Reprogramming RelA

NF- B RelA Phosphorylation Regulates RelA Acetylation†

Regulation of the RelA (p65) transactivation domain.

The RelA (p65) NF-kappaB (nuclear factor kappaB) subunit contains an extremely active C-terminal transcriptional activation domain, required for its cellular function. In the present article, we review our knowledge of this domain, its modifications and its known interacting proteins. Moreover, we discuss how analysis of its evolutionary conservation reveals distinct subdomains and conserved re...

RelA-Induced Interferon Response Negatively Regulates Proliferation

Both oncogenic and tumor-suppressor activities are attributed to the Nuclear Factor kappa B (NF-kB) pathway. Moreover, NF-kB may positively or negatively regulate proliferation. The molecular determinants of these opposing roles of NF-kB are unclear. Using primary human mammary epithelial cells (HMEC) as a model, we show that increased RelA levels and consequent increase in basal transcriptiona...

Subinhibitory Concentrations of Bacteriostatic Antibiotics Induce relA-Dependent and relA-Independent Tolerance to β-Lactams

The nucleotide (p)ppGpp is a key regulator of bacterial metabolism, growth, stress tolerance, and virulence. During amino acid starvation, the Escherichia coli (p)ppGpp synthetase RelA is activated by deacylated tRNA in the ribosomal A-site. An increase in (p)ppGpp is believed to drive the formation of antibiotic-tolerant persister cells, prompting the development of strategies to inhibit (p)pp...

Nuclear reprogramming.

There is currently particular interest in the field of nuclear reprogramming, a process by which the identity of specialised cells may be changed, typically to an embryonic-like state. Reprogramming procedures provide insight into many mechanisms of fundamental cell biology and have several promising applications, most notably in healthcare through the development of human disease models and pa...