5aba - Revision history

OCA at 11:06, 10 January 2024

2024-01-10T11:06:51Z

← Older revision		Revision as of 11:06, 10 January 2024
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	== Structural highlights ==		== Structural highlights ==
	<table><tr><td colspan='2'>[[5aba]] 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=5ABA OCA]. For a <b>guided tour on the structure components</b> use [https://proteopedia.org/fgij/fg.htm?mol=5ABA FirstGlance]. <br>		<table><tr><td colspan='2'>[[5aba]] 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=5ABA OCA]. For a <b>guided tour on the structure components</b> use [https://proteopedia.org/fgij/fg.htm?mol=5ABA FirstGlance]. <br>
	</td></tr><tr id='ligand'><td class="sblockLbl"><b>[[Ligand\|Ligands:]]</b></td><td class="sblockDat" id="ligandDat"><scene name='pdbligand=UL7:1-{1-[(3-BROMO-5-CHLORO-2-HYDROXYPHENYL)METHYL+PIPERIDIN-4-YL}PIPERIDIN-4-OL]'>UL7</scene>, <scene name='pdbligand=ZN:ZINC+ION'>ZN</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]] 1.62Å</td></tr>
			<tr id='ligand'><td class="sblockLbl"><b>[[Ligand\|Ligands:]]</b></td><td class="sblockDat" id="ligandDat"><scene name='pdbligand=UL7:1-{1-[(3-BROMO-5-CHLORO-2-HYDROXYPHENYL)METHYL+PIPERIDIN-4-YL}PIPERIDIN-4-OL]'>UL7</scene>, <scene name='pdbligand=ZN:ZINC+ION'>ZN</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=5aba FirstGlance], [http://oca.weizmann.ac.il/oca-bin/ocaids?id=5aba OCA], [https://pdbe.org/5aba PDBe], [https://www.rcsb.org/pdb/explore.do?structureId=5aba RCSB], [https://www.ebi.ac.uk/pdbsum/5aba PDBsum], [https://prosat.h-its.org/prosat/prosatexe?pdbcode=5aba 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=5aba FirstGlance], [http://oca.weizmann.ac.il/oca-bin/ocaids?id=5aba OCA], [https://pdbe.org/5aba PDBe], [https://www.rcsb.org/pdb/explore.do?structureId=5aba RCSB], [https://www.ebi.ac.uk/pdbsum/5aba PDBsum], [https://prosat.h-its.org/prosat/prosatexe?pdbcode=5aba ProSAT]</span></td></tr>
	</table>		</table>

