Type I interferons induce proteins susceptible to act as thyroid receptor (TR) corepressors and to signal the TR for destruction by the proteasome: Possible etiology for unexplained chronic fatigue

Medical Hypotheses

Volumn 60, Issue 2, 2003, Pages 175-180

  Englebienne, P ^a   Verhas, M ^a   Herst, C V ^a   De Meirleir, K ^a  

^a UNIVERSITÉ LIBRE DE BRUXELLES   (Belgium)

Author keywords

[No Author keywords available]

Indexed keywords

2',5' OLIGOADENYLATE SYNTHETASE; ALPHA INTERFERON; BETA INTERFERON; HORMONE BINDING PROTEIN; REPRESSOR PROTEIN; THYROID HORMONE RECEPTOR; THYROID HORMONE RECEPTOR INTERACTING PROTEIN 14; UBIQUITIN; UNCLASSIFIED DRUG;

AMINO ACID SEQUENCE; ARTICLE; CARBOXY TERMINAL SEQUENCE; CHRONIC FATIGUE SYNDROME; HORMONAL REGULATION; HORMONE RECEPTOR INTERACTION; HUMAN; HYPOTHESIS; HYPOTHYROIDISM; INTERFERON PRODUCTION; MOLECULAR MECHANICS; OBSERVATION; PHYSICAL DISEASE; PRIORITY JOURNAL; PROTEIN DOMAIN; PROTEIN EXPRESSION; PROTEIN INDUCTION; RECEPTOR BINDING; SEQUENCE ANALYSIS; SIGNAL TRANSDUCTION; THYROID FUNCTION; THYROID HORMONE RELEASE; TRANSACTIVATION;

EID: 0037320589     PISSN: 03069877     EISSN: None     Source Type: Journal    
DOI: 10.1016/S0306-9877(02)00353-5     Document Type: Article

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