7z72 - Revision history

OCA at 13:29, 1 February 2024

OCA — Thu, 01 Feb 2024 13:29:40 GMT

←Older revision		Revision as of 13:29, 1 February 2024
Line 4:		Line 4:
	== Structural highlights ==		== Structural highlights ==
	<table><tr><td colspan='2'>[[7z72]] is a 2 chain structure with sequence from [https://en.wikipedia.org/wiki/Homo_sapiens Homo sapiens] and [https://en.wikipedia.org/wiki/Synthetic_construct Synthetic construct]. Full crystallographic information is available from [http://oca.weizmann.ac.il/oca-bin/ocashort?id=7Z72 OCA]. For a <b>guided tour on the structure components</b> use [https://proteopedia.org/fgij/fg.htm?mol=7Z72 FirstGlance]. <br>		<table><tr><td colspan='2'>[[7z72]] is a 2 chain structure with sequence from [https://en.wikipedia.org/wiki/Homo_sapiens Homo sapiens] and [https://en.wikipedia.org/wiki/Synthetic_construct Synthetic construct]. Full crystallographic information is available from [http://oca.weizmann.ac.il/oca-bin/ocashort?id=7Z72 OCA]. For a <b>guided tour on the structure components</b> use [https://proteopedia.org/fgij/fg.htm?mol=7Z72 FirstGlance]. <br>
-	</td></tr><tr id='ligand'><td class="sblockLbl"><b>[[Ligand\|Ligands:]]</b></td><td class="sblockDat" id="ligandDat"><scene name='pdbligand=PEG:DI(HYDROXYETHYL)ETHER'>PEG</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]] 1.8Å</td></tr>
		+	<tr id='ligand'><td class="sblockLbl"><b>[[Ligand\|Ligands:]]</b></td><td class="sblockDat" id="ligandDat"><scene name='pdbligand=PEG:DI(HYDROXYETHYL)ETHER'>PEG</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=7z72 FirstGlance], [http://oca.weizmann.ac.il/oca-bin/ocaids?id=7z72 OCA], [https://pdbe.org/7z72 PDBe], [https://www.rcsb.org/pdb/explore.do?structureId=7z72 RCSB], [https://www.ebi.ac.uk/pdbsum/7z72 PDBsum], [https://prosat.h-its.org/prosat/prosatexe?pdbcode=7z72 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=7z72 FirstGlance], [http://oca.weizmann.ac.il/oca-bin/ocaids?id=7z72 OCA], [https://pdbe.org/7z72 PDBe], [https://www.rcsb.org/pdb/explore.do?structureId=7z72 RCSB], [https://www.ebi.ac.uk/pdbsum/7z72 PDBsum], [https://prosat.h-its.org/prosat/prosatexe?pdbcode=7z72 ProSAT]</span></td></tr>
	</table>		</table>
Line 11:		Line 12:
	== Function ==		== Function ==
	[https://www.uniprot.org/uniprot/P63_HUMAN P63_HUMAN] Acts as a sequence specific DNA binding transcriptional activator or repressor. The isoforms contain a varying set of transactivation and auto-regulating transactivation inhibiting domains thus showing an isoform specific activity. Isoform 2 activates RIPK4 transcription. May be required in conjunction with TP73/p73 for initiation of p53/TP53 dependent apoptosis in response to genotoxic insults and the presence of activated oncogenes. Involved in Notch signaling by probably inducing JAG1 and JAG2. Plays a role in the regulation of epithelial morphogenesis. The ratio of DeltaN-type and TA*-type isoforms may govern the maintenance of epithelial stem cell compartments and regulate the initiation of epithelial stratification from the undifferentiated embryonal ectoderm. Required for limb formation from the apical ectodermal ridge. Activates transcription of the p21 promoter.<ref>PMID:9774969</ref> <ref>PMID:11641404</ref> <ref>PMID:12446779</ref> <ref>PMID:12446784</ref> <ref>PMID:12374749</ref> <ref>PMID:20123734</ref> <ref>PMID:22197488</ref>		[https://www.uniprot.org/uniprot/P63_HUMAN P63_HUMAN] Acts as a sequence specific DNA binding transcriptional activator or repressor. The isoforms contain a varying set of transactivation and auto-regulating transactivation inhibiting domains thus showing an isoform specific activity. Isoform 2 activates RIPK4 transcription. May be required in conjunction with TP73/p73 for initiation of p53/TP53 dependent apoptosis in response to genotoxic insults and the presence of activated oncogenes. Involved in Notch signaling by probably inducing JAG1 and JAG2. Plays a role in the regulation of epithelial morphogenesis. The ratio of DeltaN-type and TA*-type isoforms may govern the maintenance of epithelial stem cell compartments and regulate the initiation of epithelial stratification from the undifferentiated embryonal ectoderm. Required for limb formation from the apical ectodermal ridge. Activates transcription of the p21 promoter.<ref>PMID:9774969</ref> <ref>PMID:11641404</ref> <ref>PMID:12446779</ref> <ref>PMID:12446784</ref> <ref>PMID:12374749</ref> <ref>PMID:20123734</ref> <ref>PMID:22197488</ref>
		+
		+	==See Also==
		+	*[[P63\|P63]]
	== References ==		== References ==
	<references/>		<references/>

