7tab - Revision history

OCA at 17:02, 18 October 2023

2023-10-18T17:02:52Z

←Older revision		Revision as of 17:02, 18 October 2023
Line 4:		Line 4:
	== Structural highlights ==		== Structural highlights ==
	<table><tr><td colspan='2'>[[7tab]] 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=7TAB OCA]. For a <b>guided tour on the structure components</b> use [https://proteopedia.org/fgij/fg.htm?mol=7TAB FirstGlance]. <br>		<table><tr><td colspan='2'>[[7tab]] 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=7TAB OCA]. For a <b>guided tour on the structure components</b> use [https://proteopedia.org/fgij/fg.htm?mol=7TAB FirstGlance]. <br>
-	</td></tr><tr id='ligand'><td class="sblockLbl"><b>[[Ligand\|Ligands:]]</b></td><td class="sblockDat" id="ligandDat"><scene name='pdbligand=GGU:2-(6-amino-5-phenylpyridazin-3-yl)phenol'>GGU</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]] 1.16Å</td></tr>
		+	<tr id='ligand'><td class="sblockLbl"><b>[[Ligand\|Ligands:]]</b></td><td class="sblockDat" id="ligandDat"><scene name='pdbligand=GGU:2-(6-amino-5-phenylpyridazin-3-yl)phenol'>GGU</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=7tab FirstGlance], [http://oca.weizmann.ac.il/oca-bin/ocaids?id=7tab OCA], [https://pdbe.org/7tab PDBe], [https://www.rcsb.org/pdb/explore.do?structureId=7tab RCSB], [https://www.ebi.ac.uk/pdbsum/7tab PDBsum], [https://prosat.h-its.org/prosat/prosatexe?pdbcode=7tab 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=7tab FirstGlance], [http://oca.weizmann.ac.il/oca-bin/ocaids?id=7tab OCA], [https://pdbe.org/7tab PDBe], [https://www.rcsb.org/pdb/explore.do?structureId=7tab RCSB], [https://www.ebi.ac.uk/pdbsum/7tab PDBsum], [https://prosat.h-its.org/prosat/prosatexe?pdbcode=7tab ProSAT]</span></td></tr>
	</table>		</table>
	== Disease ==		== Disease ==
-	[[https://www.uniprot.org/uniprot/SMCA4_HUMAN SMCA4_HUMAN]] Defects in SMARCA4 are the cause of rhabdoid tumor predisposition syndrome type 2 (RTPS2) [MIM:[https://omim.org/entry/613325 613325]]. RTPS2 is a familial cancer syndrome predisposing to renal or extrarenal malignant rhabdoid tumors and to a variety of tumors of the central nervous system, including choroid plexus carcinoma, medulloblastoma, and central primitive neuroectodermal tumors. Rhabdoid tumors are the most aggressive and lethal malignancies occurring in early childhood.<ref>PMID:20137775</ref> Defects in SMARCA4 are the cause of mental retardation autosomal dominant type 16 (MRD16) [MIM:[https://omim.org/entry/614609 614609]]. A disease characterized by multiple congenital anomalies and mental retardation. Mental retardation is defined by significantly below average general intellectual functioning associated with impairments in adaptative behavior and manifested during the developmental period. MRD16 patients manifest developmental delay, absent or hypoplastic fifth fingernails or toenails, thick eyebrows and long eyelashes, hirsutism. Additional findings include hypotonia, microcephaly, seizures, a Dandy-Walker malformation, and vision and hearing problems.<ref>PMID:22426308</ref>	+	[https://www.uniprot.org/uniprot/SMCA4_HUMAN SMCA4_HUMAN] Defects in SMARCA4 are the cause of rhabdoid tumor predisposition syndrome type 2 (RTPS2) [MIM:[https://omim.org/entry/613325 613325]. RTPS2 is a familial cancer syndrome predisposing to renal or extrarenal malignant rhabdoid tumors and to a variety of tumors of the central nervous system, including choroid plexus carcinoma, medulloblastoma, and central primitive neuroectodermal tumors. Rhabdoid tumors are the most aggressive and lethal malignancies occurring in early childhood.<ref>PMID:20137775</ref> Defects in SMARCA4 are the cause of mental retardation autosomal dominant type 16 (MRD16) [MIM:[https://omim.org/entry/614609 614609]. A disease characterized by multiple congenital anomalies and mental retardation. Mental retardation is defined by significantly below average general intellectual functioning associated with impairments in adaptative behavior and manifested during the developmental period. MRD16 patients manifest developmental delay, absent or hypoplastic fifth fingernails or toenails, thick eyebrows and long eyelashes, hirsutism. Additional findings include hypotonia, microcephaly, seizures, a Dandy-Walker malformation, and vision and hearing problems.<ref>PMID:22426308</ref>
	== Function ==		== Function ==
