4oha - Revision history

OCA at 17:14, 20 September 2023

2023-09-20T17:14:02Z

← Older revision		Revision as of 17:14, 20 September 2023
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	== Structural highlights ==		== Structural highlights ==
	<table><tr><td colspan='2'>[[4oha]] is a 2 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=4OHA OCA]. For a <b>guided tour on the structure components</b> use [https://proteopedia.org/fgij/fg.htm?mol=4OHA FirstGlance]. <br>		<table><tr><td colspan='2'>[[4oha]] is a 2 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=4OHA OCA]. For a <b>guided tour on the structure components</b> use [https://proteopedia.org/fgij/fg.htm?mol=4OHA FirstGlance]. <br>
	</td></tr><tr id='ligand'><td class="sblockLbl"><b>[[Ligand\|Ligands:]]</b></td><td class="sblockDat" id="ligandDat"><scene name='pdbligand=HFT:HYDROXYFLUTAMIDE'>HFT</scene>, <scene name='pdbligand=SO4:SULFATE+ION'>SO4</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]] 1.42Å</td></tr>
			<tr id='ligand'><td class="sblockLbl"><b>[[Ligand\|Ligands:]]</b></td><td class="sblockDat" id="ligandDat"><scene name='pdbligand=HFT:HYDROXYFLUTAMIDE'>HFT</scene>, <scene name='pdbligand=SO4:SULFATE+ION'>SO4</scene></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=4oha FirstGlance], [http://oca.weizmann.ac.il/oca-bin/ocaids?id=4oha OCA], [https://pdbe.org/4oha PDBe], [https://www.rcsb.org/pdb/explore.do?structureId=4oha RCSB], [https://www.ebi.ac.uk/pdbsum/4oha PDBsum], [https://prosat.h-its.org/prosat/prosatexe?pdbcode=4oha 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=4oha FirstGlance], [http://oca.weizmann.ac.il/oca-bin/ocaids?id=4oha OCA], [https://pdbe.org/4oha PDBe], [https://www.rcsb.org/pdb/explore.do?structureId=4oha RCSB], [https://www.ebi.ac.uk/pdbsum/4oha PDBsum], [https://prosat.h-its.org/prosat/prosatexe?pdbcode=4oha ProSAT]</span></td></tr>
	</table>		</table>

