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Development of Inhibitors of Protein-protein Interactions through REPLACE: Application to the Design and Development Non-ATP Competitive CDK Inhibitors
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Un nuevo motivo regulador en el control del ciclo celular que causa la inhibición específica de la ciclina D/CDK4
M Serrano1, G J Hannon, D Beach
1Howard Hughes Medical Institute, Cold Spring Harbor Laboratory, New York 11724.
Nature
|December 16, 1993
Resumen
Una proteína recientemente identificada, p16, se une a la cinasa dependiente de ciclina 4 (CDK4) e inhibe su actividad. Este descubrimiento revela un nuevo circuito de retroalimentación reguladora que controla la división y la proliferación celular.
Área de la Ciencia:
- Biología celular Biología celular.
- Biología Molecular Biología Molecular
- La bioquímica es la bioquímica.
Sus antecedentes:
- La división celular eucariota está regulada por las cinasas dependientes de ciclina (CDK).
- Las ciclinas CDK4 y tipo D controlan la proliferación celular durante la fase G1.
- CDK4 forma complejos con las ciclinas, el antígeno nuclear celular proliferante y p21.
Objetivo del estudio:
- Para aislar y caracterizar la proteína p16 humana.
- Investigar la interacción entre p16 y CDK4.
- Para determinar el efecto de p16 en la actividad de la enzima CDK4/ciclina D.
Principales métodos:
- Aislamiento del ADN complementario p16 humano.
- Ensayos bioquímicos para estudiar la unión a proteínas y la inhibición de enzimas.
Principales resultados:
- Se aisló con éxito el ADNc p16 humano.
- Se demostró que p16 se une a la CDK4.
- p16 inhibe la actividad catalítica de las enzimas CDK4/ciclina D.
Conclusiones:
- p16 actúa como un inhibidor de la actividad de CDK4/ciclina D.
- p16 está involucrado en un circuito de retroalimentación reguladora con CDK4, ciclinas tipo D y la proteína del retinoblastoma.
- Esta interacción es particularmente relevante en las células que carecen de la proteína funcional del retinoblastoma.
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