TGFβ family members, including TGFβs, activins and BMPs, are cytokines that control cell growth, differentiation and deposition of extracellular matrix through binding to heterodimeric cell surface receptor complexes composed of type I and II subunits, and intracellular Smad transcription factors (Shi and Massague, 2003; Feng and Derynck, 2005; Schmierer and Hill, 2007).
Previously, Aβ fibrils were proposed to attach to microglial cells by interacting with a cell surface receptor complex that includes CD47, α6β1 integrin, and CD36 [3].
MAPK activation is triggered in response to soluble Env gp120 engagement with surface receptor complex and is required for efficient production of infectious viral particles in primary T-lymphocytes and monocyte/macrophages [41] [43].
Type I IFNs signal through a universally expressed cell surface receptor complex composed of two subunits, IFNAR1 and IFNAR2 [ 8].
The cell surface receptor complex containing the receptor-like kinase, BR-insensitive 1 (Brespondssponds to BR signaling components by inducing the initial phosphorylation-dependent signal transduction cascade [ 3].
All Hh proteins bind to a surface receptor complex comprised of two transmembrane proteins Patched (Ptc), a receptor for Hh proteins and Smoothened (Smo), a signal transducer.
Once secreted from the cell, Type I IFNs bind to their cell surface receptor complex (INFAR) leading to the activation of the JAK/STAT signaling pathway.
Previous studies have suggested that successively activating the TGFβR1 TGFβR2 heterodimer, a cell surface receptor complex, is needed for the TGFβ subfamily to achieve cross-membrane signalling [ 24, 25].
Specifically, studies have demonstrated that CD36, a class B scavenger receptor, CD47, an integrin-associated protein, and α6β1-integrin form a cell surface receptor complex that mediates the binding of microglia or THP-1 monocytes to Aβ fibrils.
TGF-β inhibits the expression of MMP-1 and MMP-3 by binding to a certain cell surface receptor complex (TGF-β receptor proteins: TβR I/II/III), thus preventing the breakdown of collagens.
Previous studies have suggested that the TGFβ subfamily signals at the membrane are transmitted via a cell surface receptor complex, the TGFβR2 TGFβR1 heterodimer, thereby achieving cross-membrane signalling into the interior of the cell [ 24, 25].