OCA at 07:26, 25 January 2023

2023-01-25T07:26:17Z

← Older revision		Revision as of 07:26, 25 January 2023
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	<StructureSection load='4oha' size='340' side='right'caption='[[4oha]], [[Resolution\|resolution]] 1.42Å' scene=''>		<StructureSection load='4oha' size='340' side='right'caption='[[4oha]], [[Resolution\|resolution]] 1.42Å' scene=''>
	== Structural highlights ==		== Structural highlights ==
	<table><tr><td colspan='2'>[[4oha]] is a 2 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=4OHA OCA]. For a <b>guided tour on the structure components</b> use [~~http~~://~~oca~~.~~weizmann.ac.il/oca-docs~~/fgij/fg.htm?mol=4OHA FirstGlance]. <br>		<table><tr><td colspan='2'>[[4oha]] is a 2 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=4OHA OCA]. For a <b>guided tour on the structure components</b> use [https://proteopedia.org/fgij/fg.htm?mol=4OHA FirstGlance]. <br>
	</td></tr><tr id='ligand'><td class="sblockLbl"><b>[[Ligand\|Ligands:]]</b></td><td class="sblockDat"><scene name='pdbligand=HFT:HYDROXYFLUTAMIDE'>HFT</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" id="ligandDat"><scene name='pdbligand=HFT:HYDROXYFLUTAMIDE'>HFT</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">[[4oea\|4oea]], [[4oed\|4oed]], [[4oey\|4oey]], [[4oez\|4oez]], [[4ofr\|4ofr]], [[4ofu\|4ofu]], [[4ogh\|4ogh]], [[4oh5\|4oh5]], [[4oh6\|4oh6]], [[4oil\|4oil]], [[4oiu\|4oiu]], [[4oj9\|4oj9]], [[4ojb\|4ojb]], [[4ok1\|4ok1]], [[4okb\|4okb]], [[4okt\|4okt]], [[4okw\|4okw]], [[4okx\|4okx]], [[4olm\|4olm]]</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=4oha FirstGlance], [http://oca.weizmann.ac.il/oca-bin/ocaids?id=4oha OCA], [https://pdbe.org/4oha PDBe], [https://www.rcsb.org/pdb/explore.do?structureId=4oha RCSB], [https://www.ebi.ac.uk/pdbsum/4oha PDBsum], [https://prosat.h-its.org/prosat/prosatexe?pdbcode=4oha ProSAT]</span></td></tr>
	~~<tr id='gene'><td class="sblockLbl"><b>[[Gene\|Gene:]]</b></td><td class="sblockDat">AR, DHTR, NR3C4 ([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'>[~~http~~://~~oca~~.~~weizmann.ac.il/oca-docs~~/fgij/fg.htm?mol=4oha FirstGlance], [http://oca.weizmann.ac.il/oca-bin/ocaids?id=4oha OCA], [~~http~~://pdbe.org/4oha PDBe], [~~http~~://www.rcsb.org/pdb/explore.do?structureId=4oha RCSB], [~~http~~://www.ebi.ac.uk/pdbsum/4oha PDBsum], [~~http~~://prosat.h-its.org/prosat/prosatexe?pdbcode=4oha ProSAT]</span></td></tr>
	</table>		</table>
	== Disease ==		== Disease ==
	[~~[http~~://www.uniprot.org/uniprot/ANDR_HUMAN ANDR_HUMAN]] Defects in AR are the cause of androgen insensitivity syndrome (AIS) [MIM:[~~http~~://omim.org/entry/300068 300068]]; previously known as testicular feminization syndrome (TFM). AIS is an X-linked recessive form of pseudohermaphroditism due end-organ resistance to androgen. Affected males have female external genitalia, female breast development, blind vagina, absent uterus and female adnexa, and abdominal or inguinal testes, despite a normal 46,XY karyotype.<ref>PMID:2594783</ref> <ref>PMID:8413310</ref> <ref>PMID:1775137</ref> <ref>PMID:16129672</ref> <ref>PMID:2082179</ref> <ref>PMID:1999491</ref> <ref>PMID:1609793</ref> <ref>PMID:1426313</ref> <ref>PMID:1487249</ref> <ref>PMID:1307250</ref> <ref>PMID:1569163</ref> <ref>PMID:1464650</ref> <ref>PMID:1430233</ref> <ref>PMID:1316540</ref> <ref>PMID:1480178</ref> <ref>PMID:8224266</ref> <ref>PMID:8103398</ref> <ref>PMID:8281140</ref> <ref>PMID:8325950</ref> <ref>PMID:8096390</ref> <ref>PMID:8446106</ref> [:]<ref>PMID:8162033</ref> <ref>PMID:7981687</ref> <ref>PMID:7981689</ref> <ref>PMID:7962294</ref> <ref>PMID:8040309</ref> <ref>PMID:7929841</ref> <ref>PMID:7993455</ref> <ref>PMID:7970939</ref> <ref>PMID:8830623</ref> <ref>PMID:7641413</ref> <ref>PMID:7671849</ref> <ref>PMID:7633398</ref> <ref>PMID:7537149</ref> <ref>PMID:7581399</ref> <ref>PMID:8723113</ref> <ref>PMID:9039340</ref> <ref>PMID:9001799</ref> <ref>PMID:8626869</ref> <ref>PMID:8768864</ref> <ref>PMID:8918984</ref> <ref>PMID:8683794</ref> <ref>PMID:8647313</ref> <ref>PMID:8809734</ref> <ref>PMID:9106550</ref> <ref>PMID:9160185</ref> <ref>PMID:9007482</ref> <ref>PMID:8990010</ref> <ref>PMID:9255042</ref> <ref>PMID:9252933</ref> <ref>PMID:9328206</ref> <ref>PMID:9302173</ref> <ref>PMID:9544375</ref> <ref>PMID:9698822</ref> <ref>PMID:9788719</ref> <ref>PMID:9610419</ref> <ref>PMID:9856504</ref> <ref>PMID:9554754</ref> [:]<ref>PMID:9851768</ref> <ref>PMID:9627582</ref> <ref>PMID:10571951</ref> <ref>PMID:10221692</ref> <ref>PMID:10404311</ref> <ref>PMID:10022458</ref> <ref>PMID:10221770</ref> <ref>PMID:10590024</ref> <ref>PMID:10458483</ref> <ref>PMID:10690872</ref> <ref>PMID:11587068</ref> <ref>PMID:11744994</ref> <ref>PMID:16595706</ref> Defects in AR are the cause of spinal and bulbar muscular atrophy X-linked type 1 (SMAX1) [MIM:[~~http~~://omim.org/entry/313200 313200]]; also known as Kennedy disease. SMAX1 is an X-linked recessive form of spinal muscular atrophy. Spinal muscular atrophy refers to a group of neuromuscular disorders characterized by degeneration of the anterior horn cells of the spinal cord, leading to symmetrical muscle weakness and atrophy. SMAX1 occurs only in men. Age at onset is usually in the third to fifth decade of life, but earlier involvement has been reported. It is characterized by slowly progressive limb and bulbar muscle weakness with fasciculations, muscle atrophy, and gynecomastia. The disorder is clinically similar to classic forms of autosomal spinal muscular atrophy. Note=Caused by trinucleotide CAG repeat expansion. In SMAX1 patients the number of Gln ranges from 38 to 62. Longer expansions result in earlier onset and more severe clinical manifestations of the disease.<ref>PMID:15851746</ref> Note=Defects in AR may play a role in metastatic prostate cancer. The mutated receptor stimulates prostate growth and metastases development despite of androgen ablation. This treatment can reduce primary and metastatic lesions probably by inducing apoptosis of tumor cells when they express the wild-type receptor. Defects in AR are the cause of androgen insensitivity syndrome partial (PAIS) [MIM:[~~http~~://omim.org/entry/312300 312300]]; also known as Reifenstein syndrome. PAIS is characterized by hypospadias, hypogonadism, gynecomastia, genital ambiguity, normal XY karyotype, and a pedigree pattern consistent with X-linked recessive inheritance. Some patients present azoospermia or severe oligospermia without other clinical manifestations.		