TNF Receptor I Antibody - #AF0282

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Product: TNF Receptor I Antibody
Catalog: AF0282
Description: Rabbit polyclonal antibody to TNF Receptor I
Application: WB IHC IF/ICC
Reactivity: Human, Mouse, Rat
Prediction: Pig, Bovine, Horse, Rabbit, Dog
Mol.Wt.: 50kDa; 50kD(Calculated).
Uniprot: P19438
RRID: AB_2834164

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Related Downloads
MS Report
HPLC Report
MSDS
Data Sheet
COA
Protocols
WB Handbook
IHC Protocol
IF/ICC Protocol

Product Info

Source:
Rabbit
Application:
IHC 1:50-1:200, WB 1:500-2000, 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:
Pig(92%), Bovine(100%), Horse(100%), Rabbit(83%), Dog(100%)
Clonality:
Polyclonal
Specificity:
TNF Receptor I Antibody detects endogenous levels of total TNF Receptor I.
RRID:
AB_2834164
Cite Format: Affinity Biosciences Cat# AF0282, RRID:AB_2834164.
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

CD120a; FPF; MGC19588; p55; p55-R; p60; TBP1; TBPI; TNF R; TNF R55; TNF-R1; TNF-RI; TNFAR; TNFR-I; TNFR1; TNFR55; TNFR60; TNFRI; TNFRSF1a; TNR1A_HUMAN; Tumor necrosis factor receptor 1; Tumor necrosis factor receptor superfamily, member 1A; Tumor necrosis factor receptor type 1; Tumor necrosis factor receptor type I; Tumor necrosis factor-binding protein 1;

Immunogens

Immunogen:
Uniprot:

P19438(TNR1A_HUMAN) >>Visit HPA database.

Gene(ID):
TNFRSF1A(7132)
Description:
TNF-R1 Receptor for TNFSF2/TNF-alpha and homotrimeric TNFSF1/lymphotoxin-alpha. 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. Contributes to the induction of non-cytocidal TNF effects including anti-viral state and activation of the acid sphingomyelinase. Binding of TNF to the extracellular domain leads to homotrimerization. The aggregated death domains provide a novel molecular interface that interacts specifically with the death domain of TRADD.
Sequence:
MGLSTVPDLLLPLVLLELLVGIYPSGVIGLVPHLGDREKRDSVCPQGKYIHPQNNSICCTKCHKGTYLYNDCPGPGQDTDCRECESGSFTASENHLRHCLSCSKCRKEMGQVEISSCTVDRDTVCGCRKNQYRHYWSENLFQCFNCSLCLNGTVHLSCQEKQNTVCTCHAGFFLRENECVSCSNCKKSLECTKLCLPQIENVKGTEDSGTTVLLPLVIFFGLCLLSLLFIGLMYRYQRWKSKLYSIVCGKSTPEKEGELEGTTTKPLAPNPSFSPTPGFTPTLGFSPVPSSTFTSSSTYTPGDCPNFAAPRREVAPPYQGADPILATALASDPIPNPLQKWEDSAHKPQSLDTDDPATLYAVVENVPPLRWKEFVRRLGLSDHEIDRLELQNGRCLREAQYSMLATWRRRTPRREATLELLGRVLRDMDLLGCLEDIEEALCGPAALPPAPSLLR

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
100
Bovine
100
Dog
100
Pig
92
Rabbit
83
Sheep
0
Xenopus
0
Zebrafish
0
Chicken
0
Model Confidence:
High(score>80) Medium(80>score>50) Low(score<50) No confidence

PTMs - P19438 As Substrate

Site PTM Type Enzyme
K48 Ubiquitination
K61 Ubiquitination
K64 Ubiquitination
S86 Phosphorylation
T90 Phosphorylation
T118 Phosphorylation
K242 Ubiquitination
K250 Ubiquitination
K265 Ubiquitination
Y318 Phosphorylation
K347 Ubiquitination
T353 Phosphorylation
Y360 Phosphorylation
S381 Phosphorylation O14920 (IKBKB)
Y401 Phosphorylation
S402 Phosphorylation
T406 Phosphorylation
T417 Phosphorylation

Research Backgrounds

Function:

Receptor for TNFSF2/TNF-alpha and homotrimeric TNFSF1/lymphotoxin-alpha. 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. Contributes to the induction of non-cytocidal TNF effects including anti-viral state and activation of the acid sphingomyelinase.

PTMs:

The soluble form is produced from the membrane form by proteolytic processing.

Subcellular Location:

Cell membrane>Single-pass type I membrane protein. Golgi apparatus membrane>Single-pass type I membrane protein. Secreted.
Note: A secreted form is produced through proteolytic processing.

