7p0e - Revision history

OCA at 12:59, 1 February 2024

OCA — Thu, 01 Feb 2024 12:59:17 GMT

←Older revision		Revision as of 12:59, 1 February 2024
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	== Structural highlights ==		== Structural highlights ==
	<table><tr><td colspan='2'>[[7p0e]] 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=7P0E OCA]. For a <b>guided tour on the structure components</b> use [https://proteopedia.org/fgij/fg.htm?mol=7P0E FirstGlance]. <br>		<table><tr><td colspan='2'>[[7p0e]] 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=7P0E OCA]. For a <b>guided tour on the structure components</b> use [https://proteopedia.org/fgij/fg.htm?mol=7P0E FirstGlance]. <br>
-	</td></tr><tr id='ligand'><td class="sblockLbl"><b>[[Ligand\|Ligands:]]</b></td><td class="sblockDat" id="ligandDat"><scene name='pdbligand=EDO:1,2-ETHANEDIOL'>EDO</scene>, <scene name='pdbligand=GOL:GLYCEROL'>GOL</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]] 1.6Å</td></tr>
		+	<tr id='ligand'><td class="sblockLbl"><b>[[Ligand\|Ligands:]]</b></td><td class="sblockDat" id="ligandDat"><scene name='pdbligand=EDO:1,2-ETHANEDIOL'>EDO</scene>, <scene name='pdbligand=GOL:GLYCEROL'>GOL</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=7p0e FirstGlance], [http://oca.weizmann.ac.il/oca-bin/ocaids?id=7p0e OCA], [https://pdbe.org/7p0e PDBe], [https://www.rcsb.org/pdb/explore.do?structureId=7p0e RCSB], [https://www.ebi.ac.uk/pdbsum/7p0e PDBsum], [https://prosat.h-its.org/prosat/prosatexe?pdbcode=7p0e 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=7p0e FirstGlance], [http://oca.weizmann.ac.il/oca-bin/ocaids?id=7p0e OCA], [https://pdbe.org/7p0e PDBe], [https://www.rcsb.org/pdb/explore.do?structureId=7p0e RCSB], [https://www.ebi.ac.uk/pdbsum/7p0e PDBsum], [https://prosat.h-its.org/prosat/prosatexe?pdbcode=7p0e ProSAT]</span></td></tr>
	</table>		</table>
	== Disease ==		== Disease ==
-	[[https://www.uniprot.org/uniprot/FLNC_HUMAN FLNC_HUMAN]] Defects in FLNC are the cause of myopathy myofibrillar type 5 (MFM5) [MIM:[https://omim.org/entry/609524 609524]]. A neuromuscular disorder, usually with an adult onset, characterized by focal myofibrillar destruction and pathological cytoplasmic protein aggregations, and clinical features of a limb-girdle myopathy.<ref>PMID:15929027</ref> Defects in FLNC are the cause of myopathy distal type 4 (MPD4) [MIM:[https://omim.org/entry/614065 614065]]. MPD4 is a slowly progressive muscular disorder characterized by distal muscle weakness and atrophy affecting the upper and lower limbs. Onset occurs around the third to fourth decades of life, and patients remain ambulatory even after long disease duration. Muscle biopsy shows non-specific changes with no evidence of rods, necrosis, or inflammation.<ref>PMID:21620354</ref>	+	[https://www.uniprot.org/uniprot/FLNC_HUMAN FLNC_HUMAN] Defects in FLNC are the cause of myopathy myofibrillar type 5 (MFM5) [MIM:[https://omim.org/entry/609524 609524]. A neuromuscular disorder, usually with an adult onset, characterized by focal myofibrillar destruction and pathological cytoplasmic protein aggregations, and clinical features of a limb-girdle myopathy.<ref>PMID:15929027</ref> Defects in FLNC are the cause of myopathy distal type 4 (MPD4) [MIM:[https://omim.org/entry/614065 614065]. MPD4 is a slowly progressive muscular disorder characterized by distal muscle weakness and atrophy affecting the upper and lower limbs. Onset occurs around the third to fourth decades of life, and patients remain ambulatory even after long disease duration. Muscle biopsy shows non-specific changes with no evidence of rods, necrosis, or inflammation.<ref>PMID:21620354</ref>
	== Function ==		== Function ==
-	[[https://www.uniprot.org/uniprot/FLNC_HUMAN FLNC_HUMAN]] Muscle-specific filamin, which plays a central role in muscle cells, probably by functioning as a large actin-cross-linking protein. May be involved in reorganizing the actin cytoskeleton in response to signaling events, and may also display structural functions at the Z lines in muscle cells. Critical for normal myogenesis and for maintaining the structural integrity of the muscle fibers.	+	[https://www.uniprot.org/uniprot/FLNC_HUMAN FLNC_HUMAN] Muscle-specific filamin, which plays a central role in muscle cells, probably by functioning as a large actin-cross-linking protein. May be involved in reorganizing the actin cytoskeleton in response to signaling events, and may also display structural functions at the Z lines in muscle cells. Critical for normal myogenesis and for maintaining the structural integrity of the muscle fibers.
		+
		+	==See Also==
		+	*[[Filamin 3D structures\|Filamin 3D structures]]
	== References ==		== References ==
	<references/>		<references/>