[https://www.uniprot.org/uniprot/ANDR_HUMAN ANDR_HUMAN] Defects in AR are the cause of androgen insensitivity syndrome (AIS) [MIM:[https://omim.org/entry/300068 300068]; previously known as testicular feminization syndrome (TFM). AIS is an X-linked recessive form of pseudohermaphroditism due end-organ resistance to androgen. Affected males have female external genitalia, female breast development, blind vagina, absent uterus and female adnexa, and abdominal or inguinal testes, despite a normal 46,XY karyotype.<ref>PMID:2594783</ref> <ref>PMID:8413310</ref> <ref>PMID:1775137</ref> <ref>PMID:16129672</ref> <ref>PMID:2082179</ref> <ref>PMID:1999491</ref> <ref>PMID:1609793</ref> <ref>PMID:1426313</ref> <ref>PMID:1487249</ref> <ref>PMID:1307250</ref> <ref>PMID:1569163</ref> <ref>PMID:1464650</ref> <ref>PMID:1430233</ref> <ref>PMID:1316540</ref> <ref>PMID:1480178</ref> <ref>PMID:8224266</ref> <ref>PMID:8103398</ref> <ref>PMID:8281140</ref> <ref>PMID:8325950</ref> <ref>PMID:8096390</ref> <ref>PMID:8446106</ref> [:]<ref>PMID:8162033</ref> <ref>PMID:7981687</ref> <ref>PMID:7981689</ref> <ref>PMID:7962294</ref> <ref>PMID:8040309</ref> <ref>PMID:7929841</ref> <ref>PMID:7993455</ref> <ref>PMID:7970939</ref> <ref>PMID:8830623</ref> <ref>PMID:7641413</ref> <ref>PMID:7671849</ref> <ref>PMID:7633398</ref> <ref>PMID:7537149</ref> <ref>PMID:7581399</ref> <ref>PMID:8723113</ref> <ref>PMID:9039340</ref> <ref>PMID:9001799</ref> <ref>PMID:8626869</ref> <ref>PMID:8768864</ref> <ref>PMID:8918984</ref> <ref>PMID:8683794</ref> <ref>PMID:8647313</ref> <ref>PMID:8809734</ref> <ref>PMID:9106550</ref> <ref>PMID:9160185</ref> <ref>PMID:9007482</ref> <ref>PMID:8990010</ref> <ref>PMID:9255042</ref> <ref>PMID:9252933</ref> <ref>PMID:9328206</ref> <ref>PMID:9302173</ref> <ref>PMID:9544375</ref> <ref>PMID:9698822</ref> <ref>PMID:9788719</ref> <ref>PMID:9610419</ref> <ref>PMID:9856504</ref> <ref>PMID:9554754</ref> [:]<ref>PMID:9851768</ref> <ref>PMID:9627582</ref> <ref>PMID:10571951</ref> <ref>PMID:10221692</ref> <ref>PMID:10404311</ref> <ref>PMID:10022458</ref> <ref>PMID:10221770</ref> <ref>PMID:10590024</ref> <ref>PMID:10458483</ref> <ref>PMID:10690872</ref> <ref>PMID:11587068</ref> <ref>PMID:11744994</ref> <ref>PMID:16595706</ref> Defects in AR are the cause of spinal and bulbar muscular atrophy X-linked type 1 (SMAX1) [MIM:[https://omim.org/entry/313200 313200]; also known as Kennedy disease. SMAX1 is an X-linked recessive form of spinal muscular atrophy. Spinal muscular atrophy refers to a group of neuromuscular disorders characterized by degeneration of the anterior horn cells of the spinal cord, leading to symmetrical muscle weakness and atrophy. SMAX1 occurs only in men. Age at onset is usually in the third to fifth decade of life, but earlier involvement has been reported. It is characterized by slowly progressive limb and bulbar muscle weakness with fasciculations, muscle atrophy, and gynecomastia. The disorder is clinically similar to classic forms of autosomal spinal muscular atrophy. Note=Caused by trinucleotide CAG repeat expansion. In SMAX1 patients the number of Gln ranges from 38 to 62. Longer expansions result in earlier onset and more severe clinical manifestations of the disease.<ref>PMID:15851746</ref> Note=Defects in AR may play a role in metastatic prostate cancer. The mutated receptor stimulates prostate growth and metastases development despite of androgen ablation. This treatment can reduce primary and metastatic lesions probably by inducing apoptosis of tumor cells when they express the wild-type receptor. Defects in AR are the cause of androgen insensitivity syndrome partial (PAIS) [MIM:[https://omim.org/entry/312300 312300]; also known as Reifenstein syndrome. PAIS is characterized by hypospadias, hypogonadism, gynecomastia, genital ambiguity, normal XY karyotype, and a pedigree pattern consistent with X-linked recessive inheritance. Some patients present azoospermia or severe oligospermia without other clinical manifestations.
	== Function ==		== Function ==
	[~~[http~~://www.uniprot.org/uniprot/ANDR_HUMAN ANDR_HUMAN]] Steroid hormone receptors are ligand-activated transcription factors that regulate eukaryotic gene expression and affect cellular proliferation and differentiation in target tissues. Transcription factor activity is modulated by bound coactivator and corepressor proteins. Transcription activation is down-regulated by NR0B2. Activated, but not phosphorylated, by HIPK3 and ZIPK/DAPK3.<ref>PMID:14664718</ref> <ref>PMID:18084323</ref> <ref>PMID:19345326</ref> <ref>PMID:20980437</ref> <ref>PMID:15563469</ref> <ref>PMID:17591767</ref> <ref>PMID:17911242</ref>		[https://www.uniprot.org/uniprot/ANDR_HUMAN ANDR_HUMAN] Steroid hormone receptors are ligand-activated transcription factors that regulate eukaryotic gene expression and affect cellular proliferation and differentiation in target tissues. Transcription factor activity is modulated by bound coactivator and corepressor proteins. Transcription activation is down-regulated by NR0B2. Activated, but not phosphorylated, by HIPK3 and ZIPK/DAPK3.<ref>PMID:14664718</ref> <ref>PMID:18084323</ref> <ref>PMID:19345326</ref> <ref>PMID:20980437</ref> <ref>PMID:15563469</ref> <ref>PMID:17591767</ref> <ref>PMID:17911242</ref>
	<div style="background-color:#fffaf0;">		<div style="background-color:#fffaf0;">
	== Publication Abstract from PubMed ==		== Publication Abstract from PubMed ==
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	__TOC__		__TOC__
	</StructureSection>		</StructureSection>
	[[Category: ~~Human~~]]		[[Category: Homo sapiens]]
	[[Category: Large Structures]]		[[Category: Large Structures]]
	[[Category: Hsu~~, C L~~]]		[[Category: Hsu CL]]
	[[Category: Liu~~, J S~~]]		[[Category: Liu JS]]
	[[Category: Wu~~, W G]]~~		[[Category: Wu WG]]
	~~[[Category: Alpha-helix]]~~
	~~[[Category: Hormone receptor-peptide complex]]~~
	~~[[Category: Hormone/growth factor receptor]]~~
	~~[[Category: Phosphorylation]]~~
	~~[[Category: Signal transduction~~]]