OCA at 09:17, 28 December 2022

OCA — Wed, 28 Dec 2022 09:17:30 GMT

←Older revision		Revision as of 09:17, 28 December 2022
Line 8:		Line 8:
	</table>		</table>
	== Disease ==		== Disease ==
-	[[https://www.uniprot.org/uniprot/P63_HUMAN P63_HUMAN]] Defects in TP63 are the cause of acro-dermato-ungual-lacrimal-tooth syndrome (ADULT syndrome) [MIM:[https://omim.org/entry/103285 103285]]; a form of ectodermal dysplasia. Ectodermal dysplasias (EDs) constitute a heterogeneous group of developmental disorders affecting tissues of ectodermal origin. EDs are characterized by abnormal development of two or more ectodermal structures such as hair, teeth, nails and sweat glands, with or without any additional clinical sign. Each combination of clinical features represents a different type of ectodermal dysplasia. ADULT syndrome involves ectrodactyly, syndactyly, finger- and toenail dysplasia, hypoplastic breasts and nipples, intensive freckling, lacrimal duct atresia, frontal alopecia, primary hypodontia, and loss of permanent teeth. ADULT differs significantly from EEC3 syndrome by the absence of facial clefting. Defects in TP63 are the cause of ankyloblepharon-ectodermal defects-cleft lip/palate (AEC) [MIM:[https://omim.org/entry/106260 106260]]. AEC is an autosomal dominant condition characterized by congenital ectodermal dysplasia with coarse, wiry, sparse hair, dystrophic nails, slight hypohidrosis, scalp infections, ankyloblepharon filiform adnatum, maxillary hypoplasia, hypodontia and cleft lip/palate.<ref>PMID:11159940</ref> Defects in TP63 are the cause of ectrodactyly-ectodermal dysplasia-cleft lip/palate syndrome type 3 (EEC3) [MIM:[https://omim.org/entry/604292 604292]]. EEC3 is an autosomal dominant syndrome characterized by ectrodactyly of hands and feet, ectodermal dysplasia and facial clefting.<ref>PMID:10535733</ref> <ref>PMID:10839977</ref> <ref>PMID:11462173</ref> <ref>PMID:12838557</ref> Defects in TP63 are the cause of split-hand/foot malformation type 4 (SHFM4) [MIM:[https://omim.org/entry/605289 605289]]. Split-hand/split-foot malformation is a limb malformation involving the central rays of the autopod and presenting with syndactyly, median clefts of the hands and feet, and aplasia and/or hypoplasia of the phalanges, metacarpals, and metatarsals. There is restricted overlap between the mutational spectra of EEC3 and SHFM4.<ref>PMID:10839977</ref> <ref>PMID:11462173</ref> Defects in TP63 are the cause of limb-mammary syndrome (LMS) [MIM:[https://omim.org/entry/603543 603543]]. LMS is characterized by ectrodactyly, cleft palate and mammary-gland abnormalities.<ref>PMID:11462173</ref> Note=Defects in TP63 are a cause of cervical, colon, head and neck, lung and ovarian cancers. Defects in TP63 are a cause of ectodermal dysplasia Rapp-Hodgkin type (EDRH) [MIM:[https://omim.org/entry/129400 129400]]; also called Rapp-Hodgkin syndrome or anhidrotic ectodermal dysplasia with cleft lip/palate. Ectodermal dysplasia defines a heterogeneous group of disorders due to abnormal development of two or more ectodermal structures. EDRH is characterized by the combination of anhidrotic ectodermal dysplasia, cleft lip, and cleft palate. The clinical syndrome is comprised of a characteristic facies (narrow nose and small mouth), wiry, slow-growing, and uncombable hair, sparse eyelashes and eyebrows, obstructed lacrimal puncta/epiphora, bilateral stenosis of external auditory canals, microsomia, hypodontia, cone-shaped incisors, enamel hypoplasia, dystrophic nails, and cleft lip/cleft palate.