Secreted.
Note: Lacks a Golgi-retention motif, is not membrane bound and therefore is secreted.

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

Binding of TNF to the extracellular domain leads to homotrimerization. The aggregated death domains provide a novel molecular interface that interacts specifically with the death domain of TRADD. Various TRADD-interacting proteins such as TRAFS, RIPK1 and possibly FADD, are recruited to the complex by their association with TRADD. This complex activates at least two distinct signaling cascades, apoptosis and NF-kappa-B signaling. Interacts with BAG4, BABAM2, FEM1B, GRB2, SQSTM1 and TRPC4AP. Interacts directly with NOL3 (via CARD domain); inhibits TNF-signaling pathway (By similarity). Interacts with SH3RF2, TRADD and RIPK1. SH3RF2 facilitates the recruitment of RIPK1 and TRADD to TNFRSF1A in a TNF-alpha-dependent process.

(Microbial infection) Interacts with mumps virus protein SH; this interaction inhibits downstream NF-kappa-B pathway activation.

(Microbial infection) Interacts with HCV core protein.

(Microbial infection) Interacts with human cytomegalovirus/HHV-5 protein UL138.

(Microbial infection) Interacts with host TNFRSF1A; this interaction leads to the stimulation of both surface expression and shedding of TNFRSF1A.

Family&Domains:

The domain that induces A-SMASE is probably identical to the death domain. The N-SMASE activation domain (NSD) is both necessary and sufficient for activation of N-SMASE.

Both the cytoplasmic membrane-proximal region and the C-terminal region containing the death domain are involved in the interaction with TRPC4AP.

Research Fields

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

· Cellular Processes > Cell growth and death > Apoptosis - multiple species.   (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 > NF-kappa B signaling pathway.   (View pathway)

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

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

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

· Human Diseases > Endocrine and metabolic diseases > Insulin resistance.

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

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

· Human Diseases > Neurodegenerative diseases > Amyotrophic lateral sclerosis (ALS).

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

· Human Diseases > Infectious diseases: Parasitic > Toxoplasmosis.

· Human Diseases > Infectious diseases: Bacterial > Tuberculosis.

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

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

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

· Human Diseases > Infectious diseases: Viral > HTLV-I infection.

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

· Organismal Systems > Development > Osteoclast differentiation.   (View pathway)

· Organismal Systems > Endocrine system > Adipocytokine signaling pathway.

References

1). Silica nanoparticles cause spermatogenesis dysfunction in mice via inducing cell cycle arrest and apoptosis. ECOTOXICOLOGY AND ENVIRONMENTAL SAFETY, 2022 (PubMed: 35051769) [IF=6.8]

Application: WB    Species: mouse    Sample: testis

Fig. 7. |SiNPs affected the protein expressions of ATM/p53 and TNF-α/TNFR I-mediated signaling pathways. (A) The protein expressions of ATM, p53, Bcl-2, Bax,TNF-α, TNFR I, Caspase-8, and Caspase-3 were detected in the testis of control group and SiNPs group.
2). 20 (S)-Ginsenoside Rh2 induces caspase-dependent PML-RARA degradation in NB4 cells via Akt/Bax/caspase9 and TNF-α/caspase8 signaling cascades. Journal of Ginseng Research, 2021 (PubMed: 33841010) [IF=6.3]

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.

Application: WB    Species: Human    Sample: NB4 cells

Fig. 7 GRh2 activated the TNF-α/caspase8 cascade. (A) NB4 cells were incubated with 30 μM, 40 μM, or 50 μM GRh2 for 12 h. Protein expression levels of FasL, Fas, TNF-α, 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 = 3) ∗p < 0.05, ∗∗p < 0.01. (C) RT-PCR was used to detect the mRNA expression level of TNF-α in NB4 cells after GRh2 administration. The results are shown as the mean ± SD (n = 3) ∗∗p < 0.01, ∗∗∗p < 0.001 versus solvent. After preincubation with 1.5 μM TNF-α inhibitor, C 87, for 2 h, 30 μM, 40 μM, or 50 μM 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 = 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 Scale bar=200 μm. (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 = 3) ∗∗∗p < 0.001, #p < 0.05. GRh2, 20(S)-ginsenoside Rh2.
3). Effect of nicotine on placental inflammation and apoptosis in preeclampsia-like model. Life Sciences, 2020 (PubMed: 32835699) [IF=6.1]