OCA at 07:48, 17 April 2019

2019-04-17T07:48:41Z

← Older revision		Revision as of 07:48, 17 April 2019
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	==Crystal structure of T877A-AR-LBD bound with co-regulator peptide==		==Crystal structure of T877A-AR-LBD bound with co-regulator peptide==
	<StructureSection load='4oha' size='340' side='right' caption='[[4oha]], [[Resolution\|resolution]] 1.42Å' scene=''>		<StructureSection load='4oha' size='340' side='right'caption='[[4oha]], [[Resolution\|resolution]] 1.42Å' scene=''>
	== Structural highlights ==		== Structural highlights ==
	<table><tr><td colspan='2'>[[4oha]] is a 2 chain structure. Full crystallographic information is available from [http://oca.weizmann.ac.il/oca-bin/ocashort?id=4OHA OCA]. For a <b>guided tour on the structure components</b> use [http://oca.weizmann.ac.il/oca-docs/fgij/fg.htm?mol=4OHA FirstGlance]. <br>		<table><tr><td colspan='2'>[[4oha]] is a 2 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=4OHA OCA]. For a <b>guided tour on the structure components</b> use [http://oca.weizmann.ac.il/oca-docs/fgij/fg.htm?mol=4OHA FirstGlance]. <br>
	</td></tr><tr id='ligand'><td class="sblockLbl"><b>[[Ligand\|Ligands:]]</b></td><td class="sblockDat"><scene name='pdbligand=HFT:HYDROXYFLUTAMIDE'>HFT</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=HFT:HYDROXYFLUTAMIDE'>HFT</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">[[4oea\|4oea]], [[4oed\|4oed]], [[4oey\|4oey]], [[4oez\|4oez]], [[4ofr\|4ofr]], [[4ofu\|4ofu]], [[4ogh\|4ogh]], [[4oh5\|4oh5]], [[4oh6\|4oh6]], [[4oil\|4oil]], [[4oiu\|4oiu]], [[4oj9\|4oj9]], [[4ojb\|4ojb]], [[4ok1\|4ok1]], [[4okb\|4okb]], [[4okt\|4okt]], [[4okw\|4okw]], [[4okx\|4okx]], [[4olm\|4olm]]</td></tr>		<tr id='related'><td class="sblockLbl"><b>[[Related_structure\|Related:]]</b></td><td class="sblockDat">[[4oea\|4oea]], [[4oed\|4oed]], [[4oey\|4oey]], [[4oez\|4oez]], [[4ofr\|4ofr]], [[4ofu\|4ofu]], [[4ogh\|4ogh]], [[4oh5\|4oh5]], [[4oh6\|4oh6]], [[4oil\|4oil]], [[4oiu\|4oiu]], [[4oj9\|4oj9]], [[4ojb\|4ojb]], [[4ok1\|4ok1]], [[4okb\|4okb]], [[4okt\|4okt]], [[4okw\|4okw]], [[4okx\|4okx]], [[4olm\|4olm]]</td></tr>
			<tr id='gene'><td class="sblockLbl"><b>[[Gene\|Gene:]]</b></td><td class="sblockDat">AR, DHTR, NR3C4 ([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'>[http://oca.weizmann.ac.il/oca-docs/fgij/fg.htm?mol=4oha FirstGlance], [http://oca.weizmann.ac.il/oca-bin/ocaids?id=4oha OCA], [http://pdbe.org/4oha PDBe], [http://www.rcsb.org/pdb/explore.do?structureId=4oha RCSB], [http://www.ebi.ac.uk/pdbsum/4oha PDBsum], [http://prosat.h-its.org/prosat/prosatexe?pdbcode=4oha 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=4oha FirstGlance], [http://oca.weizmann.ac.il/oca-bin/ocaids?id=4oha OCA], [http://pdbe.org/4oha PDBe], [http://www.rcsb.org/pdb/explore.do?structureId=4oha RCSB], [http://www.ebi.ac.uk/pdbsum/4oha PDBsum], [http://prosat.h-its.org/prosat/prosatexe?pdbcode=4oha ProSAT]</span></td></tr>
	</table>		</table>
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	==See Also==		==See Also==
	*[[Androgen receptor\|Androgen receptor]]		*[[Androgen receptor 3D structures\|Androgen receptor 3D structures]]
	== References ==		== References ==
	<references/>		<references/>
	__TOC__		__TOC__
	</StructureSection>		</StructureSection>
			[[Category: Human]]
			[[Category: Large Structures]]
	[[Category: Hsu, C L]]		[[Category: Hsu, C L]]
	[[Category: Liu, J S]]		[[Category: Liu, J S]]

