8flq

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Current revision (17:06, 26 April 2023) (edit) (undo)
 
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'''Unreleased structure'''
 
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The entry 8flq is ON HOLD until 2024-12-22
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==Human PTH1R in complex with PTH(1-34) and Gs==
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<StructureSection load='8flq' size='340' side='right'caption='[[8flq]], [[Resolution|resolution]] 2.55&Aring;' scene=''>
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Authors:
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== Structural highlights ==
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<table><tr><td colspan='2'>[[8flq]] is a 6 chain structure with sequence from [https://en.wikipedia.org/wiki/Homo_sapiens Homo sapiens] and [https://en.wikipedia.org/wiki/Lama_glama Lama glama]. Full crystallographic information is available from [http://oca.weizmann.ac.il/oca-bin/ocashort?id=8FLQ OCA]. For a <b>guided tour on the structure components</b> use [https://proteopedia.org/fgij/fg.htm?mol=8FLQ FirstGlance]. <br>
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Description:
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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=8flq FirstGlance], [http://oca.weizmann.ac.il/oca-bin/ocaids?id=8flq OCA], [https://pdbe.org/8flq PDBe], [https://www.rcsb.org/pdb/explore.do?structureId=8flq RCSB], [https://www.ebi.ac.uk/pdbsum/8flq PDBsum], [https://prosat.h-its.org/prosat/prosatexe?pdbcode=8flq ProSAT]</span></td></tr>
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[[Category: Unreleased Structures]]
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</table>
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== Disease ==
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[https://www.uniprot.org/uniprot/GNAS2_HUMAN GNAS2_HUMAN] Pseudopseudohypoparathyroidism;Pseudohypoparathyroidism type 1A;Progressive osseous heteroplasia;Polyostotic fibrous dysplasia;Monostotic fibrous dysplasia;Pseudohypoparathyroidism type 1C;Pseudohypoparathyroidism type 1B;McCune-Albright syndrome. The disease is caused by mutations affecting the gene represented in this entry. The disease is caused by mutations affecting the gene represented in this entry. The disease is caused by mutations affecting the gene represented in this entry. The disease is caused by mutations affecting the gene represented in this entry. The disease is caused by mutations affecting the gene represented in this entry. The disease is caused by mutations affecting the gene represented in this entry. The disease is caused by mutations affecting the gene represented in this entry. Most affected individuals have defects in methylation of the gene. In some cases microdeletions involving the STX16 appear to cause loss of methylation at exon A/B of GNAS, resulting in PHP1B. Paternal uniparental isodisomy have also been observed. The disease is caused by mutations affecting the gene represented in this entry. The disease is caused by mutations affecting the gene represented in this entry.
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== Function ==
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[https://www.uniprot.org/uniprot/GNAS2_HUMAN GNAS2_HUMAN] Guanine nucleotide-binding proteins (G proteins) function as transducers in numerous signaling pathways controlled by G protein-coupled receptors (GPCRs) (PubMed:17110384). Signaling involves the activation of adenylyl cyclases, resulting in increased levels of the signaling molecule cAMP (PubMed:26206488, PubMed:8702665). GNAS functions downstream of several GPCRs, including beta-adrenergic receptors (PubMed:21488135). Stimulates the Ras signaling pathway via RAPGEF2 (PubMed:12391161).<ref>PMID:12391161</ref> <ref>PMID:17110384</ref> <ref>PMID:21488135</ref> <ref>PMID:26206488</ref> <ref>PMID:8702665</ref>
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== References ==
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<references/>
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__TOC__
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</StructureSection>
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[[Category: Homo sapiens]]
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[[Category: Lama glama]]
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[[Category: Large Structures]]
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[[Category: Belousoff MJ]]
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[[Category: Cary BP]]
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[[Category: Piper SJ]]
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[[Category: Sexton PM]]
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[[Category: Wootten D]]

Current revision

Human PTH1R in complex with PTH(1-34) and Gs

PDB ID 8flq

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