OCA at 05:43, 8 September 2022

OCA — Thu, 08 Sep 2022 05:43:25 GMT

←Older revision		Revision as of 05:43, 8 September 2022
Line 1:		Line 1:

	==Crystal structure of human filamin C domains 14-15 cardiovascular disease causing mutation G1676R==		==Crystal structure of human filamin C domains 14-15 cardiovascular disease causing mutation G1676R==
-	<StructureSection load='7p0e' size='340' side='right'caption='[[7p0e]]' scene=''>	+	<StructureSection load='7p0e' size='340' side='right'caption='[[7p0e]], [[Resolution\|resolution]] 1.60Å' 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=7P0E OCA]. For a <b>guided tour on the structure components</b> use [https://proteopedia.org/fgij/fg.htm?mol=7P0E FirstGlance]. <br>	+	<table><tr><td colspan='2'>[[7p0e]] 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=7P0E OCA]. For a <b>guided tour on the structure components</b> use [https://proteopedia.org/fgij/fg.htm?mol=7P0E 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=7p0e FirstGlance], [http://oca.weizmann.ac.il/oca-bin/ocaids?id=7p0e OCA], [https://pdbe.org/7p0e PDBe], [https://www.rcsb.org/pdb/explore.do?structureId=7p0e RCSB], [https://www.ebi.ac.uk/pdbsum/7p0e PDBsum], [https://prosat.h-its.org/prosat/prosatexe?pdbcode=7p0e 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=EDO:1,2-ETHANEDIOL'>EDO</scene>, <scene name='pdbligand=GOL:GLYCEROL'>GOL</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=7p0e FirstGlance], [http://oca.weizmann.ac.il/oca-bin/ocaids?id=7p0e OCA], [https://pdbe.org/7p0e PDBe], [https://www.rcsb.org/pdb/explore.do?structureId=7p0e RCSB], [https://www.ebi.ac.uk/pdbsum/7p0e PDBsum], [https://prosat.h-its.org/prosat/prosatexe?pdbcode=7p0e ProSAT]</span></td></tr>
	</table>		</table>
		+	== Disease ==
		+	[[https://www.uniprot.org/uniprot/FLNC_HUMAN FLNC_HUMAN]] Defects in FLNC are the cause of myopathy myofibrillar type 5 (MFM5) [MIM:[https://omim.org/entry/609524 609524]]. A neuromuscular disorder, usually with an adult onset, characterized by focal myofibrillar destruction and pathological cytoplasmic protein aggregations, and clinical features of a limb-girdle myopathy.<ref>PMID:15929027</ref> Defects in FLNC are the cause of myopathy distal type 4 (MPD4) [MIM:[https://omim.org/entry/614065 614065]]. MPD4 is a slowly progressive muscular disorder characterized by distal muscle weakness and atrophy affecting the upper and lower limbs. Onset occurs around the third to fourth decades of life, and patients remain ambulatory even after long disease duration. Muscle biopsy shows non-specific changes with no evidence of rods, necrosis, or inflammation.<ref>PMID:21620354</ref>
		+	== Function ==
		+	[[https://www.uniprot.org/uniprot/FLNC_HUMAN FLNC_HUMAN]] Muscle-specific filamin, which plays a central role in muscle cells, probably by functioning as a large actin-cross-linking protein. May be involved in reorganizing the actin cytoskeleton in response to signaling events, and may also display structural functions at the Z lines in muscle cells. Critical for normal myogenesis and for maintaining the structural integrity of the muscle fibers.
		+	== References ==
		+	<references/>
	__TOC__		__TOC__
	</StructureSection>		</StructureSection>
		+	[[Category: Homo sapiens]]
	[[Category: Large Structures]]		[[Category: Large Structures]]
	[[Category: Djinovic-Carugo K]]		[[Category: Djinovic-Carugo K]]
	[[Category: Mlynek G]]		[[Category: Mlynek G]]

