4u4k - Revision history

OCA: Replacing page with 'REMOVED: The PDB entry 4u4k was removed.'

OCA — Wed, 11 May 2016 03:21:48 GMT

Replacing page with 'REMOVED: The PDB entry 4u4k was removed.'

←Older revision		Revision as of 03:21, 11 May 2016
Line 1:		Line 1:
-	~~==Structure-based study to overcome cross-reactivity of novel androgen receptor inhibitors==~~	+	REMOVED: The PDB entry 4u4k was removed.
-	~~<StructureSection load='4u4k' size='340' side='right' caption='[[4u4k]], [[Resolution\|resolution]] 1.20Å' scene=''>~~	+
-	~~== Structural highlights ==~~	+
-	~~<table><tr><td colspan='2'>[[4u4k]] is a 1 chain structure. Full crystallographic information is available from [http~~:~~//oca.weizmann.ac.il/oca-bin/ocashort?id=4U4K OCA]. For a <b>guided tour on the structure components</b> use [http://oca.weizmann.ac.il/oca-docs/fgij/fg.htm?mol=4U4K FirstGlance]. <br>~~	+
-	</td></tr><tr id='ligand'><td class="sblockLbl"><b>[[Ligand\|Ligands:]]</b></td><td class="sblockDat"><scene name='pdbligand=3E0:4-[4-(3-FLUORO-2-METHOXYPHENYL)-1,3-THIAZOL-2-YL]MORPHOLINE'>3E0</scene>, <scene name='pdbligand=EDO:1,2-ETHANEDIOL'>EDO</scene></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=4u4k FirstGlance], [http://oca.weizmann.ac.il/oca-bin/ocaids?id=4u4k OCA], [http://www.rcsb.org/pdb/explore.do?structureId=4u4k RCSB], [http://www.ebi.ac.uk/pdbsum/4u4k PDBsum]</span></td></tr>	+
-	~~</table>~~	+
-	~~== 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.	+
-	~~== 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>	+
-	~~== References ==~~	+
-	~~<references/>~~	+
-	~~__TOC__~~	+
-	~~</StructureSection>~~	+
-	~~[[Category: Ban, F]]~~	+
-	~~[[Category: Cherkasov, A]]~~	+
-	~~[[Category: Chow, B]]~~	+
-	~~[[Category: Ciesielski, F]]~~	+
-	~~[[Category: Dalal, K]]~~	+
-	~~[[Category: Lallous, N]]~~	+
-	~~[[Category: Leblanc, E]]~~	+
-	~~[[Category: Li, H]]~~	+
-	~~[[Category: Morin, M]]~~	+
-	~~[[Category: Rennie, P S]]~~	+
-	~~[[Category: Singh, K]]~~	+
-	~~[[Category: Agonist]]~~	+
-	~~[[Category: Ar]]~~	+
-	~~[[Category: Hormone receptor]]~~	+

