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Transcription Factors

Tissue-specific transcription factors contribute to diverse cellular functions in mammals. For example, the gene for beta globin, a major component of hemoglobin, is present in all cells of the body. However, it is only expressed in red blood cells because the transcription factors that can bind to the promoter sequences of the beta globin gene are only expressed in these cells. Tissue-specific transcription factors also ensure that mutations in these factors may impair only the function of...
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Gene transcription is regulated by the synergistic action of several proteins that form a complex at a gene regulatory site. This is observed in eukaryotes, where the regulation of gene expression is a complex process. Regulatory proteins in eukaryotes can broadly be classified into two types – regulators that bind directly to specific DNA sequences and co-regulators that associate with regulatory proteins but cannot directly bind to the DNA. These co-regulators are further divided into...
NF-κB-dependent Signaling Pathway02:26

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The transcription factor NF-κB was discovered in 1986 in the lab of Nobel laureate Professor David Baltimore, for its interaction with the immunoglobulin light chain enhancer in B-cells. After more than three decades of study, it is now evident that NF-κB regulates the expression of over 100 genes. Most of these genes play an essential role in the innate and adaptive immune responses as well as the inflammatory responses of animals.
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Tissue-specific transcription factors contribute to diverse cellular functions in mammals. For example, the gene for beta globin, a major component of hemoglobin, is present in all cells of the body. However, it is only expressed in red blood cells because the transcription factors that can bind to the promoter sequences of the beta globin gene are only expressed in these cells. Tissue-specific transcription factors also ensure that mutations in these factors may impair only the function of...
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In Vitro Differentiation of Human CD4+FOXP3+ Induced Regulatory T Cells (iTregs) from Naïve CD4+ T Cells Using a TGF-β-containing Protocol
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Published on: December 30, 2016

FOXP3 controla la función reguladora de las células T a través de la cooperación con NFAT.

Yongqing Wu1, Madhuri Borde, Vigo Heissmeyer

  • 1Department of Chemistry and Biochemistry, University of Colorado at Boulder, Boulder, CO 80309, USA.

Cell
|July 29, 2006
PubMed
Resumen

Las células T reguladoras (Tregs) usan un complejo NFAT-FOXP3 único para suprimir las respuestas inmunes. Esta interacción cambia los programas de activación de las células T, permitiendo las funciones supresoras de Treg y el tratamiento de la diabetes autoinmune.

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Área de la Ciencia:

  • Inmunología Inmunología.
  • Biología Molecular Biología Molecular
  • Biología Estructural Biología estructural.

Sus antecedentes:

  • El factor nuclear de las células T activadas (NFAT) es crucial para la activación de las células T.
  • NFAT suele asociarse con los factores de transcripción AP-1 para regular los genes de las células T.
  • Las células T reguladoras (Tregs) poseen funciones distintas que requieren mecanismos moleculares únicos.

Objetivo del estudio:

  • Para investigar el mecanismo molecular subyacente a la función de las células T reguladoras (Treg).
  • Para identificar los factores de transcripción que cooperan con NFAT en Tregs.
  • Para aclarar la base estructural de la interacción NFAT-FOXP3 y sus consecuencias funcionales.

Principales métodos:

  • Cristalografía de rayos X para determinar la estructura de un complejo NFAT:FOXP2:ADN.
  • Mutagenesis dirigida al sitio de FOXP3 basada en conocimientos estructurales.
  • Ensayos funcionales que miden la expresión génica (IL2, CTLA4, CD25) y la actividad supresora en un modelo de ratón.

Principales resultados:

  • Identificó un nuevo complejo cooperativo entre NFAT y FOXP3 en Tregs.
  • Reveló una extensa interfaz de interacción proteína-proteína entre NFAT y FOXP3 (usando la estructura de FOXP2).
  • Se ha demostrado que la interrupción de la interacción NFAT-FOXP3 perjudica la función Treg, incluida la represión de IL2 y la actividad supresora.

Conclusiones:

  • NFAT se asocia con FOXP3 en Tregs, distinto de su papel con AP-1 en las células T convencionales.
  • Este complejo NFAT-FOXP3 es esencial para la supresión inmune mediada por Treg.
  • Dirigirse a la interacción NFAT-FOXP3 ofrece una estrategia terapéutica potencial para las enfermedades autoinmunes.