OCA at 04:49, 25 May 2023

2023-05-25T04:49:25Z

← Older revision		Revision as of 04:49, 25 May 2023
Line 3:		Line 3:
	<StructureSection load='5aba' size='340' side='right'caption='[[5aba]], [[Resolution\|resolution]] 1.62Å' scene=''>		<StructureSection load='5aba' size='340' side='right'caption='[[5aba]], [[Resolution\|resolution]] 1.62Å' scene=''>
	== Structural highlights ==		== Structural highlights ==
	<table><tr><td colspan='2'>[[5aba]] 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=5ABA OCA]. For a <b>guided tour on the structure components</b> use [~~http~~://~~oca~~.~~weizmann.ac.il/oca-docs~~/fgij/fg.htm?mol=5ABA FirstGlance]. <br>		<table><tr><td colspan='2'>[[5aba]] 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=5ABA OCA]. For a <b>guided tour on the structure components</b> use [https://proteopedia.org/fgij/fg.htm?mol=5ABA FirstGlance]. <br>
	</td></tr><tr id='ligand'><td class="sblockLbl"><b>[[Ligand\|Ligands:]]</b></td><td class="sblockDat"><scene name='pdbligand=UL7:1-{1-[(3-BROMO-5-CHLORO-2-HYDROXYPHENYL)METHYL+PIPERIDIN-4-YL}PIPERIDIN-4-OL]'>UL7</scene>, <scene name='pdbligand=ZN:ZINC+ION'>ZN</scene>~~</td></tr>~~		</td></tr><tr id='ligand'><td class="sblockLbl"><b>[[Ligand\|Ligands:]]</b></td><td class="sblockDat" id="ligandDat"><scene name='pdbligand=UL7:1-{1-[(3-BROMO-5-CHLORO-2-HYDROXYPHENYL)METHYL+PIPERIDIN-4-YL}PIPERIDIN-4-OL]'>UL7</scene>, <scene name='pdbligand=ZN:ZINC+ION'>ZN</scene></td></tr>
	~~<tr id='related'><td class="sblockLbl"><b>[[Related_structure\|Related:]]</b></td><td class="sblockDat">[[5ab9\|5ab9]]~~</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=5aba FirstGlance], [http://oca.weizmann.ac.il/oca-bin/ocaids?id=5aba OCA], [https://pdbe.org/5aba PDBe], [https://www.rcsb.org/pdb/explore.do?structureId=5aba RCSB], [https://www.ebi.ac.uk/pdbsum/5aba PDBsum], [https://prosat.h-its.org/prosat/prosatexe?pdbcode=5aba 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=5aba FirstGlance], [http://oca.weizmann.ac.il/oca-bin/ocaids?id=5aba OCA], [~~http~~://pdbe.org/5aba PDBe], [~~http~~://www.rcsb.org/pdb/explore.do?structureId=5aba RCSB], [~~http~~://www.ebi.ac.uk/pdbsum/5aba PDBsum], [~~http~~://prosat.h-its.org/prosat/prosatexe?pdbcode=5aba ProSAT]</span></td></tr>
	</table>		</table>
	== Disease ==		== Disease ==
	[~~[http~~://www.uniprot.org/uniprot/P53_HUMAN P53_HUMAN]] Note=TP53 is found in increased amounts in a wide variety of transformed cells. TP53 is frequently mutated or inactivated in about 60% of cancers. TP53 defects are found in Barrett metaplasia a condition in which the normally stratified squamous epithelium of the lower esophagus is replaced by a metaplastic columnar epithelium. The condition develops as a complication in approximately 10% of patients with chronic gastroesophageal reflux disease and predisposes to the development of esophageal adenocarcinoma. Defects in TP53 are a cause of esophageal cancer (ESCR) [MIM:[~~http~~://omim.org/entry/133239 133239]]. Defects in TP53 are a cause of Li-Fraumeni syndrome (LFS) [MIM:[~~http~~://omim.org/entry/151623 151623]]. LFS is an autosomal dominant familial cancer syndrome that in its classic form is defined by the existence of a proband affected by a sarcoma before 45 years with a first degree relative affected by any tumor before 45 years and another first degree relative with any tumor before 45 years or a sarcoma at any age. Other clinical definitions for LFS have been proposed (PubMed:8118819 and PubMed:8718514) and called Li-Fraumeni like syndrome (LFL). In these families affected relatives develop a diverse set of malignancies at unusually early ages. Four types of cancers account for 80% of tumors occurring in TP53 germline mutation carriers: breast cancers, soft tissue and bone sarcomas, brain tumors (astrocytomas) and adrenocortical carcinomas. Less frequent tumors include choroid plexus carcinoma or papilloma before the age of 15, rhabdomyosarcoma before the age of 5, leukemia, Wilms tumor, malignant phyllodes tumor, colorectal and gastric cancers.