OCA at 14:49, 29 July 2015

OCA — Wed, 29 Jul 2015 14:49:05 GMT

←Older revision		Revision as of 14:49, 29 July 2015
Line 1:		Line 1:
-	'''~~Unreleased structure~~'''	+	==Structure-based study to overcome cross-reactivity of novel androgen receptor inhibitors==
-		+	<StructureSection load='4u4k' size='340' side='right' caption='[[4u4k]], [[Resolution\|resolution]] 1.20Å' scene=''>
-	~~The entry~~ 4u4k is ~~ON HOLD until Jul 29 2016~~	+	== Structural highlights ==
-		+	<table><tr><td colspan='2'>[[4u4k]] is a 1 chain structure. Full crystallographic information is available from [http://oca.weizmann.ac.il/oca-bin/ocashort?id=4U4K OCA]. For a <b>guided tour on the structure components</b> use [http://oca.weizmann.ac.il/oca-docs/fgij/fg.htm?mol=4U4K FirstGlance]. <br>
-	~~Authors~~: ~~Lallous~~, N., Li, H., ~~Dalal~~, K., ~~Leblanc, E~~., ~~Ban~~, F., ~~Ciesielski~~, F., ~~Chow~~, B., ~~Morin, M~~., ~~Singh, K~~., ~~Rennie~~, P.S., ~~Cherkasov~~, A.	+	</td></tr><tr id='ligand'><td class="sblockLbl"><b>[[Ligand\|Ligands:]]</b></td><td class="sblockDat"><scene name='pdbligand=3E0:4-[4-(3-FLUORO-2-METHOXYPHENYL)-1,3-THIAZOL-2-YL]MORPHOLINE'>3E0</scene>, <scene name='pdbligand=EDO:1,2-ETHANEDIOL'>EDO</scene></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=4u4k FirstGlance], [http://oca.weizmann.ac.il/oca-bin/ocaids?id=4u4k OCA], [http://www.rcsb.org/pdb/explore.do?structureId=4u4k RCSB], [http://www.ebi.ac.uk/pdbsum/4u4k PDBsum]</span></td></tr>
-	~~Description~~: ~~Structure~~-~~based study to overcome cross~~-~~reactivity of novel androgen receptor inhibitors~~	+	</table>
-	[[Category: ~~Unreleased Structures~~]]	+	== 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.
		+	== 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>
		+	== References ==
		+	<references/>
		+	__TOC__
		+	</StructureSection>
		+	[[Category: Ban, F]]
	[[Category: Cherkasov, A]]		[[Category: Cherkasov, A]]
-	[[Category: Leblanc, E]]
-	[[Category: Dalal, K]]
-	[[Category: Morin, M]]
-	[[Category: Li, H]]
	[[Category: Chow, B]]		[[Category: Chow, B]]
-	[[Category: Rennie, P.S]]
-	[[Category: Ban, F]]
	[[Category: Ciesielski, F]]		[[Category: Ciesielski, F]]
		+	[[Category: Dalal, K]]
	[[Category: Lallous, N]]		[[Category: Lallous, N]]
		+	[[Category: Leblanc, E]]
		+	[[Category: Li, H]]
		+	[[Category: Morin, M]]
		+	[[Category: Rennie, P S]]
	[[Category: Singh, K]]		[[Category: Singh, K]]
		+	[[Category: Agonist]]
		+	[[Category: Ar]]
		+	[[Category: Hormone receptor]]

OCA at 10:17, 8 July 2015

OCA — Wed, 08 Jul 2015 10:17:50 GMT

←Older revision		Revision as of 10:17, 8 July 2015
Line 1:		Line 1:
	'''Unreleased structure'''		'''Unreleased structure'''

-	The entry 4u4k is ON HOLD until ~~Paper Publication~~	+	The entry 4u4k is ON HOLD until Jul 29 2016

	Authors: Lallous, N., Li, H., Dalal, K., Leblanc, E., Ban, F., Ciesielski, F., Chow, B., Morin, M., Singh, K., Rennie, P.S., Cherkasov, A.		Authors: Lallous, N., Li, H., Dalal, K., Leblanc, E., Ban, F., Ciesielski, F., Chow, B., Morin, M., Singh, K., Rennie, P.S., Cherkasov, A.

OCA at 09:24, 10 June 2015

OCA — Wed, 10 Jun 2015 09:24:09 GMT

←Older revision		Revision as of 09:24, 10 June 2015
Line 5:		Line 5:
	Authors: Lallous, N., Li, H., Dalal, K., Leblanc, E., Ban, F., Ciesielski, F., Chow, B., Morin, M., Singh, K., Rennie, P.S., Cherkasov, A.		Authors: Lallous, N., Li, H., Dalal, K., Leblanc, E., Ban, F., Ciesielski, F., Chow, B., Morin, M., Singh, K., Rennie, P.S., Cherkasov, A.

-	Description: ~~Molecular basis for accommodation of 4-(4-(3-fluoro-2-methoxyphenyl)thiazol~~-2-~~yl)morpholine into the ligand binding site~~ of ~~human~~ androgen receptor	+	Description: Structure-based study to overcome cross-reactivity of novel androgen receptor inhibitors
	[[Category: Unreleased Structures]]		[[Category: Unreleased Structures]]
	[[Category: Cherkasov, A]]		[[Category: Cherkasov, A]]

OCA at 18:08, 24 December 2014

OCA — Wed, 24 Dec 2014 18:08:18 GMT

←Older revision		Revision as of 18:08, 24 December 2014
Line 6:		Line 6:

	Description: Molecular basis for accommodation of 4-(4-(3-fluoro-2-methoxyphenyl)thiazol-2-yl)morpholine into the ligand binding site of human androgen receptor		Description: Molecular basis for accommodation of 4-(4-(3-fluoro-2-methoxyphenyl)thiazol-2-yl)morpholine into the ligand binding site of human androgen receptor
		+	[[Category: Unreleased Structures]]
		+	[[Category: Cherkasov, A]]
		+	[[Category: Leblanc, E]]
		+	[[Category: Dalal, K]]
		+	[[Category: Morin, M]]
		+	[[Category: Li, H]]
		+	[[Category: Chow, B]]
		+	[[Category: Rennie, P.S]]
		+	[[Category: Ban, F]]
		+	[[Category: Ciesielski, F]]
		+	[[Category: Lallous, N]]
		+	[[Category: Singh, K]]

OCA at 07:49, 5 November 2014

OCA — Wed, 05 Nov 2014 07:49:13 GMT

←Older revision		Revision as of 07:49, 5 November 2014
Line 1:		Line 1:
	'''Unreleased structure'''		'''Unreleased structure'''

-	The entry 4u4k is ON HOLD	+	The entry 4u4k is ON HOLD until Paper Publication

	Authors: Lallous, N., Li, H., Dalal, K., Leblanc, E., Ban, F., Ciesielski, F., Chow, B., Morin, M., Singh, K., Rennie, P.S., Cherkasov, A.		Authors: Lallous, N., Li, H., Dalal, K., Leblanc, E., Ban, F., Ciesielski, F., Chow, B., Morin, M., Singh, K., Rennie, P.S., Cherkasov, A.

	Description: Molecular basis for accommodation of 4-(4-(3-fluoro-2-methoxyphenyl)thiazol-2-yl)morpholine into the ligand binding site of human androgen receptor		Description: Molecular basis for accommodation of 4-(4-(3-fluoro-2-methoxyphenyl)thiazol-2-yl)morpholine into the ligand binding site of human androgen receptor

OCA at 01:30, 7 August 2014

OCA — Thu, 07 Aug 2014 01:30:11 GMT

←Older revision		Revision as of 01:30, 7 August 2014
Line 3:		Line 3:
	The entry 4u4k is ON HOLD		The entry 4u4k is ON HOLD

-	Authors: Lallous, N., Li, H., Dalal, K., Leblanc, E., Ban, F., Ciesielski, F., Chow, B., Morin M, Singh, K., Rennie, P.S., Cherkasov, A.	+	Authors: Lallous, N., Li, H., Dalal, K., Leblanc, E., Ban, F., Ciesielski, F., Chow, B., Morin, M., Singh, K., Rennie, P.S., Cherkasov, A.

	Description: Molecular basis for accommodation of 4-(4-(3-fluoro-2-methoxyphenyl)thiazol-2-yl)morpholine into the ligand binding site of human androgen receptor		Description: Molecular basis for accommodation of 4-(4-(3-fluoro-2-methoxyphenyl)thiazol-2-yl)morpholine into the ligand binding site of human androgen receptor

OCA: Protected "4u4k" [edit=sysop:move=sysop]

OCA — Wed, 30 Jul 2014 07:16:21 GMT

Protected "4u4k" [edit=sysop:move=sysop]

←Older revision

Revision as of 07:16, 30 July 2014

OCA: New page: '''Unreleased structure''' The entry 4u4k is ON HOLD Authors: Lallous, N., Li, H., Dalal, K., Leblanc, E., Ban, F., Ciesielski, F., Chow, B., Morin M, Singh, K., Rennie, P.S., Cherkasov...

OCA — Wed, 30 Jul 2014 07:16:20 GMT

New page: '''Unreleased structure''' The entry 4u4k is ON HOLD Authors: Lallous, N., Li, H., Dalal, K., Leblanc, E., Ban, F., Ciesielski, F., Chow, B., Morin M, Singh, K., Rennie, P.S., Cherkasov...

New page

'''Unreleased structure'''

The entry 4u4k is ON HOLD

Authors: Lallous, N., Li, H., Dalal, K., Leblanc, E., Ban, F., Ciesielski, F., Chow, B., Morin M, Singh, K., Rennie, P.S., Cherkasov, A.

Description: Molecular basis for accommodation of 4-(4-(3-fluoro-2-methoxyphenyl)thiazol-2-yl)morpholine into the ligand binding site of human androgen receptor