-	[[https://www.uniprot.org/uniprot/SMCA4_HUMAN SMCA4_HUMAN]] Transcriptional coactivator cooperating with nuclear hormone receptors to potentiate transcriptional activation. Component of the CREST-BRG1 complex, a multiprotein complex that regulates promoter activation by orchestrating a calcium-dependent release of a repressor complex and a recruitment of an activator complex. In resting neurons, transcription of the c-FOS promoter is inhibited by BRG1-dependent recruitment of a phospho-RB1-HDAC repressor complex. Upon calcium influx, RB1 is dephosphorylated by calcineurin, which leads to release of the repressor complex. At the same time, there is increased recruitment of CREBBP to the promoter by a CREST-dependent mechanism, which leads to transcriptional activation. The CREST-BRG1 complex also binds to the NR2B promoter, and activity-dependent induction of NR2B expression involves a release of HDAC1 and recruitment of CREBBP. Belongs to the neural progenitors-specific chromatin remodeling complex (npBAF complex) and the neuron-specific chromatin remodeling complex (nBAF complex). During neural development a switch from a stem/progenitor to a post-mitotic chromatin remodeling mechanism occurs as neurons exit the cell cycle and become committed to their adult state. The transition from proliferating neural stem/progenitor cells to post-mitotic neurons requires a switch in subunit composition of the npBAF and nBAF complexes. As neural progenitors exit mitosis and differentiate into neurons, npBAF complexes which contain ACTL6A/BAF53A and PHF10/BAF45A, are exchanged for homologous alternative ACTL6B/BAF53B and DPF1/BAF45B or DPF3/BAF45C subunits in neuron-specific complexes (nBAF). The npBAF complex is essential for the self-renewal/proliferative capacity of the multipotent neural stem cells. The nBAF complex along with CREST plays a role regulating the activity of genes essential for dendrite growth. SMARCA4/BAF190A may promote neural stem cell self-renewal/proliferation by enhancing Notch-dependent proliferative signals, while concurrently making the neural stem cell insensitive to SHH-dependent differentiating cues (By similarity). Also involved in vitamin D-coupled transcription regulation via its association with the WINAC complex, a chromatin-remodeling complex recruited by vitamin D receptor (VDR), which is required for the ligand-bound VDR-mediated transrepression of the CYP27B1 gene. Acts as a corepressor of ZEB1 to regulate E-cadherin transcription and is required for induction of epithelial-mesenchymal transition (EMT) by ZEB1.<ref>PMID:12837248</ref> <ref>PMID:19571879</ref> <ref>PMID:20418909</ref>	+	[https://www.uniprot.org/uniprot/SMCA4_HUMAN SMCA4_HUMAN] Transcriptional coactivator cooperating with nuclear hormone receptors to potentiate transcriptional activation. Component of the CREST-BRG1 complex, a multiprotein complex that regulates promoter activation by orchestrating a calcium-dependent release of a repressor complex and a recruitment of an activator complex. In resting neurons, transcription of the c-FOS promoter is inhibited by BRG1-dependent recruitment of a phospho-RB1-HDAC repressor complex. Upon calcium influx, RB1 is dephosphorylated by calcineurin, which leads to release of the repressor complex. At the same time, there is increased recruitment of CREBBP to the promoter by a CREST-dependent mechanism, which leads to transcriptional activation. The CREST-BRG1 complex also binds to the NR2B promoter, and activity-dependent induction of NR2B expression involves a release of HDAC1 and recruitment of CREBBP. Belongs to the neural progenitors-specific chromatin remodeling complex (npBAF complex) and the neuron-specific chromatin remodeling complex (nBAF complex). During neural development a switch from a stem/progenitor to a post-mitotic chromatin remodeling mechanism occurs as neurons exit the cell cycle and become committed to their adult state. The transition from proliferating neural stem/progenitor cells to post-mitotic neurons requires a switch in subunit composition of the npBAF and nBAF complexes. As neural progenitors exit mitosis and differentiate into neurons, npBAF complexes which contain ACTL6A/BAF53A and PHF10/BAF45A, are exchanged for homologous alternative ACTL6B/BAF53B and DPF1/BAF45B or DPF3/BAF45C subunits in neuron-specific complexes (nBAF). The npBAF complex is essential for the self-renewal/proliferative capacity of the multipotent neural stem cells. The nBAF complex along with CREST plays a role regulating the activity of genes essential for dendrite growth. SMARCA4/BAF190A may promote neural stem cell self-renewal/proliferation by enhancing Notch-dependent proliferative signals, while concurrently making the neural stem cell insensitive to SHH-dependent differentiating cues (By similarity). Also involved in vitamin D-coupled transcription regulation via its association with the WINAC complex, a chromatin-remodeling complex recruited by vitamin D receptor (VDR), which is required for the ligand-bound VDR-mediated transrepression of the CYP27B1 gene. Acts as a corepressor of ZEB1 to regulate E-cadherin transcription and is required for induction of epithelial-mesenchymal transition (EMT) by ZEB1.<ref>PMID:12837248</ref> <ref>PMID:19571879</ref> <ref>PMID:20418909</ref>
	<div style="background-color:#fffaf0;">		<div style="background-color:#fffaf0;">
	== Publication Abstract from PubMed ==		== Publication Abstract from PubMed ==

