Video Experimental Relacionado
Updated: Mar 1, 2026
06:00
Through the Looking Glass: Time-lapse Microscopy and Longitudinal Tracking of Single Cells to Study Anti-cancer Therapeutics
Published on: May 14, 2016
11.6K
El decaimiento endonucleolítico mediado por Tudor-SN de los microARN de las células humanas promueve la transición de
Reyad A Elbarbary1,2, Keita Miyoshi1,2, Jason R Myers3
1Department of Biochemistry and Biophysics, School of Medicine and Dentistry, University of Rochester, Rochester, NY 14642, USA.
Science (New York, N.Y.)
|May 27, 2017
Resumen
La endonucleasa Tudor-SN (TSN) degrada los microARN funcionales (miRNA) en las células humanas. La inhibición de la TSN detiene la progresión del ciclo celular, lo que sugiere que la TSN es un objetivo para inhibir la proliferación celular patológica.
Área de la Ciencia:
- Biología molecular
- Regulación genética
- La bioquímica
Sus antecedentes:
- Los microARN (miRNA) son reguladores cruciales de la expresión génica.
- Los mecanismos de descomposición del miRNA maduro se comprenden menos que la biogénesis del miRNA.
- Tudor-SN (TSN) es una endonucleasa con un papel potencial en la degradación del miRNA.
Objetivo del estudio:
- Investigar el papel de Tudor-SN (TSN) en la descomposición de los microARN maduros (miRNA).
- Para aclarar el mecanismo por el cual TSN media la desintegración de miRNA.
- Evaluar el impacto de la inhibición de la desintegración del miARN mediada por TSN en la progresión del ciclo celular.
Principales métodos:
- Ensayos de degradación in vitro utilizando TSN recombinante en miARN libres de proteínas y cargados con Argonaute 2.
- Secuenciación de microARN para identificar objetivos celulares de descomposición mediada por TSN.
- CRISPR-Cas9 elimina la TSN para inhibir su actividad en las células humanas.
Principales resultados:
- La TSN inicia directamente la descomposición del miRNA a través de la escisión endonucleolítica en los dinucleótidos CA y UA.
- La escisión se produce preferentemente en sitios con más de cinco nucleótidos de los extremos del miARN.
- La inhibición de TSN por el knockout de CRISPR-Cas9 condujo a la detención del ciclo celular en la transición de fase G1 a S debido a la regulación al alza del miRNA.
Conclusiones:
- TSN es una endonucleasa clave responsable de la descomposición de los miRNA funcionales en las células humanas.
- La desintegración del miRNA mediada por TSN sigue reglas específicas de escisión.
- Dirigirse a la actividad de la nucleasa TSN presenta una estrategia terapéutica potencial para inhibir la proliferación celular patológica.
Más Videos Relacionados
08:33Combining Mitotic Cell Synchronization and High Resolution Confocal Microscopy to Study the Role of Multifunctional Cell Cycle Proteins During Mitosis
Published on: December 5, 2017
15.0K
07:03Determining Genome-wide Transcript Decay Rates in Proliferating and Quiescent Human Fibroblasts
Published on: January 2, 2018
6.6K
Videos de Conceptos Relacionados
01:23Negative Regulator Molecules
38.7K
Positive regulators allow a cell to advance through cell cycle checkpoints. Negative regulators have an equally important role as they terminate a cell’s progression through the cell cycle—or pause it—until the cell meets specific criteria.
38.7K
02:34Inhibition of Cdk Activity
6.1K
The orderly progression of the cell cycle depends on the activation of Cdk protein by binding to its cyclin partner. However, the cell cycle must be restricted when undergoing abnormal changes. Most cancers correlate to the deregulated cell cycle, and since Cdks are a central component of the cell cycle, Cdk inhibitors are extensively studied to develop anticancer agents. For instance, cyclin D associates with several Cdks, such as Cdk 4/6, to form an active complex. The cyclin D-Cdk4/6 complex...
6.1K
01:22MicroRNAs
4.2K
MicroRNA (miRNA) are short, regulatory RNA transcribed from introns (non-coding regions of a gene) or intergenic regions (stretches of DNA present between genes). Several processing steps are required to form biologically active, mature miRNA. The initial transcript, called primary miRNA (pri-mRNA), base-pairs with itself, forming a stem-loop structure. Within the nucleus, an endonuclease enzyme, called Drosha, shortens the stem-loop structure into hairpin-shaped pre-miRNA. After the pre-miRNA...
4.2K
01:22MicroRNAs
24.4K
MicroRNA (miRNA) are short, regulatory RNA transcribed from introns—non-coding regions of a gene—or intergenic regions—stretches of DNA present between genes. Several processing steps are required to form biologically active, mature miRNA. The initial transcript, called primary miRNA (pri-mRNA), base-pairs with itself forming a stem-loop structure. Within the nucleus, an endonuclease enzyme, called Drosha, shortens the stem-loop structure into hairpin-shaped pre-miRNA. After...
24.4K
02:15Replicative Cell Senescence
4.5K
Replicative cell senescence is a property of cells that allows them to divide a finite number of times throughout the organism's lifespan while preventing excessive proliferation. Replicative senescence is associated with the gradual loss of the telomere — short, repetitive DNA sequences found at the end of the chromosomes. Telomeres are bound by a group of proteins to form a protective cap on the ends of chromosomes. Embryonic stem cells express telomerase — an enzyme that adds...
4.5K
02:15M-Cdk Drives Transition Into Mitosis
6.7K
Checkpoints throughout the cell cycle serve as safeguards and gatekeepers, allowing the cell cycle to progress in favorable conditions and slow or halt it in problematic ones. This regulation is known as the cell cycle control system.
Cyclin-dependent kinases, or Cdks, work in concert with cyclins to control cell cycle transitions. M-Cdk, a complex of Cdk1 bound to M cyclin, is a well-known example of this coordinated control that drives the transition from the G2 to the M phase.
M cyclin...
Cyclin-dependent kinases, or Cdks, work in concert with cyclins to control cell cycle transitions. M-Cdk, a complex of Cdk1 bound to M cyclin, is a well-known example of this coordinated control that drives the transition from the G2 to the M phase.
M cyclin...
6.7K