Product: FAS Antibody
Catalog: AF5342
Source: Rabbit
Application: WB, IHC, IF/ICC, ELISA(peptide)
Reactivity: Human, Mouse, Rat
Mol.Wt.: 37kD,50~70kD(Glycosylated); 38kD(Calculated).
Uniprot: P25445
RRID: AB_2837827

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 100ul $280 In stock
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Product Info

Source:
Rabbit
Application:
WB 1:500-1:2000, IHC 1:50-1:200, IF/ICC 1:100-1:500, ELISA(peptide) 1:20000-1:40000
*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
Clonality:
Polyclonal
Specificity:
FAS Antibody detects endogenous levels of total FAS.
RRID:
AB_2837827
Cite Format: Affinity Biosciences Cat# AF5342, RRID:AB_2837827.
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

ALPS 1A; ALPS1A; APO 1; Apo 1 antigen; APO 1 cell surface antigen; Apo-1 antigen; APO1; Apo1 antigen; APO1 cell surface antigen; Apoptosis antigen 1; Apoptosis mediating surface antigen FAS; Apoptosis-mediating surface antigen FAS; APT 1; APT1; CD 95; CD 95 antigen; CD95; CD95 antigen; Delta Fas; Delta Fas/APO 1/CD95; Delta Fas/APO1/CD95; Fas (TNF receptor superfamily, member 6); FAS 1; FAS 827dupA; Fas AMA; Fas; FAS Antigen; Fas cell surface death receptor; FAS1; FASLG receptor; FASTM; sFAS; Surface antigen APO1; TNF receptor superfamily, member 6; TNFRSF 6; TNFRSF6; TNR6_HUMAN; Tumor necrosis factor receptor superfamily member 6;

Immunogens

Immunogen:
Uniprot:
Gene(ID):
Expression:
P25445 TNR6_HUMAN:

Isoform 1 and isoform 6 are expressed at equal levels in resting peripheral blood mononuclear cells. After activation there is an increase in isoform 1 and decrease in the levels of isoform 6.

Description:
Receptor for TNFSF6/FASLG. The adapter molecule FADD recruits caspase-8 to the activated receptor. The resulting death-inducing signaling complex (DISC) performs caspase-8 proteolytic activation which initiates the subsequent cascade of caspases (aspartate-specific cysteine proteases) mediating apoptosis.
Sequence:
MLGIWTLLPLVLTSVARLSSKSVNAQVTDINSKGLELRKTVTTVETQNLEGLHHDGQFCHKPCPPGERKARDCTVNGDEPDCVPCQEGKEYTDKAHFSSKCRRCRLCDEGHGLEVEINCTRTQNTKCRCKPNFFCNSTVCEHCDPCTKCEHGIIKECTLTSNTKCKEEGSRSNLGWLCLLLLPIPLIVWVKRKEVQKTCRKHRKENQGSHESPTLNPETVAINLSDVDLSKYITTIAGVMTLSQVKGFVRKNGVNEAKIDEIKNDNVQDTAEQKVQLLRNWHQLHGKKEAYDTLIKDLKKANLCTLAEKIQTIILKDITSDSENSNFRNEIQSLV

PTMs - P25445 As Substrate

Site PTM Type Enzyme
T28 O-Glycosylation
K33 Ubiquitination
T40 O-Glycosylation
T42 O-Glycosylation
T43 O-Glycosylation
T46 O-Glycosylation
Y91 Phosphorylation
N118 N-Glycosylation
K204 Ubiquitination
S209 Phosphorylation
S212 Phosphorylation
T214 Phosphorylation
T219 Phosphorylation
S225 Phosphorylation
S230 Phosphorylation
Y232 Phosphorylation
T234 Phosphorylation
T241 Phosphorylation
S243 Phosphorylation
K263 Ubiquitination
K274 Ubiquitination
K287 Ubiquitination
K288 Ubiquitination
Y291 Phosphorylation
T293 Phosphorylation
K296 Ubiquitination
K300 Ubiquitination
T305 Phosphorylation
K309 Ubiquitination
T312 Phosphorylation
K316 Ubiquitination
S320 Phosphorylation
S322 Phosphorylation
S325 Phosphorylation
S333 Phosphorylation