OCA at 18:57, 7 September 2022

2022-09-07T18:57:28Z

←Older revision		Revision as of 18:57, 7 September 2022
Line 11:		Line 11:
	== Function ==		== Function ==
	[[https://www.uniprot.org/uniprot/SMCA4_HUMAN SMCA4_HUMAN]] Transcriptional coactivator cooperating with nuclear hormone receptors to potentiate transcriptional activation. Component of the CREST-BRG1 complex, a multiprotein complex that regulates promoter activation by orchestrating a calcium-dependent release of a repressor complex and a recruitment of an activator complex. In resting neurons, transcription of the c-FOS promoter is inhibited by BRG1-dependent recruitment of a phospho-RB1-HDAC repressor complex. Upon calcium influx, RB1 is dephosphorylated by calcineurin, which leads to release of the repressor complex. At the same time, there is increased recruitment of CREBBP to the promoter by a CREST-dependent mechanism, which leads to transcriptional activation. The CREST-BRG1 complex also binds to the NR2B promoter, and activity-dependent induction of NR2B expression involves a release of HDAC1 and recruitment of CREBBP. Belongs to the neural progenitors-specific chromatin remodeling complex (npBAF complex) and the neuron-specific chromatin remodeling complex (nBAF complex). During neural development a switch from a stem/progenitor to a post-mitotic chromatin remodeling mechanism occurs as neurons exit the cell cycle and become committed to their adult state. The transition from proliferating neural stem/progenitor cells to post-mitotic neurons requires a switch in subunit composition of the npBAF and nBAF complexes. As neural progenitors exit mitosis and differentiate into neurons, npBAF complexes which contain ACTL6A/BAF53A and PHF10/BAF45A, are exchanged for homologous alternative ACTL6B/BAF53B and DPF1/BAF45B or DPF3/BAF45C subunits in neuron-specific complexes (nBAF). The npBAF complex is essential for the self-renewal/proliferative capacity of the multipotent neural stem cells. The nBAF complex along with CREST plays a role regulating the activity of genes essential for dendrite growth. SMARCA4/BAF190A may promote neural stem cell self-renewal/proliferation by enhancing Notch-dependent proliferative signals, while concurrently making the neural stem cell insensitive to SHH-dependent differentiating cues (By similarity). Also involved in vitamin D-coupled transcription regulation via its association with the WINAC complex, a chromatin-remodeling complex recruited by vitamin D receptor (VDR), which is required for the ligand-bound VDR-mediated transrepression of the CYP27B1 gene. Acts as a corepressor of ZEB1 to regulate E-cadherin transcription and is required for induction of epithelial-mesenchymal transition (EMT) by ZEB1.<ref>PMID:12837248</ref> <ref>PMID:19571879</ref> <ref>PMID:20418909</ref>		[[https://www.uniprot.org/uniprot/SMCA4_HUMAN SMCA4_HUMAN]] Transcriptional coactivator cooperating with nuclear hormone receptors to potentiate transcriptional activation. Component of the CREST-BRG1 complex, a multiprotein complex that regulates promoter activation by orchestrating a calcium-dependent release of a repressor complex and a recruitment of an activator complex. In resting neurons, transcription of the c-FOS promoter is inhibited by BRG1-dependent recruitment of a phospho-RB1-HDAC repressor complex. Upon calcium influx, RB1 is dephosphorylated by calcineurin, which leads to release of the repressor complex. At the same time, there is increased recruitment of CREBBP to the promoter by a CREST-dependent mechanism, which