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==HUMAN MRF-2 DOMAIN, NMR, 11 STRUCTURES==
==HUMAN MRF-2 DOMAIN, NMR, 11 STRUCTURES==
<StructureSection load='1ig6' size='340' side='right' caption='[[1ig6]], [[NMR_Ensembles_of_Models | 11 NMR models]]' scene=''>
<StructureSection load='1ig6' size='340' side='right'caption='[[1ig6]]' scene=''>
== Structural highlights ==
== Structural highlights ==
<table><tr><td colspan='2'>[[1ig6]] is a 1 chain structure. This structure supersedes the now removed PDB entry [http://oca.weizmann.ac.il/oca-bin/send-pdb?obs=1&id=1bmy 1bmy]. Full experimental information is available from [http://oca.weizmann.ac.il/oca-bin/ocashort?id=1IG6 OCA]. For a <b>guided tour on the structure components</b> use [http://oca.weizmann.ac.il/oca-docs/fgij/fg.htm?mol=1IG6 FirstGlance]. <br>
<table><tr><td colspan='2'>[[1ig6]] is a 1 chain structure with sequence from [https://en.wikipedia.org/wiki/Homo_sapiens Homo sapiens]. This structure supersedes the now removed PDB entry [http://oca.weizmann.ac.il/oca-bin/send-pdb?obs=1&id=1bmy 1bmy]. Full experimental information is available from [http://oca.weizmann.ac.il/oca-bin/ocashort?id=1IG6 OCA]. For a <b>guided tour on the structure components</b> use [https://proteopedia.org/fgij/fg.htm?mol=1IG6 FirstGlance]. <br>
</td></tr><tr id='related'><td class="sblockLbl"><b>[[Related_structure|Related:]]</b></td><td class="sblockDat">[[1bmy|1bmy]]</td></tr>
</td></tr><tr id='method'><td class="sblockLbl"><b>[[Empirical_models|Method:]]</b></td><td class="sblockDat" id="methodDat">Solution NMR</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=1ig6 FirstGlance], [http://oca.weizmann.ac.il/oca-bin/ocaids?id=1ig6 OCA], [http://pdbe.org/1ig6 PDBe], [http://www.rcsb.org/pdb/explore.do?structureId=1ig6 RCSB], [http://www.ebi.ac.uk/pdbsum/1ig6 PDBsum], [http://prosat.h-its.org/prosat/prosatexe?pdbcode=1ig6 ProSAT]</span></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=1ig6 FirstGlance], [http://oca.weizmann.ac.il/oca-bin/ocaids?id=1ig6 OCA], [https://pdbe.org/1ig6 PDBe], [https://www.rcsb.org/pdb/explore.do?structureId=1ig6 RCSB], [https://www.ebi.ac.uk/pdbsum/1ig6 PDBsum], [https://prosat.h-its.org/prosat/prosatexe?pdbcode=1ig6 ProSAT]</span></td></tr>
</table>
</table>
== Disease ==
== Disease ==
[[http://www.uniprot.org/uniprot/ARI5B_HUMAN ARI5B_HUMAN]] Note=Defects in ARID5B may be a cause of susceptibility to coronary atherosclerosis in the Japanese population.  Defects in ARID5B may be a cause of susceptibility to acute lymphoblastic leukemia (ALL) [MIM:[http://omim.org/entry/613065 613065]]. Note=ALL is a subtype of acute leukemia, a cancer of the white blood cells. ALL is a malignant disease of bone marrow and the most common malignancy diagnosed in children. The malignant cells are lymphoid precursor cells (lymphoblasts) that are arrested in an early stage of development. The lymphoblasts replace the normal marrow elements, resulting in a marked decrease in the production of normal blood cells. Consequently, anemia, thrombocytopenia, and neutropenia occur to varying degrees. The lymphoblasts also proliferate in organs other than the marrow, particularly the liver, spleen, and lymphonodes.<ref>PMID:19684603</ref> <ref>PMID:19684604</ref> <ref>PMID:20042726</ref> <ref>PMID:20460642</ref> <ref>PMID:20054350</ref> <ref>PMID:20189245</ref> <ref>PMID:21098271</ref>
