6jfk - Revision history

OCA at 09:20, 20 March 2024

OCA — Wed, 20 Mar 2024 09:20:08 GMT

←Older revision		Revision as of 09:20, 20 March 2024
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	== Function ==		== Function ==
	[https://www.uniprot.org/uniprot/MFN2_HUMAN MFN2_HUMAN] Mitochondrial outer membrane GTPase that mediates mitochondrial clustering and fusion (PubMed:11181170, PubMed:11950885, PubMed:28114303). Mitochondria are highly dynamic organelles, and their morphology is determined by the equilibrium between mitochondrial fusion and fission events (PubMed:28114303). Overexpression induces the formation of mitochondrial networks (PubMed:28114303). Membrane clustering requires GTPase activity and may involve a major rearrangement of the coiled coil domains (Probable). Plays a central role in mitochondrial metabolism and may be associated with obesity and/or apoptosis processes (By similarity). Plays an important role in the regulation of vascular smooth muscle cell proliferation (By similarity). Involved in the clearance of damaged mitochondria via selective autophagy (mitophagy) (PubMed:23620051). Is required for PRKN recruitment to dysfunctional mitochondria (PubMed:23620051). Involved in the control of unfolded protein response (UPR) upon ER stress including activation of apoptosis and autophagy during ER stress (By similarity). Acts as an upstream regulator of EIF2AK3 and suppresses EIF2AK3 activation under basal conditions (By similarity).[UniProtKB:Q80U63][UniProtKB:Q8R500]<ref>PMID:11181170</ref> <ref>PMID:11950885</ref> <ref>PMID:23620051</ref> <ref>PMID:26085578</ref> <ref>PMID:28114303</ref>		[https://www.uniprot.org/uniprot/MFN2_HUMAN MFN2_HUMAN] Mitochondrial outer membrane GTPase that mediates mitochondrial clustering and fusion (PubMed:11181170, PubMed:11950885, PubMed:28114303). Mitochondria are highly dynamic organelles, and their morphology is determined by the equilibrium between mitochondrial fusion and fission events (PubMed:28114303). Overexpression induces the formation of mitochondrial networks (PubMed:28114303). Membrane clustering requires GTPase activity and may involve a major rearrangement of the coiled coil domains (Probable). Plays a central role in mitochondrial metabolism and may be associated with obesity and/or apoptosis processes (By similarity). Plays an important role in the regulation of vascular smooth muscle cell proliferation (By similarity). Involved in the clearance of damaged mitochondria via selective autophagy (mitophagy) (PubMed:23620051). Is required for PRKN recruitment to dysfunctional mitochondria (PubMed:23620051). Involved in the control of unfolded protein response (UPR) upon ER stress including activation of apoptosis and autophagy during ER stress (By similarity). Acts as an upstream regulator of EIF2AK3 and suppresses EIF2AK3 activation under basal conditions (By similarity).[UniProtKB:Q80U63][UniProtKB:Q8R500]<ref>PMID:11181170</ref> <ref>PMID:11950885</ref> <ref>PMID:23620051</ref> <ref>PMID:26085578</ref> <ref>PMID:28114303</ref>
-	<div style="background-color:#fffaf0;">
-	== Publication Abstract from PubMed ==
-	Mitofusin-2 (MFN2) is a dynamin-like GTPase that plays a central role in regulating mitochondrial fusion and cell metabolism. Mutations in MFN2 cause the neurodegenerative disease Charcot-Marie-Tooth type 2A (CMT2A). The molecular basis underlying the physiological and pathological relevance of MFN2 is unclear. Here, we present crystal structures of truncated human MFN2 in different nucleotide-loading states. Unlike other dynamin superfamily members including MFN1, MFN2 forms sustained dimers even after GTP hydrolysis via the GTPase domain (G) interface, which accounts for its high membrane-tethering efficiency. The biochemical discrepancy between human MFN2 and MFN1 largely derives from a primate-only single amino acid variance. MFN2 and MFN1 can form heterodimers via the G interface in a nucleotide-dependent manner. CMT2A-related mutations, mapping to different functional zones of MFN2, lead to changes in GTP hydrolysis and homo/hetero-association ability. Our study provides fundamental insight into how mitofusins mediate mitochondrial fusion and the ways their disruptions cause disease.
-
-	Structural insights of human mitofusin-2 into mitochondrial fusion and CMT2A onset.,Li YJ, Cao YL, Feng JX, Qi Y, Meng S, Yang JF, Zhong YT, Kang S, Chen X, Lan L, Luo L, Yu B, Chen S, Chan DC, Hu J, Gao S Nat Commun. 2019 Oct 29;10(1):4914. doi: 10.1038/s41467-019-12912-0. PMID:31664033<ref>PMID:31664033</ref>
-
-	From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine.<br>
-	</div>
-	<div class="pdbe-citations 6jfk" style="background-color:#fffaf0;"></div>
	== References ==		== References ==
	<references/>		<references/>