<ref>PMID:12939657</ref> <ref>PMID:12766194</ref> <ref>PMID:15200513</ref> <ref>PMID:16740912</ref> Defects in TP63 are the cause of non-syndromic orofacial cleft type 8 (OFC8) [MIM:[https://omim.org/entry/129400 129400]]. Non-syndromic orofacial cleft is a common birth defect consisting of cleft lips with or without cleft palate. Cleft lips are associated with cleft palate in two-third of cases. A cleft lip can occur on one or both sides and range in severity from a simple notch in the upper lip to a complete opening in the lip extending into the floor of the nostril and involving the upper gum.	+	[https://www.uniprot.org/uniprot/P63_HUMAN P63_HUMAN] Defects in TP63 are the cause of acro-dermato-ungual-lacrimal-tooth syndrome (ADULT syndrome) [MIM:[https://omim.org/entry/103285 103285]; a form of ectodermal dysplasia. Ectodermal dysplasias (EDs) constitute a heterogeneous group of developmental disorders affecting tissues of ectodermal origin. EDs are characterized by abnormal development of two or more ectodermal structures such as hair, teeth, nails and sweat glands, with or without any additional clinical sign. Each combination of clinical features represents a different type of ectodermal dysplasia. ADULT syndrome involves ectrodactyly, syndactyly, finger- and toenail dysplasia, hypoplastic breasts and nipples, intensive freckling, lacrimal duct atresia, frontal alopecia, primary hypodontia, and loss of permanent teeth. ADULT differs significantly from EEC3 syndrome by the absence of facial clefting. Defects in TP63 are the cause of ankyloblepharon-ectodermal defects-cleft lip/palate (AEC) [MIM:[https://omim.org/entry/106260 106260]. AEC is an autosomal dominant condition characterized by congenital ectodermal dysplasia with coarse, wiry, sparse hair, dystrophic nails, slight hypohidrosis, scalp infections, ankyloblepharon filiform adnatum, maxillary hypoplasia, hypodontia and cleft lip/palate.<ref>PMID:11159940</ref> Defects in TP63 are the cause of ectrodactyly-ectodermal dysplasia-cleft lip/palate syndrome type 3 (EEC3) [MIM:[https://omim.org/entry/604292 604292]. EEC3 is an autosomal dominant syndrome characterized by ectrodactyly of hands and feet, ectodermal dysplasia and facial clefting.<ref>PMID:10535733</ref> <ref>PMID:10839977</ref> <ref>PMID:11462173</ref> <ref>PMID:12838557</ref> Defects in TP63 are the cause of split-hand/foot malformation type 4 (SHFM4) [MIM:[https://omim.org/entry/605289 605289]. Split-hand/split-foot malformation is a limb malformation involving the central rays of the autopod and presenting with syndactyly, median clefts of the hands and feet, and aplasia and/or hypoplasia of the phalanges, metacarpals, and metatarsals. There is restricted overlap between the mutational spectra of EEC3 and SHFM4.<ref>PMID:10839977</ref> <ref>PMID:11462173</ref> Defects in TP63 are the cause of limb-mammary syndrome (LMS) [MIM:[https://omim.org/entry/603543 603543]. LMS is characterized by ectrodactyly, cleft palate and mammary-gland abnormalities.