leads to transcriptional activation. The CREST-BRG1 complex also binds to the NR2B promoter, and activity-dependent induction of NR2B expression involves a release of HDAC1 and recruitment of CREBBP. Belongs to the neural progenitors-specific chromatin remodeling complex (npBAF complex) and the neuron-specific chromatin remodeling complex (nBAF complex). During neural development a switch from a stem/progenitor to a post-mitotic chromatin remodeling mechanism occurs as neurons exit the cell cycle and become committed to their adult state. The transition from proliferating neural stem/progenitor cells to post-mitotic neurons requires a switch in subunit composition of the npBAF and nBAF complexes. As neural progenitors exit mitosis and differentiate into neurons, npBAF complexes which contain ACTL6A/BAF53A and PHF10/BAF45A, are exchanged for homologous alternative ACTL6B/BAF53B and DPF1/BAF45B or DPF3/BAF45C subunits in neuron-specific complexes (nBAF). The npBAF complex is essential for the self-renewal/proliferative capacity of the multipotent neural stem cells. The nBAF complex along with CREST plays a role regulating the activity of genes essential for dendrite growth. SMARCA4/BAF190A may promote neural stem cell self-renewal/proliferation by enhancing Notch-dependent proliferative signals, while concurrently making the neural stem cell insensitive to SHH-dependent differentiating cues (By similarity). Also involved in vitamin D-coupled transcription regulation via its association with the WINAC complex, a chromatin-remodeling complex recruited by vitamin D receptor (VDR), which is required for the ligand-bound VDR-mediated transrepression of the CYP27B1 gene. Acts as a corepressor of ZEB1 to regulate E-cadherin transcription and is required for induction of epithelial-mesenchymal transition (EMT) by ZEB1.<ref>PMID:12837248</ref> <ref>PMID:19571879</ref> <ref>PMID:20418909</ref>
		+	<div style="background-color:#fffaf0;">
		+	== Publication Abstract from PubMed ==
		+	Bromodomains are acetyllysine recognition domains present in a variety of human proteins. Bromodomains also bind small molecules that compete with acetyllysine, and therefore bromodomains have been targets for drug discovery efforts. Highly potent and selective ligands with good cellular permeability have been proposed as chemical probes for use in exploring the functions of many of the bromodomain proteins. We report here the discovery of a class of such inhibitors targeting the family VIII bromodomains of SMARCA2 (BRM) and SMARCA4 (BRG1), and PBRM1 (polybromo-1) bromodomain 5. We propose one example from this series, GNE-064, as a chemical probe for the bromodomains SMARCA2, SMARCA4, and PBRM1(5) with the potential for in vivo use.
		+
		+	GNE-064: A Potent, Selective, and Orally Bioavailable Chemical Probe for the Bromodomains of SMARCA2 and SMARCA4 and the Fifth Bromodomain of PBRM1.,Taylor AM, Bailey C, Belmont LD, Campbell R, Cantone N, Cote A, Crawford TD, Cummings R, DeMent K, Duplessis M, Flynn M, Good AC, Huang HR, Joshi S, Leblanc Y, Murray J, Nasveschuk CG, Neiss A, Poy F, Romero FA, Sandy P, Tang Y, Tsui V, Zawadzke L, Sims RJ 3rd, Audia JE, Bellon SF, Magnuson SR, Albrecht BK, Cochran AG J Med Chem. 2022 Aug 5. doi: 10.1021/acs.jmedchem.2c00662. PMID:35930799<ref>PMID:35930799</ref>
		+
		+	From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine.<br>
		+	</div>
		+	<div class="pdbe-citations 7tab" style="background-color:#fffaf0;"></div>
	== References ==		== References ==
	<references/>		<references/>

