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Bases estructurales para la señalización hormonal del FGF

Lingfeng Chen1,2, Lili Fu1,3,4, Jingchuan Sun1,5

  • 1Oujiang Laboratory (Zhejiang Lab for Regenerative Medicine, Vision, and Brain Health), School of Pharmaceutical Sciences, Wenzhou Medical University, Wenzhou, China.

Nature
|June 7, 2023
PubMed
Resumen
Este resumen es generado por máquina.

El sulfato de heparán (HS) actúa como coreceptor, permitiendo que las hormonas del factor de crecimiento de los fibroblastos (FGF) activen los receptores del FGF (FGFR) a través de la dimerización asimétrica. Este hallazgo desafía los modelos existentes y ofrece nuevos objetivos terapéuticos para las enfermedades metabólicas y el cáncer.

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Área de la Ciencia:

  • La bioquímica
  • Biología estructural
  • Endocrinología

Sus antecedentes:

  • Las hormonas del factor de crecimiento de los fibroblastos (FGF) requieren correceptores αKlotho y proteoglicanos de sulfato de heparan (HS) para la señalización metabólica.
  • El mecanismo molecular preciso de HS como coreceptor en la activación del complejo FGF-FGFR sigue siendo incompleto.

Objetivo del estudio:

  • Para aclarar la base estructural de la función coreceptor de HS en la señalización mediada por FGF23.
  • Determinar el mecanismo de dimerización y activación del receptor FGF.

Principales métodos:

  • Microscopía criolectrónica (crio-EM) para resolver las estructuras de los complejos cuaternarios FGF23-FGFR-αKlotho-HS.
  • Ensayos de complementación y heterodimerización de receptores basados en células.

Principales resultados:

  • La determinación estructural de tres complejos distintos de FGF23-FGFR-αKlotho-HS reveló un complejo ternario 1:1:1 que recluta un FGFR secundario a través de HS.
  • Una sola cadena HS facilita la dimerización y activación asimétrica de FGFR, un mecanismo también aplicable a la señalización paracrina de FGF.
  • Se encontró que αKlotho no participaba directamente en el reclutamiento o la dimerización de receptores secundarios.

Conclusiones:

  • El estudio invierte el modelo de dimerización simétrica de FGFR, estableciendo un mecanismo asimétrico impulsado por HS.
  • Estos hallazgos proporcionan una base estructural para el desarrollo de nuevas terapias dirigidas a la señalización de FGF en enfermedades metabólicas y cáncer.