7ztz - Revision history

OCA at 08:06, 7 February 2024

OCA — Wed, 07 Feb 2024 08:06:40 GMT

←Older revision		Revision as of 08:06, 7 February 2024
Line 4:		Line 4:
	== Structural highlights ==		== Structural highlights ==
	<table><tr><td colspan='2'>[[7ztz]] is a 1 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=7ZTZ OCA]. For a <b>guided tour on the structure components</b> use [https://proteopedia.org/fgij/fg.htm?mol=7ZTZ FirstGlance]. <br>		<table><tr><td colspan='2'>[[7ztz]] is a 1 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=7ZTZ OCA]. For a <b>guided tour on the structure components</b> use [https://proteopedia.org/fgij/fg.htm?mol=7ZTZ FirstGlance]. <br>
-	</td></tr><tr id='ligand'><td class="sblockLbl"><b>[[Ligand\|Ligands:]]</b></td><td class="sblockDat" id="ligandDat"><scene name='pdbligand=DHT:5-ALPHA-DIHYDROTESTOSTERONE'>DHT</scene>, <scene name='pdbligand=IMD:IMIDAZOLE'>IMD</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]] 1.4Å</td></tr>
		+	<tr id='ligand'><td class="sblockLbl"><b>[[Ligand\|Ligands:]]</b></td><td class="sblockDat" id="ligandDat"><scene name='pdbligand=DHT:5-ALPHA-DIHYDROTESTOSTERONE'>DHT</scene>, <scene name='pdbligand=IMD:IMIDAZOLE'>IMD</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=7ztz FirstGlance], [http://oca.weizmann.ac.il/oca-bin/ocaids?id=7ztz OCA], [https://pdbe.org/7ztz PDBe], [https://www.rcsb.org/pdb/explore.do?structureId=7ztz RCSB], [https://www.ebi.ac.uk/pdbsum/7ztz PDBsum], [https://prosat.h-its.org/prosat/prosatexe?pdbcode=7ztz 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=7ztz FirstGlance], [http://oca.weizmann.ac.il/oca-bin/ocaids?id=7ztz OCA], [https://pdbe.org/7ztz PDBe], [https://www.rcsb.org/pdb/explore.do?structureId=7ztz RCSB], [https://www.ebi.ac.uk/pdbsum/7ztz PDBsum], [https://prosat.h-its.org/prosat/prosatexe?pdbcode=7ztz ProSAT]</span></td></tr>
	</table>		</table>

OCA at 07:19, 22 March 2023

OCA — Wed, 22 Mar 2023 07:19:54 GMT

←Older revision		Revision as of 07:19, 22 March 2023
Line 1:		Line 1:
-	'''Unreleased structure'''

-	~~The entry~~ 7ztz ~~is ON HOLD until Paper Publication~~	+	==Crystal structure of mutant AR-LBD (Y764C) bound to dihydrotestosterone==
-		+	<StructureSection load='7ztz' size='340' side='right'caption='[[7ztz]], [[Resolution\|resolution]] 1.40Å' scene=''>
-	~~Authors~~: ~~Alegre~~-~~Marti~~, A., ~~Jimenez~~-~~Panizo~~, A., ~~Estebanez-Perpina~~, E., ~~Fuentes~~-~~Prior, P~~.	+	== Structural highlights ==
-		+	<table><tr><td colspan='2'>[[7ztz]] is a 1 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=7ZTZ OCA]. For a <b>guided tour on the structure components</b> use [https://proteopedia.org/fgij/fg.htm?mol=7ZTZ FirstGlance]. <br>
-	~~Description~~: ~~Crystal structure~~ of ~~mutant~~ AR-~~LBD~~ (~~Y764C~~) ~~bound~~ to ~~dihydrotestosterone~~	+	</td></tr><tr id='ligand'><td class="sblockLbl"><b>[[Ligand\|Ligands:]]</b></td><td class="sblockDat" id="ligandDat"><scene name='pdbligand=DHT:5-ALPHA-DIHYDROTESTOSTERONE'>DHT</scene>, <scene name='pdbligand=IMD:IMIDAZOLE'>IMD</scene>, <scene name='pdbligand=SO4:SULFATE+ION'>SO4</scene></td></tr>
-	[[Category: ~~Unreleased Structures~~]]	+	<tr id='resources'><td class="sblockLbl"><b>Resources:</b></td><td class="sblockDat"><span class='plainlinks'>[https://proteopedia.org/fgij/fg.htm?mol=7ztz FirstGlance], [http://oca.weizmann.ac.il/oca-bin/ocaids?id=7ztz OCA], [https://pdbe.org/7ztz PDBe], [https://www.rcsb.org/pdb/explore.do?structureId=7ztz RCSB], [https://www.ebi.ac.uk/pdbsum/7ztz PDBsum], [https://prosat.h-its.org/prosat/prosatexe?pdbcode=7ztz ProSAT]</span></td></tr>
-	[[Category: ~~Fuentes-Prior, P~~]]	+	</table>
-	[[Category: Alegre-Marti, A]]	+	== Disease ==
-	[[Category: ~~Jimenez~~-~~Panizo, A~~]]	+	[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.
-	[[Category: ~~Estebanez~~-~~Perpina, E~~]]	+	== Function ==
		+	[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>
		+	== References ==
		+	<references/>
		+	__TOC__
		+	</StructureSection>
		+	[[Category: Homo sapiens]]
		+	[[Category: Large Structures]]
		+	[[Category: Alegre-Marti A]]
		+	[[Category: Estebanez-Perpina E]]
		+	[[Category: Fuentes-Prior P]]
		+	[[Category: Jimenez-Panizo A]]

OCA at 04:03, 15 June 2022

OCA — Wed, 15 Jun 2022 04:03:32 GMT

←Older revision		Revision as of 04:03, 15 June 2022
Line 1:		Line 1:
	'''Unreleased structure'''		'''Unreleased structure'''

-	The entry 7ztz is ON HOLD	+	The entry 7ztz is ON HOLD until Paper Publication

	Authors: Alegre-Marti, A., Jimenez-Panizo, A., Estebanez-Perpina, E., Fuentes-Prior, P.		Authors: Alegre-Marti, A., Jimenez-Panizo, A., Estebanez-Perpina, E., Fuentes-Prior, P.

OCA: Protected "7ztz" [edit=sysop:move=sysop]

OCA — Wed, 18 May 2022 09:21:08 GMT

Protected "7ztz" [edit=sysop:move=sysop]

←Older revision

Revision as of 09:21, 18 May 2022

OCA: New page: '''Unreleased structure''' The entry 7ztz is ON HOLD Authors: Alegre-Marti, A., Jimenez-Panizo, A., Estebanez-Perpina, E., Fuentes-Prior, P. Description: Crystal structure of mutant AR...

OCA — Wed, 18 May 2022 09:21:07 GMT

New page: '''Unreleased structure''' The entry 7ztz is ON HOLD Authors: Alegre-Marti, A., Jimenez-Panizo, A., Estebanez-Perpina, E., Fuentes-Prior, P. Description: Crystal structure of mutant AR...

New page

'''Unreleased structure'''

The entry 7ztz is ON HOLD

Authors: Alegre-Marti, A., Jimenez-Panizo, A., Estebanez-Perpina, E., Fuentes-Prior, P.

Description: Crystal structure of mutant AR-LBD (Y764C) bound to dihydrotestosterone
[[Category: Unreleased Structures]]
[[Category: Fuentes-Prior, P]]
[[Category: Alegre-Marti, A]]
[[Category: Jimenez-Panizo, A]]
[[Category: Estebanez-Perpina, E]]