Survivin modulatory role in autoimmune and autoinflammatory diseases.
DNA damage
autoimmune disease
biomarker
epigenetic
inflammation
Journal
Journal of cellular physiology
ISSN: 1097-4652
Titre abrégé: J Cell Physiol
Pays: United States
ID NLM: 0050222
Informations de publication
Date de publication:
11 2019
11 2019
Historique:
received:
23
01
2019
revised:
06
04
2019
accepted:
11
04
2019
pubmed:
26
4
2019
medline:
30
5
2020
entrez:
26
4
2019
Statut:
ppublish
Résumé
Baculoviral IAP repeat containing 5 (BIRC5) gene encodes the important protein as survivin, a multifunctional protein, which is involved in cellular and molecular networks, progression of cell cycle, homeostasis, developmental morphogenesis, and apoptosis. The proximal BIRC5 promoter possesses specific binding sites for key transcription factors such as nuclear factor κB and signal transducer and activator of transcription 3. Upregulation of survivin exacerbates the autoimmune diseases (AIDs) including multiple sclerosis and myasthenia gravis by reducing the activity threshold of survivin-specific cytotoxic T cells. DNA damage along with upregulation or downregulation of survivin have been demonstrated in initiation and pathogenesis of cancers and AIDs. However, detailed mechanism of survivin function in pathogenesis of AIDs is not well understood. This review focuses on the structure, specificity, regulation, and function of survivin in physiologic conditions and pathogenesis of AIDs.
Substances chimiques
BIRC5 protein, human
0
NF-kappa B
0
STAT3 Transcription Factor
0
STAT3 protein, human
0
Survivin
0
Types de publication
Journal Article
Research Support, Non-U.S. Gov't
Langues
eng
Sous-ensembles de citation
IM
Pagination
19440-19450Informations de copyright
© 2019 Wiley Periodicals, Inc.