[https://www.uniprot.org/uniprot/ARI5B_HUMAN ARI5B_HUMAN] Note=Defects in ARID5B may be a cause of susceptibility to coronary atherosclerosis in the Japanese population.  Defects in ARID5B may be a cause of susceptibility to acute lymphoblastic leukemia (ALL) [MIM:[https://omim.org/entry/613065 613065]. Note=ALL is a subtype of acute leukemia, a cancer of the white blood cells. ALL is a malignant disease of bone marrow and the most common malignancy diagnosed in children. The malignant cells are lymphoid precursor cells (lymphoblasts) that are arrested in an early stage of development. The lymphoblasts replace the normal marrow elements, resulting in a marked decrease in the production of normal blood cells. Consequently, anemia, thrombocytopenia, and neutropenia occur to varying degrees. The lymphoblasts also proliferate in organs other than the marrow, particularly the liver, spleen, and lymphonodes.<ref>PMID:19684603</ref> <ref>PMID:19684604</ref> <ref>PMID:20042726</ref> <ref>PMID:20460642</ref> <ref>PMID:20054350</ref> <ref>PMID:20189245</ref> <ref>PMID:21098271</ref>  
== Function ==
== Function ==
[[http://www.uniprot.org/uniprot/ARI5B_HUMAN ARI5B_HUMAN]] Transcription coactivator that binds to the 5'-AATA[CT]-3' core sequence and plays a key role in adipogenesis and liver development. Acts by forming a complex with phosphorylated PHF2, which mediates demethylation at Lys-336, leading to target the PHF2-ARID5B complex to target promoters, where PHF2 mediates demethylation of dimethylated 'Lys-9' of histone H3 (H3K9me2), followed by transcription activation of target genes. The PHF2-ARID5B complex acts as a coactivator of HNF4A in liver. Required for adipogenesis: regulates triglyceride metabolism in adipocytes by regulating expression of adipogenic genes. Overexpression leads to induction of smooth muscle marker genes, suggesting that it may also act as a regulator of smooth muscle cell differentiation and proliferation. Represses the cytomegalovirus enhancer.<ref>PMID:21532585</ref>
[https://www.uniprot.org/uniprot/ARI5B_HUMAN ARI5B_HUMAN] Transcription coactivator that binds to the 5'-AATA[CT]-3' core sequence and plays a key role in adipogenesis and liver development. Acts by forming a complex with phosphorylated PHF2, which mediates demethylation at Lys-336, leading to target the PHF2-ARID5B complex to target promoters, where PHF2 mediates demethylation of dimethylated 'Lys-9' of histone H3 (H3K9me2), followed by transcription activation of target genes. The PHF2-ARID5B complex acts as a coactivator of HNF4A in liver. Required for adipogenesis: regulates triglyceride metabolism in adipocytes by regulating expression of adipogenic genes. Overexpression leads to induction of smooth muscle marker genes, suggesting that it may also act as a regulator of smooth muscle cell differentiation and proliferation. Represses the cytomegalovirus enhancer.<ref>PMID:21532585</ref>  
== Evolutionary Conservation ==
== Evolutionary Conservation ==
[[Image:Consurf_key_small.gif|200px|right]]
[[Image:Consurf_key_small.gif|200px|right]]
Check<jmol>
Check<jmol>
   <jmolCheckbox>
   <jmolCheckbox>
     <scriptWhenChecked>select protein; define ~consurf_to_do selected; consurf_initial_scene = true; script "/wiki/ConSurf/ig/1ig6_consurf.spt"</scriptWhenChecked>
     <scriptWhenChecked>; select protein; define ~consurf_to_do selected; consurf_initial_scene = true; script "/wiki/ConSurf/ig/1ig6_consurf.spt"</scriptWhenChecked>
     <scriptWhenUnchecked>script /wiki/extensions/Proteopedia/spt/initialview01.spt</scriptWhenUnchecked>
     <scriptWhenUnchecked>script /wiki/extensions/Proteopedia/spt/initialview01.spt</scriptWhenUnchecked>
     <text>to colour the structure by Evolutionary Conservation</text>
     <text>to colour the structure by Evolutionary Conservation</text>
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__TOC__
__TOC__
</StructureSection>
</StructureSection>
[[Category: Case, D]]
[[Category: Homo sapiens]]
[[Category: Chen, Y]]
[[Category: Large Structures]]
[[Category: Lin, D]]
[[Category: Case D]]
[[Category: Tsui, V]]
[[Category: Chen Y]]
[[Category: Yuan, Y C]]
[[Category: Lin D]]
[[Category: Dna binding protein]]
[[Category: Tsui V]]
[[Category: Dna-binding motif]]
[[Category: Yuan YC]]
[[Category: Mrf-2]]
[[Category: Protein-dna interaction]]

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