Disruption of FOXP3-EZH2 Interaction Represents a Pathobiological Mechanism in Intestinal Inflammation.
Cell Mol Gastroenterol Hepatol
; 7(1): 55-71, 2019.
Article
en En
| MEDLINE
| ID: mdl-30510991
Palabras clave
C232, cysteine 232; CD, Crohn's disease; ChIP, chromatin-immunoprecipitation; Crohn's Disease; EED, embryonic ectoderm development; EZH2, enhancer of zeste homolog 2; Epigenetics; FCS, fetal calf serum; FOXP3, forkhead domain-containing X-chromosomeencoded protein; H3K27me3, trimethylated histone H3 at lysine 27; IBD, inflammatory bowel disease; IL, interleukin; IPEX, immune dysregulation, polyendocrinopathy, enteropathy, X-linked; JAK, Janus kinase; LZ, leucine zipper; PBMC, peripheral blood mononuclear cell; PBS, phosphate-buffered saline; PLA, proximity ligation assay; PMA, phorbol 12-myristate 13-acetate; PRC2, polycomb repressive complex 2; Proinflammatory Cytokine; Regulatory T Cells; STAT, signal transducer and activator of transcription; SUZ12, suppressor of zeste; Th, T helper; Treg, regulatory T cell; WT, wild-type; co-IP, co-immunoprecipitation
Texto completo:
1
Colección:
01-internacional
Base de datos:
MEDLINE
Asunto principal:
Factores de Transcripción Forkhead
/
Proteína Potenciadora del Homólogo Zeste 2
/
Inflamación
/
Intestinos
Límite:
Adult
/
Animals
/
Female
/
Humans
/
Male
/
Middle aged
Idioma:
En
Revista:
Cell Mol Gastroenterol Hepatol
Año:
2019
Tipo del documento:
Article