<ref>PMID:10570149</ref> <ref>PMID:1933902</ref> <ref>PMID:1978757</ref> <ref>PMID:2259385</ref> <ref>PMID:1737852</ref> <ref>PMID:1565144</ref> <ref>PMID:7887414</ref> <ref>PMID:8825920</ref> <ref>PMID:9452042</ref> <ref>PMID:10484981</ref> Defects in TP53 are involved in head and neck squamous cell carcinomas (HNSCC) [MIM:[~~http~~://omim.org/entry/275355 275355]]; also known as squamous cell carcinoma of the head and neck. Defects in TP53 are a cause of lung cancer (LNCR) [MIM:[~~http~~://omim.org/entry/211980 211980]]. LNCR is a common malignancy affecting tissues of the lung. The most common form of lung cancer is non-small cell lung cancer (NSCLC) that can be divided into 3 major histologic subtypes: squamous cell carcinoma, adenocarcinoma, and large cell lung cancer. NSCLC is often diagnosed at an advanced stage and has a poor prognosis. Defects in TP53 are a cause of choroid plexus papilloma (CPLPA) [MIM:[~~http~~://omim.org/entry/260500 260500]]. Choroid plexus papilloma is a slow-growing benign tumor of the choroid plexus that often invades the leptomeninges. In children it is usually in a lateral ventricle but in adults it is more often in the fourth ventricle. Hydrocephalus is common, either from obstruction or from tumor secretion of cerebrospinal fluid. If it undergoes malignant transformation it is called a choroid plexus carcinoma. Primary choroid plexus tumors are rare and usually occur in early childhood.<ref>PMID:12085209</ref> Defects in TP53 are a cause of adrenocortical carcinoma (ADCC) [MIM:[~~http~~://omim.org/entry/202300 202300]]. ADCC is a rare childhood tumor of the adrenal cortex. It occurs with increased frequency in patients with the Beckwith-Wiedemann syndrome and is a component tumor in Li-Fraumeni syndrome.<ref>PMID:11481490</ref> Defects in TP53 are the cause of susceptibility to basal cell carcinoma 7 (BCC7) [MIM:[~~http~~://omim.org/entry/614740 614740]]. A common malignant skin neoplasm that typically appears on hair-bearing skin, most commonly on sun-exposed areas. It is slow growing and rarely metastasizes, but has potentialities for local invasion and destruction. It usually develops as a flat, firm, pale area that is small, raised, pink or red, translucent, shiny, and waxy, and the area may bleed following minor injury. Tumor size can vary from a few millimeters to several centimeters in diameter.<ref>PMID:21946351</ref>		[https://www.uniprot.org/uniprot/P53_HUMAN P53_HUMAN] Note=TP53 is found in increased amounts in a wide variety of transformed cells. TP53 is frequently mutated or inactivated in about 60% of cancers. TP53 defects are found in Barrett metaplasia a condition in which the normally stratified squamous epithelium of the lower esophagus is replaced by a metaplastic columnar epithelium. The condition develops as a complication in approximately 10% of patients with chronic gastroesophageal reflux disease and predisposes to the development of esophageal adenocarcinoma. Defects in TP53 are a cause of esophageal cancer (ESCR) [MIM:[https://omim.org/entry/133239 133239]. Defects in TP53 are a cause of Li-Fraumeni syndrome (LFS) [MIM:[https://omim.org/entry/151623 151623]. LFS is an autosomal dominant familial cancer syndrome that in its classic form is defined by the existence of a proband affected by a sarcoma before 45 years with a first degree relative affected by any tumor before 45 years and another first degree relative with any tumor before 45 years or a sarcoma at any age. Other clinical definitions for LFS have been proposed (PubMed:8118819 and PubMed:8718514) and called Li-Fraumeni like syndrome (LFL). In these families affected relatives develop a diverse set of malignancies at unusually early ages. Four types of cancers account for 80% of tumors occurring in TP53 germline mutation carriers: breast cancers, soft tissue and bone sarcomas, brain tumors (astrocytomas) and adrenocortical carcinomas. Less frequent tumors include choroid plexus carcinoma or papilloma before the age of 15, rhabdomyosarcoma before the age of 5, leukemia, Wilms tumor, malignant phyllodes tumor, colorectal and gastric cancers.<ref>PMID:10570149</ref> <ref>PMID:1933902</ref> <ref>PMID:1978757</ref> <ref>PMID:2259385</ref> <ref>PMID:1737852</ref> <ref>PMID:1565144</ref> <ref>PMID:7887414</ref> <ref>PMID:8825920</ref> <ref>PMID:9452042</ref> <ref>PMID:10484981</ref> Defects in TP53 are involved in head and neck squamous cell carcinomas (HNSCC) [MIM:[https://omim.org/entry/275355 275355]; also known as squamous cell carcinoma of the head and neck. Defects in TP53 are a cause of lung cancer (LNCR) [MIM:[https://omim.org/entry/211980 211980]. LNCR is a common malignancy affecting tissues of the lung. The most common form of lung cancer is non-small cell lung cancer (NSCLC) that can be divided into 3 major histologic subtypes: squamous cell carcinoma, adenocarcinoma, and large cell lung cancer. NSCLC is often diagnosed at an advanced stage and has a poor prognosis. Defects in TP53 are a cause of choroid plexus papilloma (CPLPA) [MIM:[https://omim.org/entry/260500 260500]. Choroid plexus papilloma is a slow-growing benign tumor of the choroid plexus that often invades the leptomeninges. In children it is usually in a lateral ventricle but in adults it is more often in the fourth ventricle. Hydrocephalus is common, either from obstruction or from tumor secretion of cerebrospinal fluid. If it undergoes malignant transformation it is called a choroid plexus carcinoma. Primary choroid plexus tumors are rare and usually occur in early childhood.