Research Backgrounds

Function:

Receptor for TNFSF6/FASLG. The adapter molecule FADD recruits caspase-8 to the activated receptor. The resulting death-inducing signaling complex (DISC) performs caspase-8 proteolytic activation which initiates the subsequent cascade of caspases (aspartate-specific cysteine proteases) mediating apoptosis. FAS-mediated apoptosis may have a role in the induction of peripheral tolerance, in the antigen-stimulated suicide of mature T-cells, or both. The secreted isoforms 2 to 6 block apoptosis (in vitro).

PTMs:

N- and O-glycosylated. O-glycosylated with core 1 or possibly core 8 glycans.

Subcellular Location:

Cell membrane>Single-pass type I membrane protein.

Secreted.

Secreted.

Secreted.

Secreted.

Secreted.

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

Isoform 1 and isoform 6 are expressed at equal levels in resting peripheral blood mononuclear cells. After activation there is an increase in isoform 1 and decrease in the levels of isoform 6.

Subunit Structure:

Binds DAXX. Interacts with HIPK3 (By similarity). Part of a complex containing HIPK3 and FADD (By similarity). Binds RIPK1 and FAIM2. Interacts with BABAM2 and FEM1B. Interacts with FADD. Interacts directly (via DED domain) with NOL3 (via CARD domain); inhibits death-inducing signaling complex (DISC) assembly by inhibiting the increase in FAS-FADD binding induced by FAS activation (By similarity). Interacts with CALM. In the absence of stimulation, interacts with BIRC2, DDX3X and GSK3B. The interaction with BIRC2 and DDX3X is further enhanced upon receptor stimulation and accompanied by DDX3X and BIRC2 cleavage.

Family&Domains:

Contains a death domain involved in the binding of FADD, and maybe to other cytosolic adapter proteins.

Research Fields

· Cellular Processes > Cell growth and death > p53 signaling pathway.   (View pathway)

· Cellular Processes > Cell growth and death > Apoptosis.   (View pathway)

· Cellular Processes > Cell growth and death > Necroptosis.   (View pathway)

· Environmental Information Processing > Signal transduction > MAPK signaling pathway.   (View pathway)

· Environmental Information Processing > Signaling molecules and interaction > Cytokine-cytokine receptor interaction.   (View pathway)

· Environmental Information Processing > Signal transduction > TNF signaling pathway.   (View pathway)

· Human Diseases > Drug resistance: Antineoplastic > Platinum drug resistance.

· Human Diseases > Endocrine and metabolic diseases > Non-alcoholic fatty liver disease (NAFLD).

· Human Diseases > Endocrine and metabolic diseases > Type I diabetes mellitus.

· Human Diseases > Neurodegenerative diseases > Alzheimer's disease.

· Human Diseases > Infectious diseases: Parasitic > Chagas disease (American trypanosomiasis).

· Human Diseases > Infectious diseases: Parasitic > African trypanosomiasis.

· Human Diseases > Infectious diseases: Viral > Hepatitis B.

· Human Diseases > Infectious diseases: Viral > Measles.

· Human Diseases > Infectious diseases: Viral > Influenza A.

· Human Diseases > Infectious diseases: Viral > Human papillomavirus infection.

· Human Diseases > Infectious diseases: Viral > Herpes simplex infection.

· Human Diseases > Cancers: Overview > Pathways in cancer.   (View pathway)

· Human Diseases > Cancers: Overview > Proteoglycans in cancer.

· Human Diseases > Immune diseases > Autoimmune thyroid disease.

· Human Diseases > Immune diseases > Allograft rejection.

