4apo: Difference between revisions
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==AIP TPR domain in complex with human Tomm20 peptide== | ==AIP TPR domain in complex with human Tomm20 peptide== | ||
<StructureSection load='4apo' size='340' side='right' caption='[[4apo]], [[Resolution|resolution]] 1.90Å' scene=''> | <StructureSection load='4apo' size='340' side='right' caption='[[4apo]], [[Resolution|resolution]] 1.90Å' scene=''> | ||
== Structural highlights == | == Structural highlights == | ||
<table><tr><td colspan='2'>[[4apo]] is a 4 chain structure with sequence from [http://en.wikipedia.org/wiki/ | <table><tr><td colspan='2'>[[4apo]] is a 4 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=4APO OCA]. For a <b>guided tour on the structure components</b> use [http://oca.weizmann.ac.il/oca-docs/fgij/fg.htm?mol=4APO FirstGlance]. <br> | ||
</td></tr><tr id='ligand'><td class="sblockLbl"><b>[[Ligand|Ligands:]]</b></td><td class="sblockDat"><scene name='pdbligand=12P:DODECAETHYLENE+GLYCOL'>12P</scene>, <scene name='pdbligand=SO4:SULFATE+ION'>SO4</scene></td></tr> | </td></tr><tr id='ligand'><td class="sblockLbl"><b>[[Ligand|Ligands:]]</b></td><td class="sblockDat"><scene name='pdbligand=12P:DODECAETHYLENE+GLYCOL'>12P</scene>, <scene name='pdbligand=SO4:SULFATE+ION'>SO4</scene></td></tr> | ||
<tr id='related'><td class="sblockLbl"><b>[[Related_structure|Related:]]</b></td><td class="sblockDat">[[4aif|4aif]]</td></tr> | <tr id='related'><td class="sblockLbl"><b>[[Related_structure|Related:]]</b></td><td class="sblockDat">[[4aif|4aif]]</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=4apo FirstGlance], [http://oca.weizmann.ac.il/oca-bin/ocaids?id=4apo OCA], [http://www.rcsb.org/pdb/explore.do?structureId=4apo RCSB], [http://www.ebi.ac.uk/pdbsum/4apo PDBsum]</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=4apo FirstGlance], [http://oca.weizmann.ac.il/oca-bin/ocaids?id=4apo OCA], [http://pdbe.org/4apo PDBe], [http://www.rcsb.org/pdb/explore.do?structureId=4apo RCSB], [http://www.ebi.ac.uk/pdbsum/4apo PDBsum], [http://prosat.h-its.org/prosat/prosatexe?pdbcode=4apo ProSAT]</span></td></tr> | ||
</table> | </table> | ||
== Disease == | == Disease == | ||
[[http://www.uniprot.org/uniprot/AIP_HUMAN AIP_HUMAN]] Acromegaly;Familial prolactinoma. Defects in AIP are a cause of growth hormone-secreting pituitary adenoma (GHSPA) [MIM:[http://omim.org/entry/102200 102200]]; also known as familial isolated somatotropinomas (FIS) or isolated familial somatotropinoma (IFS) or familial somatotrophinoma or acromegaly due to pituitary adenoma.<ref>PMID:17244780</ref> <ref>PMID:17299063</ref> <ref>PMID:17360484</ref> <ref>PMID:18410548</ref> Defects in AIP are a cause of ACTH-secreting pituitary adenoma (ASPA) [MIM:[http://omim.org/entry/219090 219090]]; also known as pituitary Cushing disease. A pituary adenoma resulting in excessive production of adrenocorticotropic hormone. This leads to hypersecretion of cortisol by the adrenal glands and ACTH-dependent Cushing syndrome. Clinical manifestations of Cushing syndrome include facial and trunkal obesity, abdominal striae, muscular weakness, osteoporosis, arterial hypertension, diabetes. Defects in AIP are a cause of prolactin-secreting pituitary adenoma (PSPA) [MIM:[http://omim.org/entry/600634 600634]]; also known as prolactinoma. Prolactin-secreting pituitary adenoma is the most common type of hormonally active pituitary adenoma. | [[http://www.uniprot.org/uniprot/AIP_HUMAN AIP_HUMAN]] Acromegaly;Familial prolactinoma. Defects in AIP are a cause of growth hormone-secreting pituitary adenoma (GHSPA) [MIM:[http://omim.org/entry/102200 102200]]; also known as familial isolated somatotropinomas (FIS) or isolated familial somatotropinoma (IFS) or familial somatotrophinoma or acromegaly due to pituitary adenoma.<ref>PMID:17244780</ref> <ref>PMID:17299063</ref> <ref>PMID:17360484</ref> <ref>PMID:18410548</ref> Defects in AIP are a cause of ACTH-secreting pituitary adenoma (ASPA) [MIM:[http://omim.org/entry/219090 219090]]; also known as pituitary Cushing disease. A pituary adenoma resulting in excessive production of adrenocorticotropic hormone. This leads to hypersecretion of cortisol by the adrenal glands and ACTH-dependent Cushing syndrome. Clinical manifestations of Cushing syndrome include facial and trunkal obesity, abdominal striae, muscular weakness, osteoporosis, arterial hypertension, diabetes. Defects in AIP are a cause of prolactin-secreting pituitary adenoma (PSPA) [MIM:[http://omim.org/entry/600634 600634]]; also known as prolactinoma. Prolactin-secreting pituitary adenoma is the most common type of hormonally active pituitary adenoma. | ||
== Function == | == Function == | ||
[[http://www.uniprot.org/uniprot/AIP_HUMAN AIP_HUMAN]] May play a positive role in AHR-mediated (aromatic hydrocarbon receptor) signaling, possibly by influencing its receptivity for ligand and/or its nuclear targeting. Cellular negative regulator of the hepatitis B virus (HBV) X protein. | [[http://www.uniprot.org/uniprot/AIP_HUMAN AIP_HUMAN]] May play a positive role in AHR-mediated (aromatic hydrocarbon receptor) signaling, possibly by influencing its receptivity for ligand and/or its nuclear targeting. Cellular negative regulator of the hepatitis B virus (HBV) X protein. [[http://www.uniprot.org/uniprot/TOM20_HUMAN TOM20_HUMAN]] Central component of the receptor complex responsible for the recognition and translocation of cytosolically synthesized mitochondrial preproteins. Together with TOM22 functions as the transit peptide receptor at the surface of the mitochondrion outer membrane and facilitates the movement of preproteins into the TOM40 translocation pore (By similarity). | ||
<div style="background-color:#fffaf0;"> | <div style="background-color:#fffaf0;"> | ||
== Publication Abstract from PubMed == | == Publication Abstract from PubMed == | ||
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From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine.<br> | From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine.<br> | ||
</div> | </div> | ||
<div class="pdbe-citations 4apo" style="background-color:#fffaf0;"></div> | |||
== References == | == References == | ||
<references/> | <references/> | ||
__TOC__ | __TOC__ | ||
</StructureSection> | </StructureSection> | ||
[[Category: | [[Category: Human]] | ||
[[Category: Morgan, R M.L]] | [[Category: Morgan, R M.L]] | ||
[[Category: Pearl, L H]] | [[Category: Pearl, L H]] | ||