OCA at 16:19, 5 August 2016

2016-08-05T16:19:33Z

← Older revision		Revision as of 16:19, 5 August 2016
Line 1:		Line 1:

	==Crystal structure of T877A-AR-LBD bound with co-regulator peptide==		==Crystal structure of T877A-AR-LBD bound with co-regulator peptide==
	<StructureSection load='4oha' size='340' side='right' caption='[[4oha]], [[Resolution\|resolution]] 1.42Å' scene=''>		<StructureSection load='4oha' size='340' side='right' caption='[[4oha]], [[Resolution\|resolution]] 1.42Å' scene=''>
Line 5:		Line 6:
	</td></tr><tr id='ligand'><td class="sblockLbl"><b>[[Ligand\|Ligands:]]</b></td><td class="sblockDat"><scene name='pdbligand=HFT:HYDROXYFLUTAMIDE'>HFT</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=HFT:HYDROXYFLUTAMIDE'>HFT</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">[[4oea\|4oea]], [[4oed\|4oed]], [[4oey\|4oey]], [[4oez\|4oez]], [[4ofr\|4ofr]], [[4ofu\|4ofu]], [[4ogh\|4ogh]], [[4oh5\|4oh5]], [[4oh6\|4oh6]], [[4oil\|4oil]], [[4oiu\|4oiu]], [[4oj9\|4oj9]], [[4ojb\|4ojb]], [[4ok1\|4ok1]], [[4okb\|4okb]], [[4okt\|4okt]], [[4okw\|4okw]], [[4okx\|4okx]], [[4olm\|4olm]]</td></tr>		<tr id='related'><td class="sblockLbl"><b>[[Related_structure\|Related:]]</b></td><td class="sblockDat">[[4oea\|4oea]], [[4oed\|4oed]], [[4oey\|4oey]], [[4oez\|4oez]], [[4ofr\|4ofr]], [[4ofu\|4ofu]], [[4ogh\|4ogh]], [[4oh5\|4oh5]], [[4oh6\|4oh6]], [[4oil\|4oil]], [[4oiu\|4oiu]], [[4oj9\|4oj9]], [[4ojb\|4ojb]], [[4ok1\|4ok1]], [[4okb\|4okb]], [[4okt\|4okt]], [[4okw\|4okw]], [[4okx\|4okx]], [[4olm\|4olm]]</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=4oha FirstGlance], [http://oca.weizmann.ac.il/oca-bin/ocaids?id=4oha OCA], [http://www.rcsb.org/pdb/explore.do?structureId=4oha RCSB], [http://www.ebi.ac.uk/pdbsum/4oha 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=4oha FirstGlance], [http://oca.weizmann.ac.il/oca-bin/ocaids?id=4oha OCA], [http://pdbe.org/4oha PDBe], [http://www.rcsb.org/pdb/explore.do?structureId=4oha RCSB], [http://www.ebi.ac.uk/pdbsum/4oha PDBsum], [http://prosat.h-its.org/prosat/prosatexe?pdbcode=4oha ProSAT]</span></td></tr>
	</table>		</table>
	== Disease ==		== Disease ==
Line 19:		Line 20:
	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 4oha" style="background-color:#fffaf0;"></div>

			==See Also==
			*[[Androgen receptor\|Androgen receptor]]
	== References ==		== References ==
	<references/>		<references/>

