7y75: Difference between revisions
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==SIT1-ACE2-BA.2 RBD== | |||
<StructureSection load='7y75' size='340' side='right'caption='[[7y75]], [[Resolution|resolution]] 3.10Å' scene=''> | |||
== Structural highlights == | |||
<table><tr><td colspan='2'>[[7y75]] is a 6 chain structure with sequence from [https://en.wikipedia.org/wiki/Homo_sapiens Homo sapiens] and [https://en.wikipedia.org/wiki/Severe_acute_respiratory_syndrome_coronavirus_2 Severe acute respiratory syndrome coronavirus 2]. Full crystallographic information is available from [http://oca.weizmann.ac.il/oca-bin/ocashort?id=7Y75 OCA]. For a <b>guided tour on the structure components</b> use [https://proteopedia.org/fgij/fg.htm?mol=7Y75 FirstGlance]. <br> | |||
</td></tr><tr id='ligand'><td class="sblockLbl"><b>[[Ligand|Ligands:]]</b></td><td class="sblockDat" id="ligandDat"><scene name='pdbligand=3PH:1,2-DIACYL-GLYCEROL-3-SN-PHOSPHATE'>3PH</scene>, <scene name='pdbligand=NAG:N-ACETYL-D-GLUCOSAMINE'>NAG</scene>, <scene name='pdbligand=ZN:ZINC+ION'>ZN</scene></td></tr> | |||
[[Category: | <tr id='resources'><td class="sblockLbl"><b>Resources:</b></td><td class="sblockDat"><span class='plainlinks'>[https://proteopedia.org/fgij/fg.htm?mol=7y75 FirstGlance], [http://oca.weizmann.ac.il/oca-bin/ocaids?id=7y75 OCA], [https://pdbe.org/7y75 PDBe], [https://www.rcsb.org/pdb/explore.do?structureId=7y75 RCSB], [https://www.ebi.ac.uk/pdbsum/7y75 PDBsum], [https://prosat.h-its.org/prosat/prosatexe?pdbcode=7y75 ProSAT]</span></td></tr> | ||
[[Category: | </table> | ||
[[Category: Li | == Disease == | ||
[[Category: Yan | [https://www.uniprot.org/uniprot/S6A20_HUMAN S6A20_HUMAN] Iminoglycinuria. 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. Haploinsufficiency of SLC6A20 combined with deficiency of the neutral amino acid transporter SLC6A19 or partially inactivating mutations in SLC36A2, is responsible for iminoglycinuria. Additional polymorphisms and mutations in SLC6A18 can contribute to the IG phenotype in some families. | ||
[[Category: Zhang | == Function == | ||
[https://www.uniprot.org/uniprot/S6A20_HUMAN S6A20_HUMAN] Mediates the Na(+)- and Cl(-)-dependent uptake of imino acids such as L-proline, N-methyl-L-proline and pipecolate as well as N-methylated amino acids (PubMed:15632147, PubMed:19033659, PubMed:33428810). Also transports glycine, regulates proline and glycine homeostasis in the brain playing a role in the modulation of NMDAR currents (PubMed:33428810).<ref>PMID:15632147</ref> <ref>PMID:19033659</ref> <ref>PMID:33428810</ref> | |||
== References == | |||
<references/> | |||
__TOC__ | |||
</StructureSection> | |||
[[Category: Homo sapiens]] | |||
[[Category: Large Structures]] | |||
[[Category: Severe acute respiratory syndrome coronavirus 2]] | |||
[[Category: Li YN]] | |||
[[Category: Shen YP]] | |||
[[Category: Yan RH]] | |||
[[Category: Zhang YY]] |
Latest revision as of 13:41, 30 November 2022
SIT1-ACE2-BA.2 RBDSIT1-ACE2-BA.2 RBD
Structural highlights
DiseaseS6A20_HUMAN Iminoglycinuria. 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. Haploinsufficiency of SLC6A20 combined with deficiency of the neutral amino acid transporter SLC6A19 or partially inactivating mutations in SLC36A2, is responsible for iminoglycinuria. Additional polymorphisms and mutations in SLC6A18 can contribute to the IG phenotype in some families. FunctionS6A20_HUMAN Mediates the Na(+)- and Cl(-)-dependent uptake of imino acids such as L-proline, N-methyl-L-proline and pipecolate as well as N-methylated amino acids (PubMed:15632147, PubMed:19033659, PubMed:33428810). Also transports glycine, regulates proline and glycine homeostasis in the brain playing a role in the modulation of NMDAR currents (PubMed:33428810).[1] [2] [3] References
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