Fas Antibody [D2F4] | Primary Antibodies

Application: Reactivity: Human

Lane 1: Hela, Lane 2: Hela (KO Fas), Lane 3: Raji, Lane 4: Ramos

Usage Information

Dilution
WB1:1000-1:10000 IHC1:250-1:500 IF1:250-1:500

Application
WB, IHC, IF

Reactivity
Human

Source
Rabbit Monoclonal Antibody

Storage Buffer
PBS, pH 7.2+50% Glycerol+0.05% BSA+0.01% NaN3

Storage (from the date of receipt)
-20°C (avoid freeze-thaw cycles), 2 years

Predicted MW Observed MW
37 kDa 37 kDa
^*Why do the predicted and actual molecular weights differ? The following reasons may explain differences between the predicted and actual protein molecular weight. Post-translational modifications(e.g., phosphorylation, glycosylation); Splice variants and isoforms; Relative charge; Multimerization.

Datasheet & SDS

Biological Description

Specificity
Fas Antibody [D2F4] detects endogenous levels of total Fas protein.

Clone
D2F4

Synonym(s)
CD95; APT1; FAS1; TNFRSF6; FAS; Tumor necrosis factor receptor superfamily member 6; Apo‑1 antigen; Apoptosis‑mediating surface antigen FAS; FASLG receptor

Background
Fas (CD95/Apo-1), a prototypical death receptor of the TNF receptor superfamily, transduces extrinsic apoptosis signals critical for immune homeostasis, lymphocyte deletion, and tumor surveillance through trimerization induced by multimeric FasL binding to its extracellular cysteine-rich domains. Ligand engagement recruits the adaptor FADD via death domain interactions, forming the death-inducing signaling complex (DISC) that docks procaspase-8 through DED-mediated oligomerization, enabling autocatalytic activation independent of mitochondrial amplification in type I cells or BID cleavage in type II cells to converge on effector caspase-3/7 execution. Membrane-bound FasL from activated CD8 T cells and NK cells potently clusters Fas trimers for full DISC assembly, whereas soluble FasL requires secondary aggregation for physiological potency, distinguishing it from agonistic antibodies that variably signal death versus survival through NF-κB/ERK non-apoptotic branches. This pathway operates stringently downstream of FADD/caspase-8 as evidenced by complete blockade in deficient cells, while remaining insensitive to Bcl-2/Bcl-xL mitochondrial regulation, establishing Fas as the dominant extrinsic apoptosis trigger in lymphocytes and hepatocytes. Physiologically, Fas governs activation-induced cell death to prevent autoimmunity, contracts immune responses post-infection, and prunes double-negative thymocytes, making it indispensable for researchers quantifying effector deletion via Annexin V or dissecting tolerance breakdown in lpr/gld models. Tumors exploit FasL expression as a counterattack mechanism, killing Fas-sensitive TILs while acquiring caspase-8 mutations for resistance, though FasL suppression paradoxically enhances tumor clearance through restored lymphocyte infiltration. Immune-privileged sites weaponize constitutive FasL to exclude Fas-bearing leukocytes.

Background

Fas (CD95/Apo-1), a prototypical death receptor of the TNF receptor superfamily, transduces extrinsic apoptosis signals critical for immune homeostasis, lymphocyte deletion, and tumor surveillance through trimerization induced by multimeric FasL binding to its extracellular cysteine-rich domains. Ligand engagement recruits the adaptor FADD via death domain interactions, forming the death-inducing signaling complex (DISC) that docks procaspase-8 through DED-mediated oligomerization, enabling autocatalytic activation independent of mitochondrial amplification in type I cells or BID cleavage in type II cells to converge on effector caspase-3/7 execution. Membrane-bound FasL from activated CD8 T cells and NK cells potently clusters Fas trimers for full DISC assembly, whereas soluble FasL requires secondary aggregation for physiological potency, distinguishing it from agonistic antibodies that variably signal death versus survival through NF-κB/ERK non-apoptotic branches. This pathway operates stringently downstream of FADD/caspase-8 as evidenced by complete blockade in deficient cells, while remaining insensitive to Bcl-2/Bcl-xL mitochondrial regulation, establishing Fas as the dominant extrinsic apoptosis trigger in lymphocytes and hepatocytes. Physiologically, Fas governs activation-induced cell death to prevent autoimmunity, contracts immune responses post-infection, and prunes double-negative thymocytes, making it indispensable for researchers quantifying effector deletion via Annexin V or dissecting tolerance breakdown in lpr/gld models. Tumors exploit FasL expression as a counterattack mechanism, killing Fas-sensitive TILs while acquiring caspase-8 mutations for resistance, though FasL suppression paradoxically enhances tumor clearance through restored lymphocyte infiltration. Immune-privileged sites weaponize constitutive FasL to exclude Fas-bearing leukocytes.

References
https://pubmed.ncbi.nlm.nih.gov/16267003/ https://www.pnas.org/doi/abs/10.1073/pnas.96.26.14871

Reference Table for Selecting PVDF Membrane Pore Size Specifications

Protein Size (kDa)	PVDF Transfer Membrane Pore Size (μm)
< 10	0.22
10-20	0.22
20-30	0.45
30-45	0.45
45-70	0.45
80-100	0.45
100-140	0.45
> 140	0.45

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Protein Size (kDa)	Separating Gel Percentage
4-40	20%
12-45	15%
10-70	12.5%
15-100	10%
25-100	8%
60-210	5%