7tqo

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Current revision (17:07, 18 October 2023) (edit) (undo)
 
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== Structural highlights ==
== Structural highlights ==
<table><tr><td colspan='2'>[[7tqo]] is a 1 chain structure with sequence from [https://en.wikipedia.org/wiki/Homo_sapiens Homo sapiens]. Full crystallographic information is available from [http://oca.weizmann.ac.il/oca-bin/ocashort?id=7TQO OCA]. For a <b>guided tour on the structure components</b> use [https://proteopedia.org/fgij/fg.htm?mol=7TQO FirstGlance]. <br>
<table><tr><td colspan='2'>[[7tqo]] is a 1 chain structure with sequence from [https://en.wikipedia.org/wiki/Homo_sapiens Homo sapiens]. Full crystallographic information is available from [http://oca.weizmann.ac.il/oca-bin/ocashort?id=7TQO OCA]. For a <b>guided tour on the structure components</b> use [https://proteopedia.org/fgij/fg.htm?mol=7TQO FirstGlance]. <br>
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</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=7tqo FirstGlance], [http://oca.weizmann.ac.il/oca-bin/ocaids?id=7tqo OCA], [https://pdbe.org/7tqo PDBe], [https://www.rcsb.org/pdb/explore.do?structureId=7tqo RCSB], [https://www.ebi.ac.uk/pdbsum/7tqo PDBsum], [https://prosat.h-its.org/prosat/prosatexe?pdbcode=7tqo ProSAT]</span></td></tr>
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</td></tr><tr id='method'><td class="sblockLbl"><b>[[Empirical_models|Method:]]</b></td><td class="sblockDat" id="methodDat">X-ray diffraction, [[Resolution|Resolution]] 1.25&#8491;</td></tr>
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<tr id='resources'><td class="sblockLbl"><b>Resources:</b></td><td class="sblockDat"><span class='plainlinks'>[https://proteopedia.org/fgij/fg.htm?mol=7tqo FirstGlance], [http://oca.weizmann.ac.il/oca-bin/ocaids?id=7tqo OCA], [https://pdbe.org/7tqo PDBe], [https://www.rcsb.org/pdb/explore.do?structureId=7tqo RCSB], [https://www.ebi.ac.uk/pdbsum/7tqo PDBsum], [https://prosat.h-its.org/prosat/prosatexe?pdbcode=7tqo ProSAT]</span></td></tr>
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</table>
== Disease ==
== Disease ==
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[[https://www.uniprot.org/uniprot/TREX1_HUMAN TREX1_HUMAN]] Retinal vasculopathy with cerebral leukoencephalopathy and systemic manifestations;Familial Chilblain lupus;Systemic lupus erythematosus;Aicardi-Goutieres syndrome. The disease is caused by variants affecting the gene represented in this entry. Disease susceptibility is associated with variants affecting the gene represented in this entry. Enhanced immune sensing of oxidized DNA may be involved in the phototoxicity experienced by SLE patients. Exposure to UV-light produces DNA oxidative damage. Oxidized DNA being a poor TREX1 substrate, it accumulates in skin, leading to enhanced auto-immune reactivity and eventually skin lesions (PubMed:23993650).<ref>PMID:23993650</ref> The disease is caused by variants affecting the gene represented in this entry. The disease is caused by variants affecting the gene represented in this entry.
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[https://www.uniprot.org/uniprot/TREX1_HUMAN TREX1_HUMAN] Retinal vasculopathy with cerebral leukoencephalopathy and systemic manifestations;Familial Chilblain lupus;Systemic lupus erythematosus;Aicardi-Goutieres syndrome. The disease is caused by variants affecting the gene represented in this entry. Disease susceptibility is associated with variants affecting the gene represented in this entry. Enhanced immune sensing of oxidized DNA may be involved in the phototoxicity experienced by SLE patients. Exposure to UV-light produces DNA oxidative damage. Oxidized DNA being a poor TREX1 substrate, it accumulates in skin, leading to enhanced auto-immune reactivity and eventually skin lesions (PubMed:23993650).<ref>PMID:23993650</ref> The disease is caused by variants affecting the gene represented in this entry. The disease is caused by variants affecting the gene represented in this entry.
== Function ==
== Function ==
