Render Target: SSR
Render Timestamp: 2025-02-27T19:12:40.872Z
Commit: cb76efb1e1bf27d454180ac9a5e8c179c097b4c4
XML generation date: 2024-10-25 16:21:15.538
Product last modified at: 2025-01-27T12:15:39.722Z
Cell Signaling Technology Logo
1% for the planet logo
PDP - Template Name: Antibody Sampler Kit
PDP - Template ID: *******4a3ef3a

Mouse Reactive Necroptosis Antibody Sampler Kit #47928

    Product Information

    Product Description

    The Mouse Reactive Necroptosis Antibody Sampler Kit provides an economical means of detecting total and phosphorylated proteins associated with necroptosis. The kit includes enough antibodies to perform two western blots with each primary antibody.

    Background

    Necroptosis, a regulated pathway for necrotic cell death, is triggered by a number of inflammatory signals, including cytokines in the tumor necrosis factor (TNF) family, pathogen sensors such as toll-like receptors (TLRs), ischemic injury, and neurodegenerative diseases (1-3). The process is negatively regulated by caspases and is initiated through a complex containing the RIP and RIP3 kinases, typically referred to as the necrosome. Necroptosis is inhibited by a small molecule inhibitor of RIP, necrostatin-1 (Nec-1) (4). RIP is phosphorylated at several sites within the kinase domain that are sensitive to Nec-1, including Ser14, Ser15, Ser161, and Ser166 (5). During necroptosis, RIP3 is phosphorylated at Ser227, leading to recruitment and phosphorylation of MLKL at Thr357 and Ser358 (6). Phosphorylation of MLKL results in its oligomerization and translocation to the plasma membrane, where it affects membrane integrity (7-10).
    In mice, activation of RIP3 is associated with phosphorylation at Thr231 and Ser232 (11), and then MLKL is phosphorylated at Ser345 by RIP3 (12).
    For Research Use Only. Not For Use In Diagnostic Procedures.
    Cell Signaling Technology is a trademark of Cell Signaling Technology, Inc.
    XP is a registered trademark of Cell Signaling Technology, Inc.
    All other trademarks are the property of their respective owners. Visit our Trademark Information page.