot:

Q9BRQ8(FSP1_HUMAN) >>Visit HPA database.

Gene(ID):
AIFM2(84883)
Expression:
Q9BRQ8 FSP1_HUMAN:

Detected in most normal tissues as two transcripts of 1.8 and 4.0 kb in length, respectively. Highly expressed in heart, moderately in liver and skeletal muscles, and expressed at low levels in placenta, lung, kidney, and pancreas. Both transcripts expressed following p53/TP53 induction. The shorter 1.8 kb transcript seems to be the major transcript in EB1 colon cancer cells.

Sequence:
MGSQVSVESGALHVVIVGGGFGGIAAASQLQALNVPFMLVDMKDSFHHNVAALRASVETGFAKKTFISYSVTFKDNFRQGLVVGIDLKNQMVLLQGGEALPFSHLILATGSTGPFPGKFNEVSSQQAAIQAYEDMVRQVQRSRFIVVVGGGSAGVEMAAEIKTEYPEKEVTLIHSQVALADKELLPSVRQEVKEILLRKGVQLLLSERVSNLEELPLNEYREYIKVQTDKGTEVATNLVILCTGIKINSSAYRKAFESRLASSGALRVNEHLQVEGHSNVYAIGDCADVRTPKMAYLAGLHANIAVANIVNSVKQRPLQAYKPGALTFLLSMGRNDGVGQISGFYVGRLMVRLTKSRDLFVSTSWKTMRQSPP

Predictions

Predictions:

Score>80(red) has high confidence and is suggested to be used for WB detection. *The prediction model is mainly based on the alignment of immunogen sequences, the results are for reference only, not as the basis of quality assurance.

Species
Results
Score
Horse
88
Bovine
88
Sheep
88
Dog
88
Xenopus
88
Rabbit
86
Chicken
83
Pig
0
Zebrafish
0
Model Confidence:
High(score>80) Medium(80>score>50) Low(score<50) No confidence

PTMs - Q9BRQ8 As Substrate

Site PTM Type Enzyme
G2 Myristoylation
K63 Ubiquitination
K168 Ubiquitination
K182 Ubiquitination
K193 Ubiquitination
K199 Ubiquitination
Y220 Phosphorylation
Y223 Phosphorylation
K225 Ubiquitination
S331 Phosphorylation
Y345 Phosphorylation
S362 Phosphorylation

Research Backgrounds

Function:

A NAD(P)H-dependent oxidoreductase involved in cellular oxidative stress response. At the plasma membrane, catalyzes reduction of coenzyme Q/ubiquinone-10 to ubiquinol-10, a lipophilic radical-trapping antioxidant that prevents lipid oxidative damage and consequently ferroptosis. Cooperates with GPX4 to suppress phospholipid peroxidation and ferroptosis. This anti-ferroptotic function is independent of cellular glutathione levels. May play a role in mitochondrial stress signaling. Upon oxidative stress, associates with the lipid peroxidation end product 4-hydroxy-2-nonenal (HNE) forming a lipid adduct devoid of oxidoreductase activity, which then translocates from mitochondria into the nucleus triggering DNA damage and cell death. Capable of DNA binding in a non-sequence specific way.

PTMs:

N-myristoylation at Gly-2 mediates the recruitment to lipid droplets and plasma membrane.

Subcellular Location:

Lipid droplet. Cell membrane>Lipid-anchor. Cytoplasm. Mitochondrion membrane. Nucleus.

Extracellular region or secreted Cytosol Plasma membrane Cytoskeleton Lysosome Endosome Peroxisome ER Golgi apparatus Nucleus Mitochondrion Manual annotation Automatic computational assertionSubcellular location
Tissue Specificity:

Detected in most normal tissues as two transcripts of 1.8 and 4.0 kb in length, respectively. Highly expressed in heart, moderately in liver and skeletal muscles, and expressed at low levels in placenta, lung, kidney, and pancreas. Both transcripts expressed following p53/TP53 induction. The shorter 1.8 kb transcript seems to be the major transcript in EB1 colon cancer cells.

Subunit Structure:

Interacts with importin subunits KPNA2 and IPO5; this interaction likely mediates the translocation into the nucleus upon oxidative stress.

Family&Domains:

Belongs to the FAD-dependent oxidoreductase family.

References

1). Oroxin A alleviates early brain injury after subarachnoid hemorrhage by regulating ferroptosis and neuroinflammation. Journal of neuroinflammation, 2024 (PubMed: 38702778) [IF=9.3]

Application: WB    Species: Mouse    Sample: hippocampal tissues

Fig. 9 OA drives the transcriptional regulator Nrf2 to upregulate GPX4 and FSP1. A: An illustrative diagram of the proposed model delineating the mechanisms of FSP1-mediated regulation of ferroptosis in EBI following SAH. B: Western blot data illustrate the levels of NQO1, FSP1, and HO-1 in the brain cortex after SAH. C: Quantification of CoQ10 among the three groups. OA increased the expression of CoQ10 (n = 3). D: Quantification of HO-1 among the three groups. OA increased the expression of HO-1 (n = 3). E: Quantification of FSP1 among the three groups. OA increased the expression of FSP1 (n = 3). F: Representative views of immunofluorescence staining of FSP1. Scale bar = 50 μm. G: Quantitative analysis of the of FSP1 (n = 3). H: Western blot data show that OA fosters the protein levels of FSP1, and Nrf2 knockout does not prevent the OA-induced escalation in GPX4 levels after SAH (n = 3)