OCA at 11:25, 24 December 2014

2014-12-24T11:25:13Z

← Older revision		Revision as of 11:25, 24 December 2014
Line 3:		Line 3:
	== Structural highlights ==		== Structural highlights ==
	<table><tr><td colspan='2'>[[4oha]] is a 2 chain structure. Full crystallographic information is available from [http://oca.weizmann.ac.il/oca-bin/ocashort?id=4OHA OCA]. For a <b>guided tour on the structure components</b> use [http://oca.weizmann.ac.il/oca-docs/fgij/fg.htm?mol=4OHA FirstGlance]. <br>		<table><tr><td colspan='2'>[[4oha]] is a 2 chain structure. Full crystallographic information is available from [http://oca.weizmann.ac.il/oca-bin/ocashort?id=4OHA OCA]. For a <b>guided tour on the structure components</b> use [http://oca.weizmann.ac.il/oca-docs/fgij/fg.htm?mol=4OHA FirstGlance]. <br>
	</td></tr><tr><td class="sblockLbl"><b>[[Ligand\|Ligands:]]</b></td><td class="sblockDat"><scene name='pdbligand=HFT:HYDROXYFLUTAMIDE'>HFT</scene>, <scene name='pdbligand=SO4:SULFATE+ION'>SO4</scene><br>		</td></tr><tr id='ligand'><td class="sblockLbl"><b>[[Ligand\|Ligands:]]</b></td><td class="sblockDat"><scene name='pdbligand=HFT:HYDROXYFLUTAMIDE'>HFT</scene>, <scene name='pdbligand=SO4:SULFATE+ION'>SO4</scene></td></tr>
	<tr><td class="sblockLbl"><b>[[Related_structure\|Related:]]</b></td><td class="sblockDat">[[4oea\|4oea]], [[4oed\|4oed]], [[4oey\|4oey]], [[4oez\|4oez]], [[4ofr\|4ofr]], [[4ofu\|4ofu]], [[4ogh\|4ogh]], [[4oh5\|4oh5]], [[4oh6\|4oh6]], [[4oil\|4oil]], [[4oiu\|4oiu]], [[4oj9\|4oj9]], [[4ojb\|4ojb]], [[4ok1\|4ok1]], [[4okb\|4okb]], [[4okt\|4okt]], [[4okw\|4okw]], [[4okx\|4okx]], [[4olm\|4olm]]</td></tr>		<tr id='related'><td class="sblockLbl"><b>[[Related_structure\|Related:]]</b></td><td class="sblockDat">[[4oea\|4oea]], [[4oed\|4oed]], [[4oey\|4oey]], [[4oez\|4oez]], [[4ofr\|4ofr]], [[4ofu\|4ofu]], [[4ogh\|4ogh]], [[4oh5\|4oh5]], [[4oh6\|4oh6]], [[4oil\|4oil]], [[4oiu\|4oiu]], [[4oj9\|4oj9]], [[4ojb\|4ojb]], [[4ok1\|4ok1]], [[4okb\|4okb]], [[4okt\|4okt]], [[4okw\|4okw]], [[4okx\|4okx]], [[4olm\|4olm]]</td></tr>
	<tr><td class="sblockLbl"><b>Resources:</b></td><td class="sblockDat"><span class='plainlinks'>[http://oca.weizmann.ac.il/oca-docs/fgij/fg.htm?mol=4oha FirstGlance], [http://oca.weizmann.ac.il/oca-bin/ocaids?id=4oha OCA], [http://www.rcsb.org/pdb/explore.do?structureId=4oha RCSB], [http://www.ebi.ac.uk/pdbsum/4oha 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=4oha FirstGlance], [http://oca.weizmann.ac.il/oca-bin/ocaids?id=4oha OCA], [http://www.rcsb.org/pdb/explore.do?structureId=4oha RCSB], [http://www.ebi.ac.uk/pdbsum/4oha PDBsum]</span></td></tr>
	<table>		</table>
	== Disease ==		== Disease ==
	[[http://www.uniprot.org/uniprot/ANDR_HUMAN ANDR_HUMAN]] Defects in AR are the cause of androgen insensitivity syndrome (AIS) [MIM:[http://omim.org/entry/300068 300068]]; previously known as testicular feminization syndrome (TFM). AIS is an X-linked recessive form of pseudohermaphroditism due end-organ resistance to androgen. Affected males have female external genitalia, female breast development, blind vagina, absent uterus and female adnexa, and abdominal or inguinal testes, despite a normal 46,XY karyotype.<ref>PMID:2594783</ref> <ref>PMID:8413310</ref> <ref>PMID:1775137</ref> <ref>PMID:16129672</ref> <ref>PMID:2082179</ref> <ref>PMID:1999491</ref> <ref>PMID:1609793</ref> <ref>PMID:1426313</ref> <ref>PMID:1487249</ref> <ref>PMID:1307250</ref> <ref>PMID:1569163</ref> <ref>PMID:1464650</ref> <ref>PMID:1430233</ref> <ref>PMID:1316540</ref> <ref>PMID:1480178</ref> <ref>PMID:8224266</ref> <ref>PMID:8103398</ref> <ref>PMID:8281140</ref> <ref>PMID:8325950</ref> <ref>PMID:8096390</ref> <ref>PMID:8446106</ref> [:]<ref>PMID:8162033</ref> <ref>PMID:7981687</ref> <ref>PMID:7981689</ref> <ref>PMID:7962294</ref> <ref>PMID:8040309</ref> <ref>PMID:7929841</ref> <ref>PMID:7993455</ref> <ref>PMID:7970939</ref> <ref>PMID:8830623</ref> <ref>PMID:7641413</ref> <ref>PMID:7671849</ref> <ref>PMID:7633398</ref> <ref>PMID:7537149</ref> <ref>PMID:7581399</ref> <ref>PMID:8723113</ref> <ref>PMID:9039340</ref> <ref>PMID:9001799</ref> <ref>PMID:8626869</ref> <ref>PMID:8768864</ref> <ref>PMID:8918984</ref> <ref>PMID:8683794</ref> <ref>PMID:8647313</ref> <ref>PMID:8809734</ref> <ref>PMID:9106550</ref> <ref>PMID:9160185</ref> <ref>PMID:9007482</ref> <ref>PMID:8990010</ref> <ref>PMID:9255042</ref> <ref>PMID:9252933</ref> <ref>PMID:9328206</ref> <ref>PMID:9302173</ref> <ref>PMID:9544375</ref> <ref>PMID:9698822</ref> <ref>PMID:9788719</ref> <ref>PMID:9610419</ref> <ref>PMID:9856504</ref> <ref>PMID:9554754</ref> [:]<ref>PMID:9851768</ref> <ref>PMID:9627582</ref> <ref>PMID:10571951</ref> <ref>PMID:10221692</ref> <ref>PMID:10404311</ref> <ref>PMID:10022458</ref> <ref>PMID:10221770</ref> <ref>PMID:10590024</ref> <ref>PMID:10458483</ref> <ref>PMID:10690872</ref> <ref>PMID:11587068</ref> <ref>PMID:11744994</ref> <ref>PMID:16595706</ref> Defects in AR are the cause of spinal and bulbar muscular atrophy X-linked type 1 (SMAX1) [MIM:[http://omim.org/entry/313200 313200]]; also known as Kennedy disease. SMAX1 is an X-linked recessive form of spinal muscular atrophy. Spinal muscular atrophy refers to a group of neuromuscular disorders characterized by degeneration of the anterior horn cells of the spinal cord, leading to symmetrical muscle weakness and atrophy. SMAX1 occurs only in men. Age at onset is usually in the third to fifth decade of life, but earlier involvement has been reported. It is characterized by slowly progressive limb and bulbar muscle weakness with fasciculations, muscle atrophy, and gynecomastia. The disorder is clinically similar to classic forms of autosomal spinal muscular atrophy. Note=Caused by trinucleotide CAG repeat expansion. In SMAX1 patients the number of Gln ranges from 38 to 62. Longer expansions result in earlier onset and more severe clinical manifestations of the disease.