This seems to be the case for the control of the toxA gene of suffer from cystic fibrosis

We did not observe an up-regulation of TRPV1 after UVirradiation, which appears to be in contrast to the observed hyperalgesia to heat. However, it can be assumed that any regulation is mainly based on the keratinocyte expression as these are primarily affected by the UV-C irradiation. Albeit there is evidence for local protein biosynthesis in dendrites and axons, potential expression changes of axonal mRNA would involve signal transport from the irradiated skin to the dorsal root ganglion, induction of expression changes and subsequent trafficking of mRNA back to the skin. Considering these events, TRPV1 expression changes at 6 and 24 h after irradiation would be expected too early. Also, if there were axonal mRNA alterations, these would not necessarily contribute to expression changes due to the massive dilution of RNA caused by resident or infiltrating cells. Moreover, our data do not contradict a role of TRPV1 underlying heat hyperalgesia, particularly as heat sensitization, for instance by TRPV1 phosphorylation or TRPV1 translocation in the sensory endings, obviously does not require expression changes. The ubiquitous Gram-negative bacterium Pseudomonas aeruginosa is an opportunistic human pathogen which is a frequent cause of hospital-acquired infections including ventilator associated pneumonia, and catheter infections in immuno-compromised patients. Furthermore, P. aeruginosa is an etiologic agent of ear infections and causes infections in severely burned individuals as well as in patients. The establishment of P. aeruginosa infection is accompanied by the synthesis of several extracellular and cell-associated virulence factors, amongst which is exotoxin A encoded by the toxA gene. Similar to other extracellular virulence factors such as diphtheria-, cholera- and pertussis-toxin, exotoxin A is an ADP-ribosyl transferase that decorates host elongation factor-2, leading to the cessation of protein synthesis and eventually causes cell death. Transcription regulation is the major method of gene expression control in prokaryotic cells and is modulated by proteins that interact with RNA polymerase, such as sigma factors and transcriptional regulators. The most common type of transcriptional regulators are made of two domains, one functioning as the sensor for signals, and the other a DNA binding domain. In some cases more than one protein is involved in the ALK5 Inhibitor II cost activation/ repression of transcription in response to a signal as is the case with two-component regulatory systems. Recently some prokaryotic regulatory systems have been revealed to be more complex with an increasing number of reports of three proteins involved in regulation. In E. coli about 50% of promoters are under the control of one specific regulator, while 50% of E. coli promoters are modulated by two or more transcriptional factors. Promoters involved in the construction of cell structures, i.e., flagella, pili, and fimbrae, and complex cellular processes, i.e., virulence, biofilm formation, are often controlled by multiple environmental signals and different transcription factors operate to modulate this control.