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adam-17  (Hamad Medical Corporation)

 
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    Hamad Medical Corporation adam-17
    Adam 17, supplied by Hamad Medical Corporation, used in various techniques. Bioz Stars score: 90/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/product/adam-17/adam+17/pm37931848-200-12-16
    Average 90 stars, based on 1 article reviews
    adam-17 - by Bioz Stars, 2026-09
    90/100 stars

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    Article Title: Evaluation and targeting of amyloid precursor protein (APP)/amyloid beta (Aβ) axis in amyloidogenic and non-amyloidogenic pathways: A time outside the tunnel.
    Article Snippet: In Alzheimer disease (AD), amyloid precursor protein (APP) and production of amyloid beta (Aβ) which is generated by amyloidogenic pathway is implicated in neurotoxicity and neuronal cell deaths.. However, physiological Aβ level is essential to improves neuronal survival, attenuates neuronal apoptosis and has neuroprotective effect.. In addition, physiological APP level has neurotrophic effect on the central nervous system (CNS).



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    Knocking down ADAM‐17 inhibits expression of IL‐6 and TNF‐α. (A and B) Three lentivirus shRNAs (sh‐ADAM17#1, sh‐ADAM17#2, or sh‐ADAM17#3) were introduced into RAW264.7 cells, and the mRNA and protein expression levels of ADAM‐17 measured by WB and qRT‐PCR. (C) NC and sh‐ADAM17#1 RAW264.7 cells were treated with LCWE (1 μg/mL) for 12 h, the protein expression levels of IL‐6, IL‐1β, MCP‐1, and TNF‐α were assayed by ELISA. (D) The mRNA expression level of Areg was measured by qRT‐PCR. (E–H) LCWE‐stimulated RAW264.7 cells were treated with or without exogenous rm‐Areg (1 μg/mL), anti‐Areg (5 μg/mL), or IgG (5 μg/mL) for 12 h, then the protein expression levels of IL‐6, IL‐1β, MCP‐1, and TNF‐α were assayed by ELISA. Results are expressed as the mean ± SD, * p < 0.05, ** p < 0.01, *** p < 0.001, **** p < 0.0001.

    Journal: Immunity, Inflammation and Disease

    Article Title: Amphiregulin Promotes Proliferation and Migration of the Damaged Endothelial Cells in Kawasaki Disease Cell Models

    doi: 10.1002/iid3.70223

    Figure Lengend Snippet: Knocking down ADAM‐17 inhibits expression of IL‐6 and TNF‐α. (A and B) Three lentivirus shRNAs (sh‐ADAM17#1, sh‐ADAM17#2, or sh‐ADAM17#3) were introduced into RAW264.7 cells, and the mRNA and protein expression levels of ADAM‐17 measured by WB and qRT‐PCR. (C) NC and sh‐ADAM17#1 RAW264.7 cells were treated with LCWE (1 μg/mL) for 12 h, the protein expression levels of IL‐6, IL‐1β, MCP‐1, and TNF‐α were assayed by ELISA. (D) The mRNA expression level of Areg was measured by qRT‐PCR. (E–H) LCWE‐stimulated RAW264.7 cells were treated with or without exogenous rm‐Areg (1 μg/mL), anti‐Areg (5 μg/mL), or IgG (5 μg/mL) for 12 h, then the protein expression levels of IL‐6, IL‐1β, MCP‐1, and TNF‐α were assayed by ELISA. Results are expressed as the mean ± SD, * p < 0.05, ** p < 0.01, *** p < 0.001, **** p < 0.0001.

    Article Snippet: Primary antibodies against GAPDH (Cat. No. 60004‐1‐Ig) and ADAM‐17 (Cat. No. 29948‐1‐AP) were purchased from Proteintech (Wuhan, China).

    Techniques: Expressing, Quantitative RT-PCR, Enzyme-linked Immunosorbent Assay