5k98: Difference between revisions
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==Structure of HipA-HipB-O2-O3 complex== | |||
<StructureSection load='5k98' size='340' side='right'caption='[[5k98]], [[Resolution|resolution]] 3.99Å' scene=''> | |||
== Structural highlights == | |||
<table><tr><td colspan='2'>[[5k98]] is a 6 chain structure with sequence from [https://en.wikipedia.org/wiki/Escherichia_coli_K-12 Escherichia coli K-12], [https://en.wikipedia.org/wiki/Escherichia_coli_MP020980.2 Escherichia coli MP020980.2] and [https://en.wikipedia.org/wiki/Synthetic_construct Synthetic construct]. Full crystallographic information is available from [http://oca.weizmann.ac.il/oca-bin/ocashort?id=5K98 OCA]. For a <b>guided tour on the structure components</b> use [https://proteopedia.org/fgij/fg.htm?mol=5K98 FirstGlance]. <br> | |||
</td></tr><tr id='method'><td class="sblockLbl"><b>[[Empirical_models|Method:]]</b></td><td class="sblockDat" id="methodDat">X-ray diffraction, [[Resolution|Resolution]] 3.99Å</td></tr> | |||
<tr id='resources'><td class="sblockLbl"><b>Resources:</b></td><td class="sblockDat"><span class='plainlinks'>[https://proteopedia.org/fgij/fg.htm?mol=5k98 FirstGlance], [http://oca.weizmann.ac.il/oca-bin/ocaids?id=5k98 OCA], [https://pdbe.org/5k98 PDBe], [https://www.rcsb.org/pdb/explore.do?structureId=5k98 RCSB], [https://www.ebi.ac.uk/pdbsum/5k98 PDBsum], [https://prosat.h-its.org/prosat/prosatexe?pdbcode=5k98 ProSAT]</span></td></tr> | |||
</table> | |||
== Function == | |||
[https://www.uniprot.org/uniprot/HIPA_ECOLI HIPA_ECOLI] Toxic component of a toxin-antitoxin (TA) module. Autophosphorylates (Ser-150) and phosphorylates EF-Tu in vitro (on 'Thr-383'), may act on other proteins as well. The hipA7 mutation leads to increased generation of persister cells, cells that survive antibiotic treatment probably by entering into a dormant state. Wild-type cells produce persisters at a frequency of 10-6 to 10-5 whereas mutant hipA7 cells produce persisters at a frequency of 10-2. Generation of persister cells requires (p)ppGpp as cells lacking relA or relA/spoT generate fewer or no persister cells respectively compared to hipA7. Low level expression of HipA causes cell filamentation and depending on the protein level is toxic enough to reduce cell growth or even kill cells. Expression of wild-type HipA also leads to high antibiotic tolerance of the survivor cells. The toxic effect of HipA is neutralized by its cognate antitoxin HipB. With HipB acts as a corepressor for transcription of the hipBA promoter.<ref>PMID:17041039</ref> <ref>PMID:6348026</ref> <ref>PMID:8021189</ref> <ref>PMID:14622409</ref> <ref>PMID:19150849</ref> | |||
==See Also== | |||
*[[Serine/threonine protein kinase 3D structures|Serine/threonine protein kinase 3D structures]] | |||
== References == | |||
[[Category: | <references/> | ||
[[Category: Schumacher | __TOC__ | ||
</StructureSection> | |||
[[Category: Escherichia coli K-12]] | |||
[[Category: Escherichia coli MP020980 2]] | |||
[[Category: Large Structures]] | |||
[[Category: Synthetic construct]] | |||
[[Category: Schumacher M]] | |||
Latest revision as of 16:04, 1 March 2024
Structure of HipA-HipB-O2-O3 complexStructure of HipA-HipB-O2-O3 complex
Structural highlights
FunctionHIPA_ECOLI Toxic component of a toxin-antitoxin (TA) module. Autophosphorylates (Ser-150) and phosphorylates EF-Tu in vitro (on 'Thr-383'), may act on other proteins as well. The hipA7 mutation leads to increased generation of persister cells, cells that survive antibiotic treatment probably by entering into a dormant state. Wild-type cells produce persisters at a frequency of 10-6 to 10-5 whereas mutant hipA7 cells produce persisters at a frequency of 10-2. Generation of persister cells requires (p)ppGpp as cells lacking relA or relA/spoT generate fewer or no persister cells respectively compared to hipA7. Low level expression of HipA causes cell filamentation and depending on the protein level is toxic enough to reduce cell growth or even kill cells. Expression of wild-type HipA also leads to high antibiotic tolerance of the survivor cells. The toxic effect of HipA is neutralized by its cognate antitoxin HipB. With HipB acts as a corepressor for transcription of the hipBA promoter.[1] [2] [3] [4] [5] See AlsoReferences
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