Application: IF/ICC    Species: Mouse    Sample: hippocampal tissues

Fig. 9 OA drives the transcriptional regulator Nrf2 to upregulate GPX4 and FSP1. A: An illustrative diagram of the proposed model delineating the mechanisms of FSP1-mediated regulation of ferroptosis in EBI following SAH. B: Western blot data illustrate the levels of NQO1, FSP1, and HO-1 in the brain cortex after SAH. C: Quantification of CoQ10 among the three groups. OA increased the expression of CoQ10 (n = 3). D: Quantification of HO-1 among the three groups. OA increased the expression of HO-1 (n = 3). E: Quantification of FSP1 among the three groups. OA increased the expression of FSP1 (n = 3). F: Representative views of immunofluorescence staining of FSP1. Scale bar = 50 μm. G: Quantitative analysis of the of FSP1 (n = 3). H: Western blot data show that OA fosters the protein levels of FSP1, and Nrf2 knockout does not prevent the OA-induced escalation in GPX4 levels after SAH (n = 3)
2). Identification of a group of bisbenzylisoquinoline (BBIQ) compounds as ferroptosis inhibitors. Cell Death & Disease, 2022 (PubMed: 36435804) [IF=9.0]
3). Netrin-1 Alleviates Early Brain Injury by Regulating Ferroptosis via the PPARγ/Nrf2/GPX4 Signaling Pathway Following Subarachnoid Hemorrhage. Translational Stroke Research, 2023 (PubMed: 36631632) [IF=6.9]
4). Circ0060467 sponges miR-6805 to promote hepatocellular carcinoma progression through regulating AIFM2 and GPX4 expression. Aging, 2024 (PubMed: 38244593) [IF=5.2]

Application: IHC    Species: Human    Sample: HCC

Figure 5 Knockdown of circ0060467 promotes ferroptosis in HCC. (A) Western blotting was performed to determine the expression levels of AIFM2, GPX4 and β-Actin. (B) Expression status of AIFM2 and GPX4 in hematoxylin-eosin-stained sections of harvested xenograft tumors. (C) Glutathione (GSH)/oxidized GSH (GSSG) ratio was determined with a GSH/GSSG Quantification Kit.
5). Etomidate Improves the Antidepressant Effect of Electroconvulsive Therapy by Suppressing Hippocampal Neuronal Ferroptosis via Upregulating BDNF/Nrf2. Molecular Neurobiology, 2023 (PubMed: 37466875) [IF=5.1]
6). DNA methylation-regulated LINC02587 inhibits ferroptosis and promotes the progression of glioma cells through the CoQ-FSP1 pathway. BMC cancer, 2023 (PubMed: 37848823) [IF=3.8]

Application: WB    Species: Human    Sample: U87 and LN229 cells

Fig. 5 LINC02587 silencing inhibits the CoQ-FSP1 pathway. (A) KEGG pathway enrichment in the si-NC and si-LINC02587-ii groups. (B) Volcano map of differentially expressed Ferroptosis-related genes.(C) Hierarchical clustering heatmap of differentially expressed Ferroptosis-related genes.(D) qRT-PCR was carried out to analyse the relative expression of Ferroptosis-related genes in the si-NC and si-LINC02587-ii groups. (E) Western blot analysis of CoQ10B, FSP1 in U87 and LN229 cells transfected with si-NC or si-LINC02587. (F) Changes in GSH levels in cells after iFSP1 and si-LINC02587-ii intervention.Data are expressed as the mean ± SD.*P 
7). MPO/HOCl Facilitates Apoptosis and Ferroptosis in the SOD1G93A Motor Neuron of Amyotrophic Lateral Sclerosis. Oxidative Medicine and Cellular Longevity, 2022 (PubMed: 35178161)

Application: WB    Species: Mice    Sample: hSOD1G93A cells

Figure 3 MPO/HOCl signaling manipulated apoptosis and ferroptosis in hSOD1G93A cells. (a) The apoptosis- and autophagy-related proteins of vector, hSOD1WT, and hSOD1G93A cells, as measured by western blot. (b) 1 μM Z-DEVD-FMK reversed cell death of hSOD1G93A cells, significantly. (c, d) Flow cytometry analysis of apoptosis in vector, hSOD1WT, and hSOD1G93A cells, in the absence or presence of ABAH. (e) Immunoblots of hSOD1G93A cells treated with NC-siRNA or MPO-siRNA. (f) The ferroptosis-related proteins of vector, hSOD1WT, and hSOD1G93A cells, as measured by western blot. (g) 1 μM ferrostatin-1 reversed the cell death in hSOD1G93A cells, significantly. (h) Immunoblots of hSOD1G93A overexpressed with vector or FSP1 cDNA. (i) Overexpression of FSP1 cDNA inhibited cell death significantly in hSOD1G93A cells. (j) Immunoblots of ferroptosis-related proteins in hSOD1G93A cells, treated with NC-siRNA or MPO-siRNA. (k) Immunoblots of hSOD1G93A overexpressed with vector or MPO cDNA. (l) Relative viability of hSOD1G93A cells with multiple treatments. (m) The MDA levels of cells in different groups. (n) Effects of different treatments on viability of NSC-34 cells overexpressed with empty vector or MPO cDNA. Quantified graphs were shown as means and SEM. ∗P < 0.05,  ∗∗P < 0.01, and∗∗∗P < 0.001. The significant difference among multiple doses was determined by one-way ANOVA followed by LSD tests. The significant difference in two datasets was analyzed by Student's t-test.

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