R-SMADs are receptor-regulated SMADs. SMADs are transcription factors that transduce extracellular TGF-β superfamily ligand signaling from cell membrane bound TGF-β receptors into the nucleus where they activate transcription TGF-β target genes. R-SMADS are directly phosphorylated on their c-terminus by type 1 TGF-β receptors through their intracellular kinase domain, leading to r-SMAD activation. R-SMADS include SMAD2 and SMAD3 from the TGF-β/Activin/Nodal branch, and SMAD1, SMAD5 and SMAD8 from the BMP/GDP branch of TGF-β signaling.
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| - R-SMADs es un tipo de proteína SMAD regulado por receptores. Las SMAD son factores de transcripción que transducen señales de la superfamilia de ligandos extracelulares TGF-β que inician en los receptores de TGF-beta a nivel de la membrana celular hasta el núcleo donde activan genes diana que transcriben TGF-β. La activación de los R-SMAD ocurre por fosforilación directa de su extremo c-terminal por el dominio cinasa intracelular del receptor de TGF-beta 1. Entre las R-SMAD se incluyen al SMAD2 y SMAD3 de la vía TGF-β/Activin/Nodal, y los SMAD1, SMAD5 y SMAD8 de la vía de señalización de la proteína morfogénica ósea (BMP).
- R-SMADs are receptor-regulated SMADs. SMADs are transcription factors that transduce extracellular TGF-β superfamily ligand signaling from cell membrane bound TGF-β receptors into the nucleus where they activate transcription TGF-β target genes. R-SMADS are directly phosphorylated on their c-terminus by type 1 TGF-β receptors through their intracellular kinase domain, leading to r-SMAD activation. R-SMADS include SMAD2 and SMAD3 from the TGF-β/Activin/Nodal branch, and SMAD1, SMAD5 and SMAD8 from the BMP/GDP branch of TGF-β signaling.
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| - R-SMADs es un tipo de proteína SMAD regulado por receptores. Las SMAD son factores de transcripción que transducen señales de la superfamilia de ligandos extracelulares TGF-β que inician en los receptores de TGF-beta a nivel de la membrana celular hasta el núcleo donde activan genes diana que transcriben TGF-β. La activación de los R-SMAD ocurre por fosforilación directa de su extremo c-terminal por el dominio cinasa intracelular del receptor de TGF-beta 1. Entre las R-SMAD se incluyen al SMAD2 y SMAD3 de la vía TGF-β/Activin/Nodal, y los SMAD1, SMAD5 y SMAD8 de la vía de señalización de la proteína morfogénica ósea (BMP).
- R-SMADs are receptor-regulated SMADs. SMADs are transcription factors that transduce extracellular TGF-β superfamily ligand signaling from cell membrane bound TGF-β receptors into the nucleus where they activate transcription TGF-β target genes. R-SMADS are directly phosphorylated on their c-terminus by type 1 TGF-β receptors through their intracellular kinase domain, leading to r-SMAD activation. R-SMADS include SMAD2 and SMAD3 from the TGF-β/Activin/Nodal branch, and SMAD1, SMAD5 and SMAD8 from the BMP/GDP branch of TGF-β signaling. In response to signals by the TGF-β superfamily of ligands these proteins associate with receptor kinases and are phosphorylated at an SSXS motif at their extreme C-terminus. These proteins then typically bind to the common mediator Smad or co-SMAD SMAD4. Smad complexes then accumulate in the cell nucleus where they regulate transcription of specific target genes:
* SMAD2 and SMAD3 are activated in response to TGF-β/Activin or Nodal signals.
* SMAD1, SMAD5 and SMAD8 (also known as SMAD9) are activated in response to BMPs bone morphogenetic protein or GDP signals. SMAD6 and SMAD7 may be referred to as I-SMADs (inhibitory SMADS), which form trimers with R-SMADS and block their ability to induce gene transcription by competing with R-SMADs for receptor binding and by marking TGF-β receptors for degradation.
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