<ref>PMID:15851746</ref> Note=Defects in AR may play a role in metastatic prostate cancer. The mutated receptor stimulates prostate growth and metastases development despite of androgen ablation. This treatment can reduce primary and metastatic lesions probably by inducing apoptosis of tumor cells when they express the wild-type receptor. Defects in AR are the cause of androgen insensitivity syndrome partial (PAIS) [MIM:[http://omim.org/entry/312300 312300]]; also known as Reifenstein syndrome. PAIS is characterized by hypospadias, hypogonadism, gynecomastia, genital ambiguity, normal XY karyotype, and a pedigree pattern consistent with X-linked recessive inheritance. Some patients present azoospermia or severe oligospermia without other clinical manifestations.		[[http://www.uniprot.org/uniprot/ANDR_HUMAN ANDR_HUMAN]] Defects in AR are the cause of androgen insensitivity syndrome (AIS) [MIM:[http://omim.org/entry/300068 300068]]; previously known as testicular feminization syndrome (TFM). AIS is an X-linked recessive form of pseudohermaphroditism due end-organ resistance to androgen. Affected males have female external genitalia, female breast development, blind vagina, absent uterus and female adnexa, and abdominal or inguinal testes, despite a normal 46,XY karyotype.<ref>PMID:2594783</ref> <ref>PMID:8413310</ref> <ref>PMID:1775137</ref> <ref>PMID:16129672</ref> <ref>PMID:2082179</ref> <ref>PMID:1999491</ref> <ref>PMID:1609793</ref> <ref>PMID:1426313</ref> <ref>PMID:1487249</ref> <ref>PMID:1307250</ref> <ref>PMID:1569163</ref> <ref>PMID:1464650</ref> <ref>PMID:1430233</ref> <ref>PMID:1316540</ref> <ref>PMID:1480178</ref> <ref>PMID:8224266</ref> <ref>PMID:8103398</ref> <ref>PMID:8281140</ref> <ref>PMID:8325950</ref> <ref>PMID:8096390</ref> <ref>PMID:8446106</ref> [:]<ref>PMID:8162033</ref> <ref>PMID:7981687</ref> <ref>PMID:7981689</ref> <ref>PMID:7962294</ref> <ref>PMID:8040309</ref> <ref>PMID:7929841</ref> <ref>PMID:7993455</ref> <ref>PMID:7970939</ref> <ref>PMID:8830623</ref> <ref>PMID:7641413</ref> <ref>PMID:7671849</ref> <ref>PMID:7633398</ref> <ref>PMID:7537149</ref> <ref>PMID:7581399</ref> <ref>PMID:8723113</ref> <ref>PMID:9039340</ref> <ref>PMID:9001799</ref> <ref>PMID:8626869</ref> <ref>PMID:8768864</ref> <ref>PMID:8918984</ref> <ref>PMID:8683794</ref> <ref>PMID:8647313</ref> <ref>PMID:8809734</ref> <ref>PMID:9106550</ref> <ref>PMID:9160185</ref> <ref>PMID:9007482</ref> <ref>PMID:8990010</ref> <ref>PMID:9255042</ref> <ref>PMID:9252933</ref> <ref>PMID:9328206</ref> <ref>PMID:9302173</ref> <ref>PMID:9544375</ref> <ref>PMID:9698822</ref> <ref>PMID:9788719</ref> <ref>PMID:9610419</ref> <ref>PMID:9856504</ref> <ref>PMID:9554754</ref> [:]<ref>PMID:9851768</ref> <ref>PMID:9627582</ref> <ref>PMID:10571951</ref> <ref>PMID:10221692</ref> <ref>PMID:10404311</ref> <ref>PMID:10022458</ref> <ref>PMID:10221770</ref> <ref>PMID:10590024</ref> <ref>PMID:10458483</ref> <ref>PMID:10690872</ref> <ref>PMID:11587068</ref> <ref>PMID:11744994</ref> <ref>PMID:16595706</ref> Defects in AR are the cause of spinal and bulbar muscular atrophy X-linked type 1 (SMAX1) [MIM:[http://omim.org/entry/313200 313200]]; also known as Kennedy disease. SMAX1 is an X-linked recessive form of spinal muscular atrophy. Spinal muscular atrophy refers to a group of neuromuscular disorders characterized by degeneration of the anterior horn cells of the spinal cord, leading to symmetrical muscle weakness and atrophy. SMAX1 occurs only in men. Age at onset is usually in the third to fifth decade of life, but earlier involvement has been reported. It is characterized by slowly progressive limb and bulbar muscle weakness with fasciculations, muscle atrophy, and gynecomastia. The disorder is clinically similar to classic forms of autosomal spinal muscular atrophy. Note=Caused by trinucleotide CAG repeat expansion. In SMAX1 patients the number of Gln ranges from 38 to 62. Longer expansions result in earlier onset and more severe clinical manifestations of the disease.<ref>PMID:15851746</ref> Note=Defects in AR may play a role in metastatic prostate cancer. The mutated receptor stimulates prostate growth and metastases development despite of androgen ablation. This treatment can reduce primary and metastatic lesions probably by inducing apoptosis of tumor cells when they express the wild-type receptor. Defects in AR are the cause of androgen insensitivity syndrome partial (PAIS) [MIM:[http://omim.org/entry/312300 312300]]; also known as Reifenstein syndrome. PAIS is characterized by hypospadias, hypogonadism, gynecomastia, genital ambiguity, normal XY karyotype, and a pedigree pattern consistent with X-linked recessive inheritance. Some patients present azoospermia or severe oligospermia without other clinical manifestations.
Line 23:		Line 23:
	__TOC__		__TOC__
	</StructureSection>		</StructureSection>
	[[Category: Hsu, C L.]]		[[Category: Hsu, C L]]
	[[Category: Liu, J S.]]		[[Category: Liu, J S]]
	[[Category: Wu, W G.]]		[[Category: Wu, W G]]
	[[Category: Alpha-helix]]		[[Category: Alpha-helix]]
	[[Category: Hormone receptor-peptide complex]]		[[Category: Hormone receptor-peptide complex]]

