Detection of Human and Mouse MCPIP1 by Western Blot.
Western blot shows lysates of untreated (-) HeLa human cervical epithelial carcinoma cell line and RAW 264.7 mouse monocyte/macrophage cell line and THP‑1 human acute monocytic leukemia cell line untreated (-) or treated (+) with 1 µg/mL LPS for 24 hours or 10 µg/mL LPS for 3 hours, respectively. PVDF membrane was probed with 1 µg/mL of Mouse Anti-Human MCPIP1 Monoclonal Antibody (Catalog # MAB7875) followed by HRP-conjugated Anti-Mouse IgG Secondary Antibody (Catalog # HAF018). A specific band was detected for MCPIP1 at approximately 70 kDa (as indicated). This experiment was conducted under reducing conditions and using Immunoblot Buffer Group 1.
Preparation and Storage
Sterile PBS to a final concentration of 0.5 mg/mL.
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.
Human MCP-induced protein (MCPIP), also known as ZC3H12A, is an approximately 66 kDa intracellular protein that contains one RNAse domain (aa 134-290), one zinc finger (aa 301-324), and a proline-rich region (aa 458-536). Within aa 426-599, human MCPIP shares approximately 79% aa sequence identity with mouse and rat MCPIP. Its expression is induced by inflammatory stimulation and cellular stress. It acts to dampen inflammatory responses by promoting the degradation of proinflammatory cytokine mRNAs, inhibiting NFkB activation, and antagonizing TLR signaling. MCPIP exhibits deubiquitinase activity and inhibits the biogenesis of miRNA. It also enhances inflammation-induced angiogenesis, osteocyte and adipocyte differentiation, and the cell death of cardiac myocytes.
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