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Rage antagonist peptide rap

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The RAGE antagonist peptide (RAP) is a laboratory reagent used in research applications. It functions as an antagonist to the receptor for advanced glycation end products (RAGE), a cell surface receptor involved in various cellular processes. RAP can be utilized in experimental studies to investigate the role of RAGE signaling. No further details on intended use are provided.

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Lab products found in correlation

Lipofectamine 2000, by Thermo Fisher Scientific (2 mentions) Ifn γ, by R&D Systems (2 mentions) Fps zm1, by Cayman Chemical (2 mentions) Pam3csk4, by InvivoGen (2 mentions)

2 protocols using rage antagonist peptide rap

1

Quantifying Cell Death and Cytokine Secretion

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To assess cell death and IL-1β secretion, cells were primed with IFN-γ (10 ng/mL; R&D Systems) and Pam3CSK4 (0.5 μg/mL; InvivoGen) for 3 h and stimulated with 1 μg LPS or transfected with LPS (1 μg)-Lipofectamine 2000 (Invitrogen). Supernatants were collected 16 h post-stimulation and cell death was measured by LDH release. IL-1β levels in the supernatant was measured by ELISA. To visualize LPS internalization, BMDMs were stimulated with FITC-LPS (100 ng/mL) or FITC-LPS pre-incubated with recombinant HMGB1 (400 ng/mL) for 20 min at room temperature as described previously (Deng et al., 2018 (link)). RAGE-mediated FITC-LPS internalization was assessed by treating BMDMs with DMSO or RAGE inhibitors (1 μM FPS-ZM1 (Cayman), or 10 μM RAGE antagonist peptide (RAP; Millipore) (Deng et al., 2018 (link); Senatus et al., 2020 )) 1 h before LPS treatment. Cells were washed with PBS 2 h later, fixed, permeabilized, and blocked as described above and stained with antibodies against FITC and CD45.
Vasudevan S.O., Russo A.J., Kumari P., Vanaja S.K, & Rathinam V.A. (2022). A TLR4-independent critical role for CD14 in intracellular LPS sensing. Cell reports, 39(5), 110755.
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2

Quantifying Cell Death and Cytokine Secretion

Check if the same lab product or an alternative is used in the 5 most similar protocols
To assess cell death and IL-1β secretion, cells were primed with IFN-γ (10 ng/mL; R&D Systems) and Pam3CSK4 (0.5 μg/mL; InvivoGen) for 3 h and stimulated with 1 μg LPS or transfected with LPS (1 μg)-Lipofectamine 2000 (Invitrogen). Supernatants were collected 16 h post-stimulation and cell death was measured by LDH release. IL-1β levels in the supernatant was measured by ELISA. To visualize LPS internalization, BMDMs were stimulated with FITC-LPS (100 ng/mL) or FITC-LPS pre-incubated with recombinant HMGB1 (400 ng/mL) for 20 min at room temperature as described previously (Deng et al., 2018 (link)). RAGE-mediated FITC-LPS internalization was assessed by treating BMDMs with DMSO or RAGE inhibitors (1 μM FPS-ZM1 (Cayman), or 10 μM RAGE antagonist peptide (RAP; Millipore) (Deng et al., 2018 (link); Senatus et al., 2020 )) 1 h before LPS treatment. Cells were washed with PBS 2 h later, fixed, permeabilized, and blocked as described above and stained with antibodies against FITC and CD45.
Vasudevan S.O., Russo A.J., Kumari P., Vanaja S.K, & Rathinam V.A. (2022). A TLR4-independent critical role for CD14 in intracellular LPS sensing. Cell reports, 39(5), 110755.
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