Product Description
Size: 100µL
SLAP2 overexpression 293T lysate (whole cell) suitable for WB. View our extensive range of validated lysates from normal and diseased human, mouse and rat tissue.
Key facts
Species or organism:Human,
Form:LiquidSee storage information
Product details:
ab94209 is a 293T cell transfected lysate in which Human SLAP2 has been transiently over-expressed using a pCMV-SLAP2 plasmid. The lysate is provided in 1X Sample Buffer.
Properties and Storage Information:
Shipped at conditions-Dry Ice, Appropriate short-term storage conditions--20°C, Appropriate long-term storage conditions--20°C, Aliquoting information-Upon delivery aliquot, Storage information-Avoid freeze / thaw cycle
Supplementary Information:
This supplementary information is collated from multiple sources and compiled automatically.
Src-like adapter protein 2 (SLAP2) also known as SLAP2 functions as an adaptor protein involved in signal transduction. It mediates interactions between membrane receptors and intracellular signaling components. SLAP2 is a protein of approximately 32 kDa and expression levels vary across different tissues including high expression in immune cells such as lymphocytes and macrophages. The protein has SH2 and SH3 domains which allow it to bind to phosphorylated tyrosines on its target proteins facilitating their degradation or modification.
Biological function summary
SLAP2 has a major role in regulating the immune response. By forming complexes with the components of the signal transduction machinery SLAP2 modulates the activity of key receptors such as the T-cell receptor (TCR) and B-cell receptor (BCR). These interactions influence cellular responses such as proliferation differentiation and apoptosis. Through its action SLAP2 acts as a negative regulator preventing overactivation of immune responses and maintaining homeostasis.
Pathways
Studies have shown that SLAP2 participates in both the T-cell receptor signaling pathway and the B-cell receptor signaling pathway. In these pathways SLAP2 interacts with kinases associated with these receptors such as Lck and Fyn influencing downstream signaling events. SLAP2 can inhibit excessive activation of these pathways by promoting the degradation of key signaling molecules ensuring that cells respond appropriately to external signals during immune activation.
SLAP2 has been linked to certain types of cancer and autoimmune diseases. For example alterations in SLAP2 expression or function may contribute to lymphomas where disrupted signaling processes lead to uncontrolled cell growth. In autoimmune diseases aberrant SLAP2 activity could result in improper immune cell activation potentially linked to proteins like ZAP-70 which are also involved in disease modulation. Understanding SLAP2's regulation and interaction with signaling proteins could offer insights for therapeutic interventions in these conditions.
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Collaboration
Tony Tang
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