· Human Diseases > Immune diseases > Graft-versus-host disease.

· Organismal Systems > Immune system > Natural killer cell mediated cytotoxicity.   (View pathway)

References

1). Yang Y et al. Amelioration of nonalcoholic fatty liver disease by swertiamarin in fructose-fed mice. Phytomedicine 2019 Jun;59:152782 (PubMed: 31005808) [IF=6.656]

Application: IHC    Species: mouse    Sample: liver

Figure.7. |Effect of swertiamarin (25, 50 and 100 mg/kg) and silibinin on (A) ACC1 expression by western blotting analysis. Immunohistochemical stainings of (B) SREBP-1 and (C) FAS in liver tissue of mice. Scale bar represents 30 μm. Representative analysis from six animals in each group.Significance is represented as ##P ≤ 0.01 and ###P ≤ 0.001 compared to the normal control group,*P ≤ 0.05 and **P ≤ 0.01 compared to the fructose group.

2). Xu Q et al. Propionate Ameliorates Alcohol-Induced Liver Injury in Mice via the Gut–Liver Axis: Focus on the Improvement of Intestinal Permeability. J Agric Food Chem 2022 May 12. (PubMed: 35549256) [IF=5.895]

3). Zhu S et al. 20 (S)-Ginsenoside Rh2 induces caspase-dependent PML-RARA degradation in NB4 cells via Akt/Bax/caspase9 and TNF-α/caspase8 signaling cascades. J Ginseng Res 2021 Mar;45(2):295-304. (PubMed: 33841010) [IF=5.735]

Application: WB    Species: Human    Sample: NB4 cells

Fig. 7. GRh2 activated the TNF-a/caspase8 cascade. (A) NB4 cells were incubated with 30 mM, 40 mM, or 50 mM GRh2 for 12 h. Protein expression levels of FasL, Fas, TNF-a, and TNFR1 in NB4 cells were detected via Western blot. A representative picture of three replicates is shown. (B) Quantitative statistical graph of the relative protein expression levels. The results are shown as the mean  SD (n ¼ 3) *p < 0.05, **p < 0.01. (C) RT-PCR was used to detect the mRNA expression level of TNF-a in NB4 cells after GRh2 administration. The results are shown as the mean  SD (n ¼ 3) **p < 0.01, ***p < 0.001 versus solvent. After preincubation with 1.5 mM TNF-a inhibitor, C 87, for 2 h, 30 mM, 40 mM, or 50 mM GRh2 was applied for another 12 h. (D) CCK-8 assay measured the NB4 cell viability. The results are shown as the mean  SD (n ¼ 6) ***p < 0.001, ###p < 0.001. (E) Hoechst 33258 staining was used to observe changes in nuclear morphology of NB4 cells after GRh2 and C 87 administration (800  ). (F) Quantitative statistical graph of caspase8 cleavage activation levels in NB4 cells. The Ac-IETD-pNA method was used. The results are shown as the mean  SD (n ¼ 3) ***p < 0.001, #p < 0.05. GRh2, 20(S)-ginsenoside Rh2.

4). Liu Y et al. The Association Between Thyroid Injury and Apoptosis, and Alterations of Bax, Bcl-2, and Caspase-3 mRNA/Protein Expression Induced by Nickel Sulfate in Wistar Rats. Biol Trace Elem Res 2019 Aug 8 (PubMed: 31392545) [IF=4.081]

Application: IHC    Species: rat    Sample: thyroid

Fig. 6| Effect of NiSO4 on expression of Fas protein in rat thyroid tissue by immunohistochemistry. The expression of Fas protein in control group, low dose group,and middle dose group were positive, while that in high dose group was strong. The difference was statistically significant. N control group, L low dose group,M middle dose group, H high dose group

5). Liu YX et al. PD-1 inhibitor induces myocarditis by reducing regulatory T cells, activating inflammatory responses, promoting myocardial apoptosis and autophagy. Cytokine 2022 Jun 9;157:155932. (PubMed: 35691121) [IF=3.926]