Application: IF/ICC    Species: rat    Sample: Placental

Fig. 9. |Nicotine treatment inhibited the expression of TNFR1 (a receptor in the TNF-α-induced extrinsic apoptosis signaling) in placenta in experimental PE rats. (A)Placental tissue sections were stained with anti-TNFR1 by immunofluorescence. Nuclei were visualized with DAPI. White dotted lines show the positive staining.
4). Atsttrin regulates osteoblastogenesis and osteoclastogenesis through the TNFR pathway. Communications biology, 2023 (PubMed: 38081906) [IF=5.9]

Application: WB    Species: Mouse    Sample: RAW264.7 cells

Fig. 3 Atsttrin inhibited TNF-α-induced osteoclastogenesis via TNFR1. a Western blot analysis to examine the knockdown efficacy of siRNA against TNFR1 in RAW264.7 cells and BMDMs. b BMDMs transfected with scrambled control siRNA (scRNAi) or TNFR1 RNAi were treated with RANKL (100 ng/ml), TNF-α (10 ng/mL), and Atsttrin (500 ng/ml) for 48 h. The protein levels of TRAP and CTSK were measured by Western blotting (n = 3). The bands in the figure are not all derived from the same membrane. c, d Western blot gray value analysis of TNFR1 and TRAP in BMDMs. e, f BMDMs transfected with scrambled control siRNA (scRNAi) or TNFR1 RNAi were cultured with RANKL (100 ng/ml), TNF-α (10 ng/ml), and Atsttrin (500 ng/ml) for 7 days, and TRAP staining was performed. Scale bar, 200 µm. The TRAP-positive multinuclear cells were counted. Each experiment was performed three times independently. g–i RAW264.7 cells transfected with scrambled control siRNA (scRNAi) or TNFR1 RNAi were treated with RANKL (100 ng/ml), TNF-α (10 ng/ml), and Atsttrin (500 ng/ml) for 8 h. The mRNA levels of TRAP, Cathepsin K, and Calcitonin Receptor were measured by real-time PCR (n = 3). Significant differences are indicated as follows: nsP > 0.05, ∗P 
5). Fexofenadine Protects Against Intervertebral Disc Degeneration Through TNF Signaling. Frontiers in Cell and Developmental Biology, 2021 (PubMed: 34504840) [IF=5.5]
6). Mechanism of Xiaojianzhong decoction in alleviating aspirin-induced gastric mucosal injury revealed by transcriptomics and metabolomics. Journal of ethnopharmacology, 2024 (PubMed: 37453623) [IF=5.4]
7). Macrophage Membrane-Derived Biomimetic Nanoparticles for Treatment of Cytokine Release Syndrome. Journal of Biomedical Nanotechnology, 2022 (PubMed: 35854441) [IF=2.9]
8). Mechanistic investigation of the ameliorative effect of liquiritin on hypoxia/reoxygenation‑induced cardiomyocyte injury based on network pharmacology and in vitro validation. Experimental and therapeutic medicine, 2024 (PubMed: 38361515) [IF=2.7]
9). Huangjia Ruangan Granule Inhibits Inflammation in a Rat Model with Liver Fibrosis by Regulating TNF/MAPK and NF-κB Signaling Pathways. Evidence-based Complementary and Alternative Medicine, 2022 (PubMed: 35942372)

Application: WB    Species: Rat    Sample: liver

Figure 7 HJRG regulated TNF/MAPK and NF-κB signaling pathways in rats. Representative images of western blot analysis and the protein expression statistics of TNFR1, p-IκBα, p-P65/P65, p-ERK/ERK, p-JNK/JNK, and MAPK p-P38/P38 in the liver. (n = 5). #p < 0.05 and ##p < 0.01, compared with the control group; ∗p < 0.05 and ∗∗p < 0.01, compared with the model group. Control: control group; Model: model group; Silymarin: silymarin group; HJRG-L: Huangjia Ruangan granule low-dose group; HJRG-M: Huangjia Ruangan granule medium-dose group; HJRG-H: Huangjia Ruangan granule high-dose group.
10). Therapeutic Effect of Macrophage-Derived Biomimetic Nanoparticles for Cytokine Release Syndrome. , 2021

Application: WB    Species: Mouse    Sample:

Figure 2. Characterization of biomimetic nanoparticles. (A) The particle size and zeta potential of PLGA nanoparticles and PNP@MP were detected by DLS; (B) Particle size distribution range of PLGA and PNP@MP; (C) Transmission electron microscope image of PNP@MP negatively stained with phosphotungstic acid; (D) Stability of PNP@MP in PBS or PBS containing 10% FBS within 72 h;(E) Characteristic protein bands of macrophage cell lysates, membrane-derived biomimetic nanoparticles resolved by Western blotting.
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