Product: TRADD Antibody
Catalog: DF6279
Description: Rabbit polyclonal antibody to TRADD
Application: WB IHC IF/ICC
Reactivity: Human, Mouse, Rat
Prediction: Pig, Bovine, Sheep
Mol.Wt.: 34kDa; 34kD(Calculated).
Uniprot: Q15628
RRID: AB_2838245

View similar products>>

   Size Price Inventory
 100ul $280 In stock
 200ul $350 In stock

Lead Time: Same day delivery

For pricing and ordering contact:
Local distributors

Product Info

Source:
Rabbit
Application:
WB 1:500-1:2000, IHC 1:50-1:200, 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(80%), Bovine(80%), Sheep(80%)
Clonality:
Polyclonal
Specificity:
TRADD Antibody detects endogenous levels of total TRADD.
RRID:
AB_2838245
Cite Format: Affinity Biosciences Cat# DF6279, RRID:AB_2838245.
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

9130005N23Rik; AA930854; TNFR1 associated DEATH domain protein; TNFR1-associated DEATH domain protein; TNFRSF1A associated via death domain; TNFRSF1A-associated via death domain; tradd; TRADD_HUMAN; Tumor necrosis factor receptor type 1 associated DEATH domain protein; Tumor necrosis factor receptor type 1-associated DEATH domain protein;

Immunogens

Immunogen:
Uniprot:
Gene(ID):
Expression:
Q15628 TRADD_HUMAN:

Found in all examined tissues.

Description:
Apoptosis mediated by death factors like FasL and TNF-α involves the formation of a death-inducing signaling complex (DISC) to their respective receptors (1). Upon ligand activation to their receptors, Fas and TNF-R1 associate with death domain (DD) containing adaptor proteins FADD (Fas associated death domain) (2,3) and TRADD (TNF-R1 associated death domain) (4). In addition to its carboxy-terminal DD, FADD contains an amino-terminal death effector domain (DED) that binds to DEDs found on caspase-8 which leads to activation of this initiator caspase (5,6). Caspase-8 subsequently activates downstream effector caspases, like caspase-3, resulting in the cleavage of proteins involved in the execution of apoptosis. Unlike FADD, TRADD does not contain a DED (4). Apoptosis driven by TNF-R1 binding to TRADD involves association of TRADD and FADD which then leads to activation of caspase-8 (7).
Sequence:
MAAGQNGHEEWVGSAYLFVESSLDKVVLSDAYAHPQQKVAVYRALQAALAESGGSPDVLQMLKIHRSDPQLIVQLRFCGRQPCGRFLRAYREGALRAALQRSLAAALAQHSVPLQLELRAGAERLDALLADEERCLSCILAQQPDRLRDEELAELEDALRNLKCGSGARGGDGEVASAPLQPPVPSLSEVKPPPPPPPAQTFLFQGQPVVNRPLSLKDQQTFARSVGLKWRKVGRSLQRGCRALRDPALDSLAYEYEREGLYEQAFQLLRRFVQAEGRRATLQRLVEALEENELTSLAEDLLGLTDPNGGLA

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
Pig
80
Bovine
80
Sheep
80
Horse
70
Rabbit
70
Dog
0
Xenopus
0
Zebrafish
0
Chicken
0
Model Confidence:
High(score>80) Medium(80>score>50) Low(score<50) No confidence

PTMs - Q15628 As Substrate

Site PTM Type Enzyme
K38 Ubiquitination
Y42 Phosphorylation
K163 Ubiquitination
S215 Phosphorylation
K229 Ubiquitination
S296 Phosphorylation

Research Backgrounds

Function:

The nuclear form acts as a tumor suppressor by preventing ubiquitination and degradation of isoform p19ARF/ARF of CDKN2A by TRIP12: acts by interacting with TRIP12, leading to disrupt interaction between TRIP12 and isoform p19ARF/ARF of CDKN2A (By similarity). Adapter molecule for TNFRSF1A/TNFR1 that specifically associates with the cytoplasmic domain of activated TNFRSF1A/TNFR1 mediating its interaction with FADD. Overexpression of TRADD leads to two major TNF-induced responses, apoptosis and activation of NF-kappa-B.