<ref>PMID:11462173</ref> Note=Defects in TP63 are a cause of cervical, colon, head and neck, lung and ovarian cancers. Defects in TP63 are a cause of ectodermal dysplasia Rapp-Hodgkin type (EDRH) [MIM:[https://omim.org/entry/129400 129400]; also called Rapp-Hodgkin syndrome or anhidrotic ectodermal dysplasia with cleft lip/palate. Ectodermal dysplasia defines a heterogeneous group of disorders due to abnormal development of two or more ectodermal structures. EDRH is characterized by the combination of anhidrotic ectodermal dysplasia, cleft lip, and cleft palate. The clinical syndrome is comprised of a characteristic facies (narrow nose and small mouth), wiry, slow-growing, and uncombable hair, sparse eyelashes and eyebrows, obstructed lacrimal puncta/epiphora, bilateral stenosis of external auditory canals, microsomia, hypodontia, cone-shaped incisors, enamel hypoplasia, dystrophic nails, and cleft lip/cleft palate.<ref>PMID:12939657</ref> <ref>PMID:12766194</ref> <ref>PMID:15200513</ref> <ref>PMID:16740912</ref> Defects in TP63 are the cause of non-syndromic orofacial cleft type 8 (OFC8) [MIM:[https://omim.org/entry/129400 129400]. Non-syndromic orofacial cleft is a common birth defect consisting of cleft lips with or without cleft palate. Cleft lips are associated with cleft palate in two-third of cases. A cleft lip can occur on one or both sides and range in severity from a simple notch in the upper lip to a complete opening in the lip extending into the floor of the nostril and involving the upper gum.
	== Function ==		== Function ==
-	[[https://www.uniprot.org/uniprot/P63_HUMAN P63_HUMAN]] Acts as a sequence specific DNA binding transcriptional activator or repressor. The isoforms contain a varying set of transactivation and auto-regulating transactivation inhibiting domains thus showing an isoform specific activity. Isoform 2 activates RIPK4 transcription. May be required in conjunction with TP73/p73 for initiation of p53/TP53 dependent apoptosis in response to genotoxic insults and the presence of activated oncogenes. Involved in Notch signaling by probably inducing JAG1 and JAG2. Plays a role in the regulation of epithelial morphogenesis. The ratio of DeltaN-type and TA*-type isoforms may govern the maintenance of epithelial stem cell compartments and regulate the initiation of epithelial stratification from the undifferentiated embryonal ectoderm. Required for limb formation from the apical ectodermal ridge. Activates transcription of the p21 promoter.<ref>PMID:9774969</ref> <ref>PMID:11641404</ref> <ref>PMID:12446779</ref> <ref>PMID:12446784</ref> <ref>PMID:12374749</ref> <ref>PMID:20123734</ref> <ref>PMID:22197488</ref>	+	[https://www.uniprot.org/uniprot/P63_HUMAN P63_HUMAN] Acts as a sequence specific DNA binding transcriptional activator or repressor. The isoforms contain a varying set of transactivation and auto-regulating transactivation inhibiting domains thus showing an isoform specific activity. Isoform 2 activates RIPK4 transcription. May be required in conjunction with TP73/p73 for initiation of p53/TP53 dependent apoptosis in response to genotoxic insults and the presence of activated oncogenes. Involved in Notch signaling by probably inducing JAG1 and JAG2. Plays a role in the regulation of epithelial morphogenesis. The ratio of DeltaN-type and TA*-type isoforms may govern the maintenance of epithelial stem cell compartments and regulate the initiation of epithelial stratification from the undifferentiated embryonal ectoderm. Required for limb formation from the apical ectodermal ridge. Activates transcription of the p21 promoter.<ref>PMID:9774969</ref> <ref>PMID:11641404</ref> <ref>PMID:12446779</ref> <ref>PMID:12446784</ref> <ref>PMID:12374749</ref> <ref>PMID:20123734</ref> <ref>PMID:22197488</ref>
	== References ==		== References ==
	<references/>		<references/>

