Antibody data
- Antibody Data
- Antigen structure
- References [2]
- Comments [0]
- Validations
- Immunocytochemistry [1]
- Other assay [6]
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- Product number
- PA5-17490 - Provider product page

- Provider
- Invitrogen Antibodies
- Product name
- IRAK1 Polyclonal Antibody
- Antibody type
- Polyclonal
- Antigen
- Synthetic peptide
- Description
- It is not recommended to aliquot this antibody.
- Reactivity
- Human
- Host
- Rabbit
- Isotype
- IgG
- Vial size
- 100 μL
- Concentration
- 26.4 μg/mL
- Storage
- -20°C
Submitted references Viperin interacts with the kinase IRAK1 and the E3 ubiquitin ligase TRAF6, coupling innate immune signaling to antiviral ribonucleotide synthesis.
Human Cytomegalovirus miR-UL112-3p Targets TLR2 and Modulates the TLR2/IRAK1/NFκB Signaling Pathway.
Dumbrepatil AB, Ghosh S, Zegalia KA, Malec PA, Hoff JD, Kennedy RT, Marsh ENG
The Journal of biological chemistry 2019 Apr 26;294(17):6888-6898
The Journal of biological chemistry 2019 Apr 26;294(17):6888-6898
Human Cytomegalovirus miR-UL112-3p Targets TLR2 and Modulates the TLR2/IRAK1/NFκB Signaling Pathway.
Landais I, Pelton C, Streblow D, DeFilippis V, McWeeney S, Nelson JA
PLoS pathogens 2015 May;11(5):e1004881
PLoS pathogens 2015 May;11(5):e1004881
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Supportive validation
- Submitted by
- Invitrogen Antibodies (provider)
- Main image

- Experimental details
- Immunofluorescent analysis of IRAK1 in HT-1080 cells using an IRAK1 polyclonal antibody (Product # PA5-17490) (green). Actin filaments are labeled with a fluorescent red phalloidin. DNA is labeled using a fluorescent blue dye.
Supportive validation
- Submitted by
- Invitrogen Antibodies (provider)
- Main image

- Experimental details
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- Invitrogen Antibodies (provider)
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- Invitrogen Antibodies (provider)
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- Invitrogen Antibodies (provider)
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- Invitrogen Antibodies (provider)
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- Invitrogen Antibodies (provider)
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- Experimental details
- Fig 5 miR-UL112-3p inhibits TLR2-dependent activation of IRAK1. (A) Schematic of the upper section of the TLR2/NFkappaB pathway with known factors and post-translational modifications of IRAK4 and IRAK1 upon stimulation with TLR2 agonists. Grey ellipse, agonist; P, phosphorylation; K63, Lys63 poly-ubiquitin chain. (B) IRAK1 undergoes post-translational modifications upon stimulation with a TLR2/TLR1 agonist (PAM3CSK4, 100ng/ml) but not with a TLR4 agonist (LPS). TPA-differentiated THP-1 cells were treated as described in panel A. Unmodified and post-translationally modified forms of IRAK1 were detected by IB. (C) miR-UL112-3p inhibits FSL-1 induced IRAK1 post-translational modifications. TLR2, beta-actin and IRAK1 unmodified and modified forms were detected by IB. Numbers below the IRAK1 blot represent quantification (in relative units) of the unmodified protein signal.