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<StructureSection load='6e3k' size='340' side='right'caption='[[6e3k]], [[Resolution|resolution]] 3.25&Aring;' scene=''>
<StructureSection load='6e3k' size='340' side='right'caption='[[6e3k]], [[Resolution|resolution]] 3.25&Aring;' scene=''>
== Structural highlights ==
== Structural highlights ==
<table><tr><td colspan='2'>[[6e3k]] is a 6 chain structure with sequence from [http://en.wikipedia.org/wiki/Human Human]. Full crystallographic information is available from [http://oca.weizmann.ac.il/oca-bin/ocashort?id=6E3K OCA]. For a <b>guided tour on the structure components</b> use [http://oca.weizmann.ac.il/oca-docs/fgij/fg.htm?mol=6E3K FirstGlance]. <br>
<table><tr><td colspan='2'>[[6e3k]] is a 6 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=6E3K OCA]. For a <b>guided tour on the structure components</b> use [https://proteopedia.org/fgij/fg.htm?mol=6E3K FirstGlance]. <br>
</td></tr><tr id='ligand'><td class="sblockLbl"><b>[[Ligand|Ligands:]]</b></td><td class="sblockDat"><scene name='pdbligand=BMA:BETA-D-MANNOSE'>BMA</scene>, <scene name='pdbligand=CYS:CYSTEINE'>CYS</scene>, <scene name='pdbligand=EDO:1,2-ETHANEDIOL'>EDO</scene>, <scene name='pdbligand=MAN:ALPHA-D-MANNOSE'>MAN</scene>, <scene name='pdbligand=NAG:N-ACETYL-D-GLUCOSAMINE'>NAG</scene></td></tr>
</td></tr><tr id='method'><td class="sblockLbl"><b>[[Empirical_models|Method:]]</b></td><td class="sblockDat" id="methodDat">X-ray diffraction, [[Resolution|Resolution]] 3.25&#8491;</td></tr>
<tr id='related'><td class="sblockLbl"><b>[[Related_structure|Related:]]</b></td><td class="sblockDat">[[6e3l|6e3l]]</td></tr>
<tr id='ligand'><td class="sblockLbl"><b>[[Ligand|Ligands:]]</b></td><td class="sblockDat" id="ligandDat"><scene name='pdbligand=BMA:BETA-D-MANNOSE'>BMA</scene>, <scene name='pdbligand=CYS:CYSTEINE'>CYS</scene>, <scene name='pdbligand=EDO:1,2-ETHANEDIOL'>EDO</scene>, <scene name='pdbligand=MAN:ALPHA-D-MANNOSE'>MAN</scene>, <scene name='pdbligand=NAG:N-ACETYL-D-GLUCOSAMINE'>NAG</scene></td></tr>
<tr id='gene'><td class="sblockLbl"><b>[[Gene|Gene:]]</b></td><td class="sblockDat">IFNG ([http://www.ncbi.nlm.nih.gov/Taxonomy/Browser/wwwtax.cgi?mode=Info&srchmode=5&id=9606 HUMAN]), IFNGR1 ([http://www.ncbi.nlm.nih.gov/Taxonomy/Browser/wwwtax.cgi?mode=Info&srchmode=5&id=9606 HUMAN]), IFNGR2, IFNGT1 ([http://www.ncbi.nlm.nih.gov/Taxonomy/Browser/wwwtax.cgi?mode=Info&srchmode=5&id=9606 HUMAN])</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=6e3k FirstGlance], [http://oca.weizmann.ac.il/oca-bin/ocaids?id=6e3k OCA], [https://pdbe.org/6e3k PDBe], [https://www.rcsb.org/pdb/explore.do?structureId=6e3k RCSB], [https://www.ebi.ac.uk/pdbsum/6e3k PDBsum], [https://prosat.h-its.org/prosat/prosatexe?pdbcode=6e3k ProSAT]</span></td></tr>
<tr id='resources'><td class="sblockLbl"><b>Resources:</b></td><td class="sblockDat"><span class='plainlinks'>[http://oca.weizmann.ac.il/oca-docs/fgij/fg.htm?mol=6e3k FirstGlance], [http://oca.weizmann.ac.il/oca-bin/ocaids?id=6e3k OCA], [http://pdbe.org/6e3k PDBe], [http://www.rcsb.org/pdb/explore.do?structureId=6e3k RCSB], [http://www.ebi.ac.uk/pdbsum/6e3k PDBsum], [http://prosat.h-its.org/prosat/prosatexe?pdbcode=6e3k ProSAT]</span></td></tr>
</table>
</table>
== Disease ==
== Disease ==
[[http://www.uniprot.org/uniprot/IFNG_HUMAN IFNG_HUMAN]] In Caucasians, genetic variation in IFNG is associated with the risk of aplastic anemia (AA) [MIM:[http://omim.org/entry/609135 609135]]. AA is a rare disease in which the reduction of the circulating blood cells results from damage to the stem cell pool in bone marrow. In most patients, the stem cell lesion is caused by an autoimmune attack. T-lymphocytes, activated by an endogenous or exogenous, and most often unknown antigenic stimulus, secrete cytokines, including IFN-gamma, which would in turn be able to suppress hematopoiesis. [[http://www.uniprot.org/uniprot/INGR2_HUMAN INGR2_HUMAN]] Autosomal recessive mendelian susceptibility to mycobacterial diseases due to partial IFNgammaR2 deficiency;Autosomal dominant mendelian susceptibility to mycobacterial diseases due to partial IFNgammaR2 deficiency;Mendelian susceptibility to mycobacterial diseases due to complete IFNgammaR2 deficiency. The disease is caused by mutations affecting the gene represented in this entry. [[http://www.uniprot.org/uniprot/INGR1_HUMAN INGR1_HUMAN]] Defects in IFNGR1 are a cause of