OCA at 06:50, 8 September 2022

OCA — Thu, 08 Sep 2022 06:50:16 GMT

←Older revision		Revision as of 06:50, 8 September 2022
Line 1:		Line 1:

-	====	+	==Crystal structure of p63 SAM in complex with darpin A5==
-	<StructureSection load='7z72' size='340' side='right'caption='[[7z72]]' scene=''>	+	<StructureSection load='7z72' size='340' side='right'caption='[[7z72]], [[Resolution\|resolution]] 1.80Å' scene=''>
	== Structural highlights ==		== Structural highlights ==
-	<table><tr><td colspan='2'>Full crystallographic information is available from [http://oca.weizmann.ac.il/oca-bin/ocashort?id= OCA]. For a <b>guided tour on the structure components</b> use [https://proteopedia.org/fgij/fg.htm?mol= FirstGlance]. <br>	+	<table><tr><td colspan='2'>[[7z72]] is a 2 chain structure with sequence from [https://en.wikipedia.org/wiki/Homo_sapiens Homo sapiens] and [https://en.wikipedia.org/wiki/Synthetic_construct Synthetic construct]. Full crystallographic information is available from [http://oca.weizmann.ac.il/oca-bin/ocashort?id=7Z72 OCA]. For a <b>guided tour on the structure components</b> use [https://proteopedia.org/fgij/fg.htm?mol=7Z72 FirstGlance]. <br>
-	</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=7z72 FirstGlance], [http://oca.weizmann.ac.il/oca-bin/ocaids?id=7z72 OCA], [https://pdbe.org/7z72 PDBe], [https://www.rcsb.org/pdb/explore.do?structureId=7z72 RCSB], [https://www.ebi.ac.uk/pdbsum/7z72 PDBsum], [https://prosat.h-its.org/prosat/prosatexe?pdbcode=7z72 ProSAT]</span></td></tr>	+	</td></tr><tr id='ligand'><td class="sblockLbl"><b>[[Ligand\|Ligands:]]</b></td><td class="sblockDat" id="ligandDat"><scene name='pdbligand=PEG:DI(HYDROXYETHYL)ETHER'>PEG</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=7z72 FirstGlance], [http://oca.weizmann.ac.il/oca-bin/ocaids?id=7z72 OCA], [https://pdbe.org/7z72 PDBe], [https://www.rcsb.org/pdb/explore.do?structureId=7z72 RCSB], [https://www.ebi.ac.uk/pdbsum/7z72 PDBsum], [https://prosat.h-its.org/prosat/prosatexe?pdbcode=7z72 ProSAT]</span></td></tr>
	</table>		</table>
		+	== Disease ==
		+	[[https://www.uniprot.org/uniprot/P63_HUMAN P63_HUMAN]] Defects in TP63 are the cause of acro-dermato-ungual-lacrimal-tooth syndrome (ADULT syndrome) [MIM:[https://omim.org/entry/103285 103285]]; a form of ectodermal dysplasia. Ectodermal dysplasias (EDs) constitute a heterogeneous group of developmental disorders affecting tissues of ectodermal origin. EDs are characterized by abnormal development of two or more ectodermal structures such as hair, teeth, nails and sweat glands, with or without any additional clinical sign. Each combination of clinical features represents a different type of ectodermal dysplasia. ADULT syndrome involves ectrodactyly, syndactyly, finger- and toenail dysplasia, hypoplastic breasts and nipples, intensive freckling, lacrimal duct atresia, frontal alopecia, primary hypodontia, and loss of permanent teeth. ADULT differs significantly from EEC3 syndrome by the absence of facial clefting. Defects in TP63 are the cause of ankyloblepharon-ectodermal defects-cleft lip/palate (AEC) [MIM:[https://omim.org/entry/106260 106260]]. AEC is an autosomal dominant condition characterized by congenital ectodermal dysplasia with coarse, wiry, sparse hair, dystrophic nails, slight hypohidrosis, scalp infections, ankyloblepharon filiform adnatum, maxillary hypoplasia, hypodontia and cleft lip/palate.<ref>PMID:11159940</ref> Defects in TP63 are the cause of ectrodactyly-ectodermal dysplasia-cleft lip/palate syndrome type 3 (EEC3) [MIM:[https://omim.org/entry/604292 604292]]. EEC3 is an autosomal dominant syndrome characterized by ectrodactyly of hands and feet, ectodermal dysplasia and facial clefting.