OCA at 16:16, 20 August 2014

2014-08-20T16:16:20Z

@@ Line 1: / Line 1: @@
-'''Unreleased structure'''
+==Crystal structure of T877A-AR-LBD bound with co-regulator peptide==
-The entry 4oha is ON HOLD  until Paper Publication
+Identification of a new androgen receptor (AR) co-regulator BUD31 and related peptides to suppress wild-type and mutated AR-mediated prostate cancer growth via peptide screening and X-ray structure analysis.,Hsu CL, Liu JS, Wu PL, Guan HH, Chen YL, Lin AC, Ting HJ, Pang ST, Yeh SD, Ma WL, Chen CJ, Wu WG, Chang C Mol Oncol. 2014 Jun 24. pii: S1574-7891(14)00133-1. doi:, 10.1016/j.molonc.2014.06.009. PMID:25091737<ref>PMID:25091737</ref>
-Authors: Liu, J.S., Hsu, C.L., Wu, W.G.
+From MEDLINE&reg;/PubMed&reg;, a database of the U.S. National Library of Medicine.<br>
+</div>
-Description: Crystal structure of T877A-AR-LBD bound with co-regulator peptide
+== References ==

OCA at 06:16, 30 April 2014

2014-04-30T06:16:26Z

← Older revision		Revision as of 06:16, 30 April 2014
Line 1:		Line 1:
	'''Unreleased structure'''		'''Unreleased structure'''

	The entry 4oha is ON HOLD		The entry 4oha is ON HOLD until Paper Publication

	Authors: Liu, J.S., Hsu, C.L., Wu, W.G.		Authors: Liu, J.S., Hsu, C.L., Wu, W.G.

	Description: Crystal structure of T877A-AR-LBD bound with co-regulator peptide		Description: Crystal structure of T877A-AR-LBD bound with co-regulator peptide

OCA at 07:18, 23 April 2014

2014-04-23T07:18:03Z

← Older revision		Revision as of 07:18, 23 April 2014
Line 5:		Line 5:
	Authors: Liu, J.S., Hsu, C.L., Wu, W.G.		Authors: Liu, J.S., Hsu, C.L., Wu, W.G.

	Description: ~~crystals~~ of T877A-AR-LBD bound with ~~variant peptides~~		Description: Crystal structure of T877A-AR-LBD bound with co-regulator peptide

OCA: Protected "4oha" [edit=sysop:move=sysop]

2014-01-29T07:08:24Z

Protected "4oha" [edit=sysop:move=sysop]

← Older revision	Revision as of 07:08, 29 January 2014
(No difference)

OCA: New page: '''Unreleased structure''' The entry 4oha is ON HOLD Authors: Liu, J.S., Hsu, C.L., Wu, W.G. Description: crystals of T877A-AR-LBD bound with variant peptides

2014-01-29T07:08:23Z

New page: '''Unreleased structure''' The entry 4oha is ON HOLD Authors: Liu, J.S., Hsu, C.L., Wu, W.G. Description: crystals of T877A-AR-LBD bound with variant peptides

New page

'''Unreleased structure'''

The entry 4oha is ON HOLD

Authors: Liu, J.S., Hsu, C.L., Wu, W.G.

Description: crystals of T877A-AR-LBD bound with variant peptides