Subcellular Location:

Nucleus. Cytoplasm. Cytoplasm>Cytoskeleton.
Note: Shuttles between the cytoplasm and the 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:

Found in all examined tissues.

Subunit Structure:

Stimulation of TNF-alpha receptor TNFRSF1A leads to the formation of two distinct signaling complexes. Plasma membrane-bound complex I is composed of TNFRSF1A, TRADD, RIPK1, TRAF2 and BIRC2/c-IAP1 or BIRC3 which interacts with CHUCK/IKK-alpha, IKBKB/IKK-beta and IKBKG/IKK-gamma promoting cell survival. Subsequently, TRADD, RIPK1 and TRAF2 dissociate from TNFRSF1A and form cytoplasmic complex II with FADD and caspase CASP8 promoting cell apoptosis. Within complex I, interacts with TNFRSF1A/TNFR1, TRAF2 and kinase RIPK1. Within complex I, interacts with TRPC4AP; the interaction promotes NF-kappa B activation. UXT1 associates with complex I; the interaction prevents the formation of complex II. Within complex I Interacts with scaffold protein DAB2IP. Interacts with autophagy receptor SQSTM1. Interacts with E3 ligase TRIP12 (By similarity). Interacts with kinase HIPK2. Interacts with keratin KRT14. Interacts with keratin KRT18. Interacts with keratins KRT16 and KRT17 (By similarity). Interacts with FADD (By similarity).

Family&Domains:

Requires the intact death domain to associate with TNFRSF1A/TNFR1.

Research Fields

· 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 > Signal transduction > NF-kappa B signaling pathway.   (View pathway)

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

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

· Human Diseases > Infectious diseases: Bacterial > Tuberculosis.

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

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

· Human Diseases > Infectious diseases: Viral > Epstein-Barr virus infection.

· Human Diseases > Cancers: Overview > Viral carcinogenesis.

· Organismal Systems > Immune system > RIG-I-like receptor signaling pathway.   (View pathway)

· Organismal Systems > Immune system > IL-17 signaling pathway.   (View pathway)

· Organismal Systems > Endocrine system > Adipocytokine signaling pathway.

References

1). Extracellular vesicles of Fusobacterium nucleatum compromise intestinal barrier through targeting RIPK1-mediated cell death pathway. Gut Microbes, 2021 (PubMed: 33769187) [IF=12.2]

2). 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]

3). Corilagin Interferes With Toll-Like Receptor 3-Mediated Immune Response in Herpes Simplex Encephalitis. Frontiers in Molecular Neuroscience, 2019 (PubMed: 31080403) [IF=4.8]

Application: WB    Species: mouse    Sample: BV-2 cells

Figure 2. |Poly (I:C) and HSV-1 increased the expression of TLR3 signaling components in BV-2 cells. BV2 cells were stimulated by poly(I:C) (10μg/mL )and HSV-1 (100TCID50, 10-2.67/0.1 mL) for 6 h, then the fresh medium was added in for culturing another 24h. (A) The total RNA was extracted from activated BV-2 cells.The mRNA levels of TLR3 and its downstream molecules were measured by RT-PCR.(B) The protein levels of TLR3 and its downstream molecules were detected by western blotting.

4). The intervention mechanism of emodin on TLR3 pathway in the process of central nervous system injury caused by herpes virus infection. NEUROLOGICAL RESEARCH, 2021 (PubMed: 33274693) [IF=1.9]

Application: WB    Species: Mice    Sample: brain tissues

Figure 4. The protein expression of TLR3 and its downstream protein in brain tissues of mice.

Restrictive clause

 

Affinity Biosciences tests all products strictly. Citations are provided as a resource for additional applications that have not been validated by Affinity Biosciences. Please choose the appropriate format for each application and consult Materials and Methods sections for additional details about the use of any product in these publications.

For Research Use Only.
Not for use in diagnostic or therapeutic procedures. Not for resale. Not for distribution without written consent. Affinity Biosciences will not be held responsible for patent infringement or other violations that may occur with the use of our products. Affinity Biosciences, Affinity Biosciences Logo and all other trademarks are the property of Affinity Biosciences LTD.