<ref>PMID:10535733</ref> <ref>PMID:10839977</ref> <ref>PMID:11462173</ref> <ref>PMID:12838557</ref> Defects in TP63 are the cause of split-hand/foot malformation type 4 (SHFM4) [MIM:[https://omim.org/entry/605289 605289]]. Split-hand/split-foot malformation is a limb malformation involving the central rays of the autopod and presenting with syndactyly, median clefts of the hands and feet, and aplasia and/or hypoplasia of the phalanges, metacarpals, and metatarsals. There is restricted overlap between the mutational spectra of EEC3 and SHFM4.<ref>PMID:10839977</ref> <ref>PMID:11462173</ref> Defects in TP63 are the cause of limb-mammary syndrome (LMS) [MIM:[https://omim.org/entry/603543 603543]]. LMS is characterized by ectrodactyly, cleft palate and mammary-gland abnormalities.<ref>PMID:11462173</ref> Note=Defects in TP63 are a cause of cervical, colon, head and neck, lung and ovarian cancers. Defects in TP63 are a cause of ectodermal dysplasia Rapp-Hodgkin type (EDRH) [MIM:[https://omim.org/entry/129400 129400]]; also called Rapp-Hodgkin syndrome or anhidrotic ectodermal dysplasia with cleft lip/palate. Ectodermal dysplasia defines a heterogeneous group of disorders due to abnormal development of two or more ectodermal structures. EDRH is characterized by the combination of anhidrotic ectodermal dysplasia, cleft lip, and cleft palate. The clinical syndrome is comprised of a characteristic facies (narrow nose and small mouth), wiry, slow-growing, and uncombable hair, sparse eyelashes and eyebrows, obstructed lacrimal puncta/epiphora, bilateral stenosis of external auditory canals, microsomia, hypodontia, cone-shaped incisors, enamel hypoplasia, dystrophic nails, and cleft lip/cleft palate.<ref>PMID:12939657</ref> <ref>PMID:12766194</ref> <ref>PMID:15200513</ref> <ref>PMID:16740912</ref> Defects in TP63 are the cause of non-syndromic orofacial cleft type 8 (OFC8) [MIM:[https://omim.org/entry/129400 129400]]. Non-syndromic orofacial cleft is a common birth defect consisting of cleft lips with or without cleft palate. Cleft lips are associated with cleft palate in two-third of cases. A cleft lip can occur on one or both sides and range in severity from a simple notch in the upper lip to a complete opening in the lip extending into the floor of the nostril and involving the upper gum.
		+	== Function ==
		+	[[https://www.uniprot.org/uniprot/P63_HUMAN P63_HUMAN]] Acts as a sequence specific DNA binding transcriptional activator or repressor. The isoforms contain a varying set of transactivation and auto-regulating transactivation inhibiting domains thus showing an isoform specific activity. Isoform 2 activates RIPK4 transcription. May be required in conjunction with TP73/p73 for initiation of p53/TP53 dependent apoptosis in response to genotoxic insults and the presence of activated oncogenes. Involved in Notch signaling by probably inducing JAG1 and JAG2. Plays a role in the regulation of epithelial morphogenesis. The ratio of DeltaN-type and TA*-type isoforms may govern the maintenance of epithelial stem cell compartments and regulate the initiation of epithelial stratification from the undifferentiated embryonal ectoderm. Required for limb formation from the apical ectodermal ridge. Activates transcription of the p21 promoter.<ref>PMID:9774969</ref> <ref>PMID:11641404</ref> <ref>PMID:12446779</ref> <ref>PMID:12446784</ref> <ref>PMID:12374749</ref> <ref>PMID:20123734</ref> <ref>PMID:22197488</ref>
		+	== References ==
		+	<references/>
	__TOC__		__TOC__
	</StructureSection>		</StructureSection>
		+	[[Category: Homo sapiens]]
	[[Category: Large Structures]]		[[Category: Large Structures]]
-	[[Category: ~~Z-disk~~]]	+	[[Category: Synthetic construct]]
		+	[[Category: Chaikuad A]]
		+	[[Category: Doetsch V]]
		+	[[Category: Knapp S]]
		+	[[Category: Strubel A]]