6). Ding S et al. Combined effects of ambient particulate matter exposure and a high-fat diet on oxidative stress and steatohepatitis in mice. PLoS One 2019 Mar 28;14(3):e0214680 (PubMed: 30921449) [IF=3.752]

Application: WB    Species: mouse    Sample: liver

Fig 3. |Ambient PM exposure leads to hepatic steatosis by impairing hepatic lipid metabolism. (A) Oil Red O staining observation of liver (×200, scale bars = 100 μm). (B) H&E staining observation of liver (×200, scale bars = 50 μm). (C) The volume density of quantitation of hepatic steatosis (n = 5). (D) The genes expression involved in fatty acid β-oxidation in liver (n = 5). (E) The mRNA expression of genes involved in lipogenesis and FXR in liver (n = 5). (F) Bands of PPARα,PPARγ, ACOX1, FAS, SREBP-1c, SCD1.

7). Yu PM et al. Low-Frequency Vibration Promotes Tumor Necrosis Factor-α Production to Increase Cartilage Degeneration in Knee Osteoarthritis. Cartilage 2020 Jun 12;1947603520931178. (PubMed: 32532183) [IF=3.117]

Application: WB    Species: Human    Sample: 293T cells

Figure 4. TNF-α upregulates inflammation or apoptosis through FAH. (A) 293T cells were transfected with FAH-Luc and renila, with or without TNF-α; 48 hours after transfection, cells was performed luciferase assay. The luciferase activity was normalized to Renilla control, and expressed as fold increase (mean ± SD). Experiments were performed 2 times in triplicate. (B and C) SW1353 were co-transfected with TNF-α and FAH or FAH-siRNA; 48 hours after transfection, cells were harvested for immunoblot analysis with indicated antibodies. FAH = fumarylacetoacetase hydrolase; TNF-α = tumor necrosis factor-α.

8). Cui Z et al. Receptor Activator of Nuclear Factor (Nf)-kb Ligand Promotes T Helper 17 Cell Differentiation through Fas. Immunol Invest 2021 Jul 8;1-13. (PubMed: 34238108) [IF=3.044]

Application: WB    Species: Mice    Sample: T helper 17 (Th17) cells

Figure 3. Fas regulated Th17 cell differentiation. (a) PCR analysis of Fas expression (n = 5). (b) The protein level of Rank and Fas detected by western blotting analyzed by using integrated density (area*mean gray value) (n = 5). (c) PCR analysis of IL-17, IL-21, RORγt, IFN-γ, Klrd1 and T-bet expression (n = 5). (d) Flow cytometry analysis of CD4 and IL-17 or IFN-γ positive cells (n = 5). (e) ELISA analysis of IL-17 and IFN-γ levels in cell culture media. (f) The protein level of SATA1 and STAT3 level by western blotting analyzed by using integrated density (n = 5). * Indicates that there was a significant difference between two groups, P < .05; N.S. meant there was no significant difference between two groups. DF: differentiated CD4 + T cells; DF NC: differentiated negative control siRNA pretreated CD4 + T cells; DF F-ko: differentiated siRNA of Fas pretreated CD4 + T cells. “n = 5” means the five repeats.

9). Jiang D et al. Metabolomics Study of Whole-body Vibration on Lipid Metabolism of Skeletal Muscle in Aging Mice. Int J Sports Med 2021 May;42(5):464-477. (PubMed: 33124015)

Application: WB    Species: mouse    Sample: gastrocnemius

Fig. 5| Protein expression of FAS, HSL, IL-6, and MCP-1 in gastrocnemius after vibration for 12 weeks.

10). Yao Y et al. Passive smoking induces rat testicular injury via the FAS/FASL pathway. Drug Chem Toxicol 2019 Sep 3:1-9 (PubMed: 31476926)

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