Detection of Human IRAK4 by Western Blot.
Western blot shows lysates of A431 human epithelial carcinoma cell line and K562 human chronic myelogenous leukemia cell line. PVDF membrane was probed with 1 µg/mL Goat Anti-Human IRAK4 Antigen Affinity-purified Polyclonal Antibody (Catalog # AF3919) followed by HRP-conjugated Anti-Goat IgG Secondary Antibody (Catalog # HAF109). For additional reference, recombinant human IRAK1, IRAK2, and IRAK4 (2 ng/lane) were included. A specific band for IRAK4 was detected at approximately 55 kDa (as indicated). This experiment was conducted under reducing conditions and using Immunoblot Buffer Group 1.
IRAK4 in THP‑1 Human Cell Line.
IRAK4 was detected in immersion fixed THP‑1 human acute monocytic leukemia cell line using Goat Anti-Human IRAK4 Antigen Affinity-purified Polyclonal Antibody (Catalog # AF3919) at 15 µg/mL for 3 hours at room temperature. Cells were stained using the NorthernLights™ 557-conjugated Anti-Goat IgG Secondary Antibody (red; Catalog # NL001) and counterstained with DAPI (blue). Specific staining was localized to cytoplasm. View our protocol for Fluorescent ICC Staining of Non-adherent Cells.
Preparation and Storage
Reconstitute at 0.2 mg/mL in sterile PBS.
Reconstitution Buffer Available
The product is shipped at ambient temperature. Upon receipt, store it immediately at the temperature recommended below. *Small pack size (SP) is shipped with polar packs. Upon receipt, store it immediately at -20 to -70 °C
Stability & Storage
Use a manual defrost freezer and avoid repeated freeze-thaw cycles.
12 months from date of receipt, -20 to -70 °C as supplied.
1 month, 2 to 8 °C under sterile conditions after reconstitution.
6 months, -20 to -70 °C under sterile conditions after reconstitution.
IL-1 receptor-associated kinases (IRAKs) are serine/threonine kinases that help mediate signaling from Toll-like receptor (TLR) and IL-1 receptor family members. Four human IRAKs have been identified: IRAK1, IRAK2, IRAK-M, and IRAK4. Upon TLR ligand challenge, IRAK4 knockout mice exhibit severely impaired NF-kappa B activation. IRAK4 mutations have been described in patients with recurrent bacterial infections and poor inflammatory responses.
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