OCA at 16:48, 7 September 2022

2022-09-07T16:48:48Z

←Older revision		Revision as of 16:48, 7 September 2022
Line 1:		Line 1:

	==G-925 bound to the SMARCA4 (BRG1) Bromodomain==		==G-925 bound to the SMARCA4 (BRG1) Bromodomain==
-	<StructureSection load='7tab' size='340' side='right'caption='[[7tab]]' scene=''>	+	<StructureSection load='7tab' size='340' side='right'caption='[[7tab]], [[Resolution\|resolution]] 1.16Å' 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=7TAB OCA]. For a <b>guided tour on the structure components</b> use [https://proteopedia.org/fgij/fg.htm?mol=7TAB FirstGlance]. <br>	+	<table><tr><td colspan='2'>[[7tab]] 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=7TAB OCA]. For a <b>guided tour on the structure components</b> use [https://proteopedia.org/fgij/fg.htm?mol=7TAB 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=7tab FirstGlance], [http://oca.weizmann.ac.il/oca-bin/ocaids?id=7tab OCA], [https://pdbe.org/7tab PDBe], [https://www.rcsb.org/pdb/explore.do?structureId=7tab RCSB], [https://www.ebi.ac.uk/pdbsum/7tab PDBsum], [https://prosat.h-its.org/prosat/prosatexe?pdbcode=7tab 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=GGU:2-(6-amino-5-phenylpyridazin-3-yl)phenol'>GGU</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=7tab FirstGlance], [http://oca.weizmann.ac.il/oca-bin/ocaids?id=7tab OCA], [https://pdbe.org/7tab PDBe], [https://www.rcsb.org/pdb/explore.do?structureId=7tab RCSB], [https://www.ebi.ac.uk/pdbsum/7tab PDBsum], [https://prosat.h-its.org/prosat/prosatexe?pdbcode=7tab ProSAT]</span></td></tr>
	</table>		</table>
		+	== Disease ==
		+	[[https://www.uniprot.org/uniprot/SMCA4_HUMAN SMCA4_HUMAN]] Defects in SMARCA4 are the cause of rhabdoid tumor predisposition syndrome type 2 (RTPS2) [MIM:[https://omim.org/entry/613325 613325]]. RTPS2 is a familial cancer syndrome predisposing to renal or extrarenal malignant rhabdoid tumors and to a variety of tumors of the central nervous system, including choroid plexus carcinoma, medulloblastoma, and central primitive neuroectodermal tumors. Rhabdoid tumors are the most aggressive and lethal malignancies occurring in early childhood.<ref>PMID:20137775</ref> Defects in SMARCA4 are the cause of mental retardation autosomal dominant type 16 (MRD16) [MIM:[https://omim.org/entry/614609 614609]]. A disease characterized by multiple congenital anomalies and mental retardation. Mental retardation is defined by significantly below average general intellectual functioning associated with impairments in adaptative behavior and manifested during the developmental period. MRD16 patients manifest developmental delay, absent or hypoplastic fifth fingernails or toenails, thick eyebrows and long eyelashes, hirsutism. Additional findings include hypotonia, microcephaly, seizures, a Dandy-Walker malformation, and vision and hearing problems.<ref>PMID:22426308</ref>
		+	== Function ==
