TY - JOUR
TI - Inflammation and tissue homeostasis: the NF-κB system in physiology and malignant progression
AU - Lambrou, G.I.
AU - Hatziagapiou, K.
AU - Vlahopoulos, S.
JO - Current Molecular Biology Reports
PY - 2020
VL - 47
TODO - 5
SP - 4047-4063
PB - Springer-Verlag
SN - 2198-6428
TODO - 10.1007/s11033-020-05410-w
TODO - cytokine;  hormone;  immunoglobulin enhancer binding protein;  interleukin 1beta;  interleukin 6;  mitogen activated protein kinase;  Myc protein;  STAT3 protein;  immunoglobulin enhancer binding protein, antiapoptosis;  cancer growth;  carcinogenesis;  cell stress;  cell survival;  disease association;  gene expression;  homeostasis;  human;  immune system;  inflammation;  innate immunity;  malignant neoplasm;  nonhuman;  oxidative stress;  physiology;  proapoptotic activity;  protein function;  Review;  stress;  tissue stress;  animal;  gene expression regulation;  genetics;  homeostasis;  inflammation;  metabolism, Animals;  Gene Expression;  Gene Expression Regulation;  Homeostasis;  Humans;  Inflammation;  NF-kappa B
TODO - Disruption of tissue function activates cellular stress which triggers a number of mechanisms that protect the tissue from further damage. These mechanisms involve a number of homeostatic modules, which are regulated at the level of gene expression by the transactivator NF-κB. This transcription factor shifts between activation and repression of discrete, cell-dependent gene expression clusters. Some of its target genes provide feedback to NF-κB itself, thereby strengthening the inflammatory response of the tissue and later terminating inflammation to facilitate restoration of tissue homeostasis. Disruption of key feedback modules for NF-κB in certain cell types facilitates the survival of clones with genomic aberrations, and protects them from being recognized and eliminated by the immune system, to enable thereby carcinogenesis. © 2020, Springer Nature B.V.
ER -