OCA at 16:16, 6 July 2022

OCA — Wed, 06 Jul 2022 16:16:13 GMT

←Older revision		Revision as of 16:16, 6 July 2022
Line 1:		Line 1:
-	'''Unreleased structure'''

-	~~The entry~~ 7z72 ~~is ON HOLD until Paper Publication~~	+	====
-		+	<StructureSection load='7z72' size='340' side='right'caption='[[7z72]]' scene=''>
-	~~Authors~~: ~~Chaikuad, A~~.~~, Strubel, A~~.~~, Doetsch, V~~.~~, Knapp, S~~.~~, Structural Genomics Consortium (SGC)~~	+	== Structural highlights ==
-		+	<table><tr><td colspan='2'>Full crystallographic information is available from [http://oca.weizmann.ac.il/oca-bin/ocashort?id= OCA]. For a <b>guided tour on the structure components</b> use [https://proteopedia.org/fgij/fg.htm?mol= FirstGlance]. <br>
-	~~Description: Crystal~~ structure ~~of p63 SAM in complex with darpin A5~~	+	</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=7z72 FirstGlance], [http://oca.weizmann.ac.il/oca-bin/ocaids?id=7z72 OCA], [https://pdbe.org/7z72 PDBe], [https://www.rcsb.org/pdb/explore.do?structureId=7z72 RCSB], [https://www.ebi.ac.uk/pdbsum/7z72 PDBsum], [https://prosat.h-its.org/prosat/prosatexe?pdbcode=7z72 ProSAT]</span></td></tr>
-	[~~[Category~~: ~~Unreleased Structures]~~]	+	</table>
-	[~~[Category~~: ~~Doetsch~~, V]]	+	__TOC__
-	[~~[Category~~: ~~Chaikuad~~, A]]	+	</StructureSection>
-	[~~[Category~~: ~~Knapp~~, S]]	+	[[Category: Large Structures]]
-	[[Category: ~~Strubel, A~~]]	+	[[Category: Z-disk]]
-	[[Category: ~~Structural Genomics Consortium (Sgc)~~]]	+

OCA at 08:45, 13 April 2022

OCA — Wed, 13 Apr 2022 08:45:45 GMT

←Older revision		Revision as of 08:45, 13 April 2022
Line 1:		Line 1:
	'''Unreleased structure'''		'''Unreleased structure'''

-	The entry 7z72 is ON HOLD	+	The entry 7z72 is ON HOLD until Paper Publication

	Authors: Chaikuad, A., Strubel, A., Doetsch, V., Knapp, S., Structural Genomics Consortium (SGC)		Authors: Chaikuad, A., Strubel, A., Doetsch, V., Knapp, S., Structural Genomics Consortium (SGC)
Line 9:		Line 9:
	[[Category: Doetsch, V]]		[[Category: Doetsch, V]]
	[[Category: Chaikuad, A]]		[[Category: Chaikuad, A]]
-	[[Category: Strubel, A]]
	[[Category: Knapp, S]]		[[Category: Knapp, S]]
		+	[[Category: Strubel, A]]
	[[Category: Structural Genomics Consortium (Sgc)]]		[[Category: Structural Genomics Consortium (Sgc)]]

OCA: Protected "7z72" [edit=sysop:move=sysop]

OCA — Wed, 23 Mar 2022 10:09:15 GMT

Protected "7z72" [edit=sysop:move=sysop]

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Revision as of 10:09, 23 March 2022

OCA: New page: '''Unreleased structure''' The entry 7z72 is ON HOLD Authors: Chaikuad, A., Strubel, A., Doetsch, V., Knapp, S., Structural Genomics Consortium (SGC) Description: Crystal structure of ...

OCA — Wed, 23 Mar 2022 10:09:14 GMT

New page: '''Unreleased structure''' The entry 7z72 is ON HOLD Authors: Chaikuad, A., Strubel, A., Doetsch, V., Knapp, S., Structural Genomics Consortium (SGC) Description: Crystal structure of ...

New page

'''Unreleased structure'''

The entry 7z72 is ON HOLD

Authors: Chaikuad, A., Strubel, A., Doetsch, V., Knapp, S., Structural Genomics Consortium (SGC)

Description: Crystal structure of p63 SAM in complex with darpin A5
[[Category: Unreleased Structures]]
[[Category: Doetsch, V]]
[[Category: Chaikuad, A]]
[[Category: Strubel, A]]
[[Category: Knapp, S]]
[[Category: Structural Genomics Consortium (Sgc)]]