OCA at 05:14, 13 July 2022

OCA — Wed, 13 Jul 2022 05:14:18 GMT

←Older revision		Revision as of 05:14, 13 July 2022
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-	'''Unreleased structure'''

-	~~The entry 7p0e is ON HOLD until Paper Publication~~	+	==Crystal structure of human filamin C domains 14-15 cardiovascular disease causing mutation G1676R==
-		+	<StructureSection load='7p0e' size='340' side='right'caption='[[7p0e]]' scene=''>
-	~~Authors: Mlynek, G., Djinovic-Carugo, K.~~	+	== Structural highlights ==
-		+	<table><tr><td colspan='2'>Full crystallographic information is available from [http://oca.weizmann.ac.il/oca-bin/ocashort?id=7P0E OCA]. For a <b>guided tour on the structure components</b> use [https://proteopedia.org/fgij/fg.htm?mol=7P0E FirstGlance]. <br>
-	~~Description:~~ Crystal structure of human filamin C domains 14-15 cardiovascular disease causing mutation G1676R	+	</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=7p0e FirstGlance], [http://oca.weizmann.ac.il/oca-bin/ocaids?id=7p0e OCA], [https://pdbe.org/7p0e PDBe], [https://www.rcsb.org/pdb/explore.do?structureId=7p0e RCSB], [https://www.ebi.ac.uk/pdbsum/7p0e PDBsum], [https://prosat.h-its.org/prosat/prosatexe?pdbcode=7p0e ProSAT]</span></td></tr>
-	[[Category: ~~Unreleased~~ Structures]]	+	</table>
-	[[Category: Djinovic-Carugo, K]]	+	__TOC__
-	[[Category: Mlynek, G]]	+	</StructureSection>
		+	[[Category: Large Structures]]
		+	[[Category: Djinovic-Carugo K]]
		+	[[Category: Mlynek G]]

OCA at 09:11, 4 August 2021

OCA — Wed, 04 Aug 2021 09:11:27 GMT

←Older revision		Revision as of 09:11, 4 August 2021
Line 1:		Line 1:
	'''Unreleased structure'''		'''Unreleased structure'''

-	The entry 7p0e is ON HOLD	+	The entry 7p0e is ON HOLD until Paper Publication

	Authors: Mlynek, G., Djinovic-Carugo, K.		Authors: Mlynek, G., Djinovic-Carugo, K.

OCA: Protected "7p0e" [edit=sysop:move=sysop]

OCA — Wed, 07 Jul 2021 08:54:11 GMT

Protected "7p0e" [edit=sysop:move=sysop]

←Older revision

Revision as of 08:54, 7 July 2021

OCA: New page: '''Unreleased structure''' The entry 7p0e is ON HOLD Authors: Mlynek, G., Djinovic-Carugo, K. Description: Crystal structure of human filamin C domains 14-15 cardiovascular disease cau...

OCA — Wed, 07 Jul 2021 08:54:10 GMT

New page: '''Unreleased structure''' The entry 7p0e is ON HOLD Authors: Mlynek, G., Djinovic-Carugo, K. Description: Crystal structure of human filamin C domains 14-15 cardiovascular disease cau...

New page

'''Unreleased structure'''

The entry 7p0e is ON HOLD

Authors: Mlynek, G., Djinovic-Carugo, K.

Description: Crystal structure of human filamin C domains 14-15 cardiovascular disease causing mutation G1676R
[[Category: Unreleased Structures]]
[[Category: Djinovic-Carugo, K]]
[[Category: Mlynek, G]]