<ref>PMID:12085209</ref> Defects in TP53 are a cause of adrenocortical carcinoma (ADCC) [MIM:[https://omim.org/entry/202300 202300]. ADCC is a rare childhood tumor of the adrenal cortex. It occurs with increased frequency in patients with the Beckwith-Wiedemann syndrome and is a component tumor in Li-Fraumeni syndrome.<ref>PMID:11481490</ref> Defects in TP53 are the cause of susceptibility to basal cell carcinoma 7 (BCC7) [MIM:[https://omim.org/entry/614740 614740]. A common malignant skin neoplasm that typically appears on hair-bearing skin, most commonly on sun-exposed areas. It is slow growing and rarely metastasizes, but has potentialities for local invasion and destruction. It usually develops as a flat, firm, pale area that is small, raised, pink or red, translucent, shiny, and waxy, and the area may bleed following minor injury. Tumor size can vary from a few millimeters to several centimeters in diameter.<ref>PMID:21946351</ref>
	== Function ==		== Function ==
	[~~[http~~://www.uniprot.org/uniprot/P53_HUMAN P53_HUMAN]] Acts as a tumor suppressor in many tumor types; induces growth arrest or apoptosis depending on the physiological circumstances and cell type. Involved in cell cycle regulation as a trans-activator that acts to negatively regulate cell division by controlling a set of genes required for this process. One of the activated genes is an inhibitor of cyclin-dependent kinases. Apoptosis induction seems to be mediated either by stimulation of BAX and FAS antigen expression, or by repression of Bcl-2 expression. In cooperation with mitochondrial PPIF is involved in activating oxidative stress-induced necrosis; te function is largely independent of transcription. Induces the transcription of long intergenic non-coding RNA p21 (lincRNA-p21) and lincRNA-Mkln1. LincRNA-p21 participates in TP53-dependent transcriptional repression leading to apoptosis and seem to have to effect on cell-cycle regulation. Implicated in Notch signaling cross-over. Prevents CDK7 kinase activity when associated to CAK complex in response to DNA damage, thus stopping cell cycle progression. Isoform 2 enhances the transactivation activity of isoform 1 from some but not all TP53-inducible promoters. Isoform 4 suppresses transactivation activity and impairs growth suppression mediated by isoform 1. Isoform 7 inhibits isoform 1-mediated apoptosis.<ref>PMID:9840937</ref> <ref>PMID:11025664</ref> <ref>PMID:12810724</ref> <ref>PMID:15186775</ref> <ref>PMID:15340061</ref> <ref>PMID:17317671</ref> <ref>PMID:17349958</ref> <ref>PMID:19556538</ref> <ref>PMID:20673990</ref> <ref>PMID:20959462</ref> <ref>PMID:22726440</ref>		[https://www.uniprot.org/uniprot/P53_HUMAN P53_HUMAN] Acts as a tumor suppressor in many tumor types; induces growth arrest or apoptosis depending on the physiological circumstances and cell type. Involved in cell cycle regulation as a trans-activator that acts to negatively regulate cell division by controlling a set of genes required for this process. One of the activated genes is an inhibitor of cyclin-dependent kinases. Apoptosis induction seems to be mediated either by stimulation of BAX and FAS antigen expression, or by repression of Bcl-2 expression. In cooperation with mitochondrial PPIF is involved in activating oxidative stress-induced necrosis; te function is largely independent of transcription. Induces the transcription of long intergenic non-coding RNA p21 (lincRNA-p21) and lincRNA-Mkln1. LincRNA-p21 participates in TP53-dependent transcriptional repression leading to apoptosis and seem to have to effect on cell-cycle regulation. Implicated in Notch signaling cross-over. Prevents CDK7 kinase activity when associated to CAK complex in response to DNA damage, thus stopping cell cycle progression. Isoform 2 enhances the transactivation activity of isoform 1 from some but not all TP53-inducible promoters. Isoform 4 suppresses transactivation activity and impairs growth suppression mediated by isoform 1. Isoform 7 inhibits isoform 1-mediated apoptosis.<ref>PMID:9840937</ref> <ref>PMID:11025664</ref> <ref>PMID:12810724</ref> <ref>PMID:15186775</ref> <ref>PMID:15340061</ref> <ref>PMID:17317671</ref> <ref>PMID:17349958</ref> <ref>PMID:19556538</ref> <ref>PMID:20673990</ref> <ref>PMID:20959462</ref> <ref>PMID:22726440</ref>
	<div style="background-color:#fffaf0;">		<div style="background-color:#fffaf0;">
	== Publication Abstract from PubMed ==		== Publication Abstract from PubMed ==
Line 23:		Line 22:

	==See Also==		==See Also==
	*[[P53\|P53]]		*[[P53 3D structures\|P53 3D structures]]
	== References ==		== References ==
	<references/>		<references/>
	__TOC__		__TOC__
	</StructureSection>		</StructureSection>
	[[Category: ~~Human~~]]		[[Category: Homo sapiens]]
	[[Category: Large Structures]]		[[Category: Large Structures]]
	[[Category: Joerger~~, A C]]~~		[[Category: Joerger AC]]
	~~[[Category: Cancer]]~~
	~~[[Category: Cancer therapy]]~~
	~~[[Category: Dna binding]]~~
	~~[[Category: Halogen bonding]]~~
	~~[[Category: Molecular chaperone]]~~
	~~[[Category: Small molecule stabilizer]]~~
	~~[[Category: Transcription]]~~
	~~[[Category: Tumor suppression~~]]

OCA at 12:56, 10 May 2019

2019-05-10T12:56:53Z

← Older revision		Revision as of 12:56, 10 May 2019
Line 1:		Line 1:

	==Structure of the p53 cancer mutant Y220C with bound small-molecule stabilizer PhiKan5149==		==Structure of the p53 cancer mutant Y220C with bound small-molecule stabilizer PhiKan5149==
	<StructureSection load='5aba' size='340' side='right' caption='[[5aba]], [[Resolution\|resolution]] 1.62Å' scene=''>		<StructureSection load='5aba' size='340' side='right'caption='[[5aba]], [[Resolution\|resolution]] 1.62Å' scene=''>
	== Structural highlights ==		== Structural highlights ==
	<table><tr><td colspan='2'>[[5aba]] is a 2 chain structure. Full crystallographic information is available from [http://oca.weizmann.ac.il/oca-bin/ocashort?id=5ABA OCA]. For a <b>guided tour on the structure components</b> use [http://oca.weizmann.ac.il/oca-docs/fgij/fg.htm?mol=5ABA FirstGlance]. <br>		<table><tr><td colspan='2'>[[5aba]] 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=5ABA OCA]. For a <b>guided tour on the structure components</b> use [http://oca.weizmann.ac.il/oca-docs/fgij/fg.htm?mol=5ABA FirstGlance]. <br>
	</td></tr><tr id='ligand'><td class="sblockLbl"><b>[[Ligand\|Ligands:]]</b></td><td class="sblockDat"><scene name='pdbligand=UL7:1-{1-[(3-BROMO-5-CHLORO-2-HYDROXYPHENYL)METHYL+PIPERIDIN-4-YL}PIPERIDIN-4-OL]'>UL7</scene>, <scene name='pdbligand=ZN:ZINC+ION'>ZN</scene></td></tr>		</td></tr><tr id='ligand'><td class="sblockLbl"><b>[[Ligand\|Ligands:]]</b></td><td class="sblockDat"><scene name='pdbligand=UL7:1-{1-[(3-BROMO-5-CHLORO-2-HYDROXYPHENYL)METHYL+PIPERIDIN-4-YL}PIPERIDIN-4-OL]'>UL7</scene>, <scene name='pdbligand=ZN:ZINC+ION'>ZN</scene></td></tr>
	<tr id='related'><td class="sblockLbl"><b>[[Related_structure\|Related:]]</b></td><td class="sblockDat">[[5ab9\|5ab9]]</td></tr>		<tr id='related'><td class="sblockLbl"><b>[[Related_structure\|Related:]]</b></td><td class="sblockDat">[[5ab9\|5ab9]]</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=5aba FirstGlance], [http://oca.weizmann.ac.il/oca-bin/ocaids?id=5aba OCA], [http://pdbe.org/5aba PDBe], [http://www.rcsb.org/pdb/explore.do?structureId=5aba RCSB], [http://www.ebi.ac.uk/pdbsum/5aba 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=5aba FirstGlance], [http://oca.weizmann.ac.il/oca-bin/ocaids?id=5aba OCA], [http://pdbe.org/5aba PDBe], [http://www.rcsb.org/pdb/explore.do?structureId=5aba RCSB], [http://www.ebi.ac.uk/pdbsum/5aba PDBsum], [http://prosat.h-its.org/prosat/prosatexe?pdbcode=5aba ProSAT]</span></td></tr>
	</table>		</table>
	== Disease ==		== Disease ==
Line 20:		Line 21:
	</div>		</div>
	<div class="pdbe-citations 5aba" style="background-color:#fffaf0;"></div>		<div class="pdbe-citations 5aba" style="background-color:#fffaf0;"></div>

