LEADER 04192nam 2200889z- 450 001 9910674020103321 005 20231214132829.0 035 $a(CKB)5400000000042053 035 $a(oapen)https://directory.doabooks.org/handle/20.500.12854/76444 035 $a(EXLCZ)995400000000042053 100 $a20202201d2021 |y 0 101 0 $aeng 135 $aurmn|---annan 181 $ctxt$2rdacontent 182 $cc$2rdamedia 183 $acr$2rdacarrier 200 10$aToxin-Antitoxin Systems in Pathogenic Bacteria 210 $aBasel, Switzerland$cMDPI - Multidisciplinary Digital Publishing Institute$d2021 215 $a1 electronic resource (170 p.) 311 $a3-0365-0674-8 311 $a3-0365-0675-6 330 $aBacterial toxin?antitoxin (TA) systems, which are ubiquitously present in bacterial genomes, are not essential for normal cell proliferation. The TA systems regulate fundamental cellular processes, facilitate survival under stress conditions, have essential roles in virulence and represent potential therapeutic targets. These genetic TA loci are also shown to be involved in the maintenance of successful multidrug-resistant mobile genetic elements. The TA systems are classified as types I to VI, according to the nature of the antitoxin and to the mode of toxin inhibition. Type II TA systems encode a labile antitoxin and its stable toxin; degradation of the antitoxin renders a free toxin, which is bacteriostatic by nature. A free toxin generates a reversible state with low metabolic activity (quiescence) by affecting important functions of bacterial cells such as transcription, translation, DNA replication, replication and cell-wall synthesis, biofilm formation, phage predation, the regulation of nucleotide pool, etc., whereas antitoxins are toxin inhibitors. Under stress conditions, the TA systems might form networks. To understand the basis of the unique response of TA systems to stress, the prime causes of the emergence of drug-resistant strains, and their contribution to therapy failure and the development of chronic and recurrent infections, must be known in order to grasp how TA systems contribute to the mechanisms of phenotypic heterogeneity and pathogenesis that will enable the rational development of new treatments for infections caused by pathogens. 606 $aMedicine$2bicssc 610 $atuberculosis 610 $atoxin-antitoxin systems 610 $abacterial cell death 610 $aNAD+ 610 $astress-response 610 $atoxin-antitoxin system 610 $amazF 610 $atype II 610 $atoxin 610 $amRNA interferase 610 $aX-ray crystallography 610 $acognate interactions 610 $across-interactions 610 $amolecular insulation 610 $aantitoxin 610 $aTA systems 610 $aaddiction 610 $aanti-addiction 610 $atype I toxin-antitoxin system 610 $asmall protein toxin structure 610 $aFst/Ldr family 610 $atoxin-antitoxin 610 $aM. tuberculosis 610 $abacteria 610 $apathogenesis 610 $aprotein-protein interactions 610 $across-talk 610 $aprotein interface 610 $atolerance 610 $apersistence 610 $across-resistance 610 $atoxin-antitoxin system 610 $aPemI/PemK 610 $aKlebsiella pneumoniae 610 $atoxin-antitoxin systems 610 $atoxin activation 610 $aantibacterial agents 610 $abacterial persistence 610 $aStenotrophomonas maltophilia 610 $aopportunistic pathogen 610 $aclinical origin 610 $aenvironmental origin 610 $abiofilm 610 $aantibiotic resistance 610 $acell wall inhibition 610 $anucleotide hydrolysis 610 $auridine diphosphate-N-acetylglucosamine 615 7$aMedicine 700 $aAlonso$b Juan Carlos$4edt$01339342 702 $aAlonso$b Juan Carlos$4oth 906 $aBOOK 912 $a9910674020103321 996 $aToxin-Antitoxin Systems in Pathogenic Bacteria$93060081 997 $aUNINA