		+	[[https://www.uniprot.org/uniprot/SMCA4_HUMAN SMCA4_HUMAN]] Transcriptional coactivator cooperating with nuclear hormone receptors to potentiate transcriptional activation. Component of the CREST-BRG1 complex, a multiprotein complex that regulates promoter activation by orchestrating a calcium-dependent release of a repressor complex and a recruitment of an activator complex. In resting neurons, transcription of the c-FOS promoter is inhibited by BRG1-dependent recruitment of a phospho-RB1-HDAC repressor complex. Upon calcium influx, RB1 is dephosphorylated by calcineurin, which leads to release of the repressor complex. At the same time, there is increased recruitment of CREBBP to the promoter by a CREST-dependent mechanism, which leads to transcriptional activation. The CREST-BRG1 complex also binds to the NR2B promoter, and activity-dependent induction of NR2B expression involves a release of HDAC1 and recruitment of CREBBP. Belongs to the neural progenitors-specific chromatin remodeling complex (npBAF complex) and the neuron-specific chromatin remodeling complex (nBAF complex). During neural development a switch from a stem/progenitor to a post-mitotic chromatin remodeling mechanism occurs as neurons exit the cell cycle and become committed to their adult state. The transition from proliferating neural stem/progenitor cells to post-mitotic neurons requires a switch in subunit composition of the npBAF and nBAF complexes. As neural progenitors exit mitosis and differentiate into neurons, npBAF complexes which contain ACTL6A/BAF53A and PHF10/BAF45A, are exchanged for homologous alternative ACTL6B/BAF53B and DPF1/BAF45B or DPF3/BAF45C subunits in neuron-specific complexes (nBAF). The npBAF complex is essential for the self-renewal/proliferative capacity of the multipotent neural stem cells. The nBAF complex along with CREST plays a role regulating the activity of genes essential for dendrite growth. SMARCA4/BAF190A may promote neural stem cell self-renewal/proliferation by enhancing Notch-dependent proliferative signals, while concurrently making the neural stem cell insensitive to SHH-dependent differentiating cues (By similarity). Also involved in vitamin D-coupled transcription regulation via its association with the WINAC complex, a chromatin-remodeling complex recruited by vitamin D receptor (VDR), which is required for the ligand-bound VDR-mediated transrepression of the CYP27B1 gene. Acts as a corepressor of ZEB1 to regulate E-cadherin transcription and is required for induction of epithelial-mesenchymal transition (EMT) by ZEB1.<ref>PMID:12837248</ref> <ref>PMID:19571879</ref> <ref>PMID:20418909</ref>
		+	== References ==
		+	<references/>
	__TOC__		__TOC__
	</StructureSection>		</StructureSection>
		+	[[Category: Homo sapiens]]
	[[Category: Large Structures]]		[[Category: Large Structures]]
	[[Category: Bellon SF]]		[[Category: Bellon SF]]

OCA at 06:19, 18 August 2022

2022-08-18T06:19:45Z

←Older revision		Revision as of 06:19, 18 August 2022
Line 1:		Line 1:
-	'''Unreleased structure'''