			==See Also==
			*[[P53\|P53]]
	== References ==		== References ==
	<references/>		<references/>
	__TOC__		__TOC__
	</StructureSection>		</StructureSection>
			[[Category: Human]]
			[[Category: Large Structures]]
	[[Category: Joerger, A C]]		[[Category: Joerger, A C]]
	[[Category: Cancer]]		[[Category: Cancer]]

OCA at 13:48, 16 December 2015

2015-12-16T13:48:33Z

@@ Line 1: / Line 1: @@
-'''Unreleased structure'''
+==Structure of the p53 cancer mutant Y220C with bound small-molecule stabilizer PhiKan5149==
-The entry 5aba is ON HOLD  until Paper Publication
+Exploiting Transient Protein States for the Design of Small-Molecule Stabilizers of Mutant p53.,Joerger AC, Bauer MR, Wilcken R, Baud MG, Harbrecht H, Exner TE, Boeckler FM, Spencer J, Fersht AR Structure. 2015 Dec 1;23(12):2246-55. doi: 10.1016/j.str.2015.10.016. PMID:26636255<ref>PMID:26636255</ref>
-Authors: Joerger, A.C.
+From MEDLINE&reg;/PubMed&reg;, a database of the U.S. National Library of Medicine.<br>
+</div>
-Description: Structure of the p53 cancer mutant Y220C with bound small-molecule stabilizer PhiKan5149
+<div class="pdbe-citations 5aba" style="background-color:#fffaf0;"></div>
-[[Category: Unreleased Structures]]
+== References ==
-[[Category: Joerger, A.C]]
+<references/>

OCA at 11:02, 30 September 2015

2015-09-30T11:02:22Z

← Older revision		Revision as of 11:02, 30 September 2015
Line 1:		Line 1:
	'''Unreleased structure'''		'''Unreleased structure'''

	The entry 5aba is ON HOLD		The entry 5aba is ON HOLD until Paper Publication

	Authors: Joerger, A.C.		Authors: Joerger, A.C.

OCA: Protected "5aba" [edit=sysop:move=sysop]

2015-08-12T12:14:09Z

Protected "5aba" [edit=sysop:move=sysop]

← Older revision	Revision as of 12:14, 12 August 2015
(No difference)

OCA: New page: '''Unreleased structure''' The entry 5aba is ON HOLD Authors: Joerger, A.C. Description: Structure of the p53 cancer mutant Y220C with bound small-molecule stabilizer PhiKan5149 [[Cate...

2015-08-12T12:14:07Z

New page: '''Unreleased structure''' The entry 5aba is ON HOLD Authors: Joerger, A.C. Description: Structure of the p53 cancer mutant Y220C with bound small-molecule stabilizer PhiKan5149 [[Cate...

New page

'''Unreleased structure'''

The entry 5aba is ON HOLD

Authors: Joerger, A.C.

Description: Structure of the p53 cancer mutant Y220C with bound small-molecule stabilizer PhiKan5149
[[Category: Unreleased Structures]]
[[Category: Joerger, A.C]]