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[[https://www.uniprot.org/uniprot/TREX1_HUMAN TREX1_HUMAN]] Major cellular 3'-to-5' DNA exonuclease which digests single-stranded DNA (ssDNA) and double-stranded DNA (dsDNA) with mismatched 3' termini (PubMed:10391904, PubMed:10393201, PubMed:17293595). Prevents cell-intrinsic initiation of autoimmunity (PubMed:10391904, PubMed:10393201, PubMed:17293595). Acts by metabolizing DNA fragments from endogenous retroelements, including L1, LTR and SINE elements (PubMed:10391904, PubMed:10393201, PubMed:17293595). Plays a key role in degradation of DNA fragments at cytosolic micronuclei arising from genome instability: its association with the endoplasmic reticulum membrane directs TREX1 to ruptured micronuclei, leading to micronuclear DNA degradation (PubMed:33476576). Micronuclear DNA degradation is required to limit CGAS activation and subsequent inflammation (PubMed:33476576). Unless degraded, these DNA fragments accumulate in the cytosol and activate the cGAS-STING innate immune signaling, leading to the production of type I interferon (PubMed:33476576). Prevents chronic ATM-dependent checkpoint activation, by processing ssDNA polynucleotide species arising from the processing of aberrant DNA replication intermediates (PubMed:18045533). Inefficiently degrades oxidized DNA, such as that generated upon antimicrobial reactive oxygen production or upon absorption of UV light (PubMed:23993650). During GZMA-mediated cell death, contributes to DNA damage in concert with NME1 (PubMed:16818237). NME1 nicks one strand of DNA and TREX1 removes bases from the free 3' end to enhance DNA damage and prevent DNA end reannealing and rapid repair (PubMed:16818237).<ref>PMID:10391904</ref> <ref>PMID:10393201</ref> <ref>PMID:16818237</ref> <ref>PMID:17293595</ref> <ref>PMID:18045533</ref> <ref>PMID:23993650</ref> <ref>PMID:33476576</ref>
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[https://www.uniprot.org/uniprot/TREX1_HUMAN TREX1_HUMAN] Major cellular 3'-to-5' DNA exonuclease which digests single-stranded DNA (ssDNA) and double-stranded DNA (dsDNA) with mismatched 3' termini (PubMed:10391904, PubMed:10393201, PubMed:17293595). Prevents cell-intrinsic initiation of autoimmunity (PubMed:10391904, PubMed:10393201, PubMed:17293595). Acts by metabolizing DNA fragments from endogenous retroelements, including L1, LTR and SINE elements (PubMed:10391904, PubMed:10393201, PubMed:17293595). Plays a key role in degradation of DNA fragments at cytosolic micronuclei arising from genome instability: its association with the endoplasmic reticulum membrane directs TREX1 to ruptured micronuclei, leading to micronuclear DNA degradation (PubMed:33476576). Micronuclear DNA degradation is required to limit CGAS activation and subsequent inflammation (PubMed:33476576). Unless degraded, these DNA fragments accumulate in the cytosol and activate the cGAS-STING innate immune signaling, leading to the production of type I interferon (PubMed:33476576). Prevents chronic ATM-dependent checkpoint activation, by processing ssDNA polynucleotide species arising from the processing of aberrant DNA replication intermediates (PubMed:18045533). Inefficiently degrades oxidized DNA, such as that generated upon antimicrobial reactive oxygen production or upon absorption of UV light (PubMed:23993650). During GZMA-mediated cell death, contributes to DNA damage in concert with NME1 (PubMed:16818237). NME1 nicks one strand of DNA and TREX1 removes bases from the free 3' end to enhance DNA damage and prevent DNA end reannealing and rapid repair (PubMed:16818237).<ref>PMID:10391904</ref> <ref>PMID:10393201</ref> <ref>PMID:16818237</ref> <ref>PMID:17293595</ref> <ref>PMID:18045533</ref> <ref>PMID:23993650</ref> <ref>PMID:33476576</ref>
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== Publication Abstract from PubMed ==
== Publication Abstract from PubMed ==
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<div class="pdbe-citations 7tqo" style="background-color:#fffaf0;"></div>
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==See Also==
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*[[Exonuclease 3D structures|Exonuclease 3D structures]]
== References ==
== References ==
<references/>
<references/>

Current revision

Structure of human TREX1

PDB ID 7tqo

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