Mendelian susceptibility to mycobacterial disease (MSMD) [MIM:[http://omim.org/entry/209950 209950]]; also known as familial disseminated atypical mycobacterial infection. This rare condition confers predisposition to illness caused by moderately virulent mycobacterial species, such as Bacillus Calmette-Guerin (BCG) vaccine and environmental non-tuberculous mycobacteria, and by the more virulent Mycobacterium tuberculosis. Other microorganisms rarely cause severe clinical disease in individuals with susceptibility to mycobacterial infections, with the exception of Salmonella which infects less than 50% of these individuals. The pathogenic mechanism underlying MSMD is the impairment of interferon-gamma mediated immunity whose severity determines the clinical outcome. Some patients die of overwhelming mycobacterial disease with lepromatous-like lesions in early childhood, whereas others develop, later in life, disseminated but curable infections with tuberculoid granulomas. MSMD is a genetically heterogeneous disease with autosomal recessive, autosomal dominant or X-linked inheritance.<ref>PMID:9389728</ref> <ref>PMID:10811850</ref> 
[https://www.uniprot.org/uniprot/IFNG_HUMAN IFNG_HUMAN] In Caucasians, genetic variation in IFNG is associated with the risk of aplastic anemia (AA) [MIM:[https://omim.org/entry/609135 609135]. AA is a rare disease in which the reduction of the circulating blood cells results from damage to the stem cell pool in bone marrow. In most patients, the stem cell lesion is caused by an autoimmune attack. T-lymphocytes, activated by an endogenous or exogenous, and most often unknown antigenic stimulus, secrete cytokines, including IFN-gamma, which would in turn be able to suppress hematopoiesis.
== Function ==
== Function ==
[[http://www.uniprot.org/uniprot/IFNG_HUMAN IFNG_HUMAN]] Produced by lymphocytes activated by specific antigens or mitogens. IFN-gamma, in addition to having antiviral activity, has important immunoregulatory functions. It is a potent activator of macrophages, it has antiproliferative effects on transformed cells and it can potentiate the antiviral and antitumor effects of the type I interferons. [[http://www.uniprot.org/uniprot/INGR2_HUMAN INGR2_HUMAN]] Associates with IFNGR1 to form a receptor for the cytokine interferon gamma (IFNG) (PubMed:8124716, PubMed:7673114,PubMed:7615558). Ligand binding stimulates activation of the JAK/STAT signaling pathway (PubMed:8124716, PubMed:7673114, PubMed:15356148). Required for signal transduction in contrast to other receptor subunit responsible for ligand binding (PubMed:7673114).<ref>PMID:15356148</ref> <ref>PMID:7615558</ref> <ref>PMID:7673114</ref> <ref>PMID:8124716</ref>  [[http://www.uniprot.org/uniprot/INGR1_HUMAN INGR1_HUMAN]] Receptor for interferon gamma. Two receptors bind one interferon gamma dimer.  
[https://www.uniprot.org/uniprot/IFNG_HUMAN IFNG_HUMAN] Produced by lymphocytes activated by specific antigens or mitogens. IFN-gamma, in addition to having antiviral activity, has important immunoregulatory functions. It is a potent activator of macrophages, it has antiproliferative effects on transformed cells and it can potentiate the antiviral and antitumor effects of the type I interferons.
<div style="background-color:#fffaf0;">
<div style="background-color:#fffaf0;">
== Publication Abstract from PubMed ==
== Publication Abstract from PubMed ==
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</div>
</div>
<div class="pdbe-citations 6e3k" style="background-color:#fffaf0;"></div>
<div class="pdbe-citations 6e3k" style="background-color:#fffaf0;"></div>
==See Also==
*[[Interferon 3D structures|Interferon 3D structures]]
*[[Interferon receptor 3D structures|Interferon receptor 3D structures]]
== References ==
== References ==
<references/>
<references/>
__TOC__
__TOC__
</StructureSection>
</StructureSection>
[[Category: Human]]
[[Category: Homo sapiens]]
[[Category: Large Structures]]
[[Category: Large Structures]]
[[Category: Garcia, K C]]
[[Category: Garcia KC]]
[[Category: Jude, K M]]
[[Category: Jude KM]]
[[Category: Mendoza, J L]]
[[Category: Mendoza JL]]
[[Category: Cytokine]]
[[Category: Cytokine receptor]]
[[Category: Protein complex]]
[[Category: Protein engineering]]

Latest revision as of 06:18, 11 October 2023

Interferon gamma signalling complex with IFNGR1 and IFNGR2

6e3k, resolution 3.25Å

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