-	~~The entry~~ 7tab ~~is ON HOLD~~	+	==G-925 bound to the SMARCA4 (BRG1) Bromodomain==
-		+	<StructureSection load='7tab' size='340' side='right'caption='[[7tab]]' scene=''>
-	~~Authors~~: ~~Tang~~, Y., ~~Poy, F~~., ~~Taylor, A~~.M., ~~Cochran, A~~.G., ~~Bellon, S~~.F.	+	== Structural highlights ==
-		+	<table><tr><td colspan='2'>Full crystallographic information is available from [http://oca.weizmann.ac.il/oca-bin/ocashort?id=7TAB OCA]. For a <b>guided tour on the structure components</b> use [https://proteopedia.org/fgij/fg.htm?mol=7TAB FirstGlance]. <br>
-	~~Description: G-925 bound to the SMARCA4 (BRG1) Bromodomain~~	+	</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=7tab FirstGlance], [http://oca.weizmann.ac.il/oca-bin/ocaids?id=7tab OCA], [https://pdbe.org/7tab PDBe], [https://www.rcsb.org/pdb/explore.do?structureId=7tab RCSB], [https://www.ebi.ac.uk/pdbsum/7tab PDBsum], [https://prosat.h-its.org/prosat/prosatexe?pdbcode=7tab ProSAT]</span></td></tr>
-	[[Category: ~~Unreleased~~ Structures]]	+	</table>
-	[[Category: ~~Cochran, A.G~~]]	+	__TOC__
-	[[Category: ~~Taylor, A.M~~]]	+	</StructureSection>
-	[[Category: ~~Tang, Y~~]]	+	[[Category: Large Structures]]
-	[[Category: ~~Bellon, S.F~~]]	+	[[Category: Bellon SF]]
-	[[Category: ~~Poy, F~~]]	+	[[Category: Cochran AG]]
		+	[[Category: Poy F]]
		+	[[Category: Tang Y]]
		+	[[Category: Taylor AM]]

OCA at 03:34, 3 August 2022

2022-08-03T03:34:01Z

←Older revision		Revision as of 03:34, 3 August 2022
Line 5:		Line 5:
	Authors: Tang, Y., Poy, F., Taylor, A.M., Cochran, A.G., Bellon, S.F.		Authors: Tang, Y., Poy, F., Taylor, A.M., Cochran, A.G., Bellon, S.F.

-	Description: ~~GNE~~-~~064~~ bound to the SMARCA4 (BRG1) Bromodomain	+	Description: G-925 bound to the SMARCA4 (BRG1) Bromodomain
	[[Category: Unreleased Structures]]		[[Category: Unreleased Structures]]
	[[Category: Cochran, A.G]]		[[Category: Cochran, A.G]]
-	[[Category: Tang, Y]]
	[[Category: Taylor, A.M]]		[[Category: Taylor, A.M]]
		+	[[Category: Tang, Y]]
	[[Category: Bellon, S.F]]		[[Category: Bellon, S.F]]
	[[Category: Poy, F]]		[[Category: Poy, F]]

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

2021-12-29T12:06:50Z

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

←Older revision

Revision as of 12:06, 29 December 2021

OCA: New page: '''Unreleased structure''' The entry 7tab is ON HOLD Authors: Tang, Y., Poy, F., Taylor, A.M., Cochran, A.G., Bellon, S.F. Description: GNE-064 bound to the SMARCA4 (BRG1) Bromodomain ...

2021-12-29T12:06:49Z

New page: '''Unreleased structure''' The entry 7tab is ON HOLD Authors: Tang, Y., Poy, F., Taylor, A.M., Cochran, A.G., Bellon, S.F. Description: GNE-064 bound to the SMARCA4 (BRG1) Bromodomain ...

New page

'''Unreleased structure'''

The entry 7tab is ON HOLD

Authors: Tang, Y., Poy, F., Taylor, A.M., Cochran, A.G., Bellon, S.F.

Description: GNE-064 bound to the SMARCA4 (BRG1) Bromodomain
[[Category: Unreleased Structures]]
[[Category: Cochran, A.G]]
[[Category: Tang, Y]]
[[Category: Taylor, A.M]]
[[Category: Bellon, S.F]]
[[Category: Poy, F]]