OCA at 10:08, 22 November 2023

OCA — Wed, 22 Nov 2023 10:08:04 GMT

←Older revision		Revision as of 10:08, 22 November 2023
Line 3:		Line 3:
	<StructureSection load='6jfk' size='340' side='right'caption='[[6jfk]], [[Resolution\|resolution]] 2.00Å' scene=''>		<StructureSection load='6jfk' size='340' side='right'caption='[[6jfk]], [[Resolution\|resolution]] 2.00Å' scene=''>
	== Structural highlights ==		== Structural highlights ==
-	<table><tr><td colspan='2'>[[6jfk]] is a 1 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=6JFK OCA]. For a <b>guided tour on the structure components</b> use [~~http~~://~~oca~~.~~weizmann.ac.il/oca-docs~~/fgij/fg.htm?mol=6JFK FirstGlance]. <br>	+	<table><tr><td colspan='2'>[[6jfk]] 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=6JFK OCA]. For a <b>guided tour on the structure components</b> use [https://proteopedia.org/fgij/fg.htm?mol=6JFK FirstGlance]. <br>
-	</td></tr><tr id='ligand'><td class="sblockLbl"><b>[[Ligand\|Ligands:]]</b></td><td class="sblockDat"><scene name='pdbligand=CIT:CITRIC+ACID'>CIT</scene>, <scene name='pdbligand=GDP:GUANOSINE-5-DIPHOSPHATE'>GDP</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]] 1.997Å</td></tr>
-	~~<tr id='gene'><td class="sblockLbl"><b>[[Gene\|Gene:]]</b></td><td class="sblockDat">MFN2, CPRP1, KIAA0214 ([http://www.ncbi.nlm.nih.gov/Taxonomy/Browser/wwwtax.cgi?mode=Info&srchmode=5&id=9606 HUMAN])~~</td></tr>	+	<tr id='ligand'><td class="sblockLbl"><b>[[Ligand\|Ligands:]]</b></td><td class="sblockDat" id="ligandDat"><scene name='pdbligand=CIT:CITRIC+ACID'>CIT</scene>, <scene name='pdbligand=GDP:GUANOSINE-5-DIPHOSPHATE'>GDP</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'>[~~http~~://~~oca~~.~~weizmann.ac.il/oca-docs~~/fgij/fg.htm?mol=6jfk FirstGlance], [http://oca.weizmann.ac.il/oca-bin/ocaids?id=6jfk OCA], [~~http~~://pdbe.org/6jfk PDBe], [~~http~~://www.rcsb.org/pdb/explore.do?structureId=6jfk RCSB], [~~http~~://www.ebi.ac.uk/pdbsum/6jfk PDBsum], [~~http~~://prosat.h-its.org/prosat/prosatexe?pdbcode=6jfk 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=6jfk FirstGlance], [http://oca.weizmann.ac.il/oca-bin/ocaids?id=6jfk OCA], [https://pdbe.org/6jfk PDBe], [https://www.rcsb.org/pdb/explore.do?structureId=6jfk RCSB], [https://www.ebi.ac.uk/pdbsum/6jfk PDBsum], [https://prosat.h-its.org/prosat/prosatexe?pdbcode=6jfk ProSAT]</span></td></tr>
	</table>		</table>
	== Disease ==		== Disease ==
-	[~~[http~~://www.uniprot.org/uniprot/MFN2_HUMAN MFN2_HUMAN]] Multiple symmetric lipomatosis;Autosomal dominant Charcot-Marie-Tooth disease type 2A2;Severe early-onset axonal neuropathy due to MFN2 deficiency;Hereditary motor and sensory neuropathy type 5;Hereditary motor and sensory neuropathy type 6. The disease is caused by mutations affecting the gene represented in this entry. The disease is caused by mutations affecting the gene represented in this entry. The disease is caused by mutations affecting the gene represented in this entry.	+	[https://www.uniprot.org/uniprot/MFN2_HUMAN MFN2_HUMAN] Multiple symmetric lipomatosis;Autosomal dominant Charcot-Marie-Tooth disease type 2A2;Severe early-onset axonal neuropathy due to MFN2 deficiency;Hereditary motor and sensory neuropathy type 5;Hereditary motor and sensory neuropathy type 6. The disease is caused by mutations affecting the gene represented in this entry. The disease is caused by mutations affecting the gene represented in this entry. The disease is caused by mutations affecting the gene represented in this entry.
	== Function ==		== Function ==
-	[~~[http~~://www.uniprot.org/uniprot/MFN2_HUMAN MFN2_HUMAN]] Mitochondrial outer membrane GTPase that mediates mitochondrial clustering and fusion (PubMed:11181170, PubMed:11950885, PubMed:28114303). Mitochondria are highly dynamic organelles, and their morphology is determined by the equilibrium between mitochondrial fusion and fission events (PubMed:28114303). Overexpression induces the formation of mitochondrial networks (PubMed:28114303). Membrane clustering requires GTPase activity and may involve a major rearrangement of the coiled coil domains (Probable). Plays a central role in mitochondrial metabolism and may be associated with obesity and/or apoptosis processes (By similarity). Plays an important role in the regulation of vascular smooth muscle cell proliferation (By similarity). Involved in the clearance of damaged mitochondria via selective autophagy (mitophagy) (PubMed:23620051). Is required for PRKN recruitment to dysfunctional mitochondria (PubMed:23620051). Involved in the control of unfolded protein response (UPR) upon ER stress including activation of apoptosis and autophagy during ER stress (By similarity). Acts as an upstream regulator of EIF2AK3 and suppresses EIF2AK3 activation under basal conditions (By similarity).[UniProtKB:Q80U63][UniProtKB:Q8R500]<ref>PMID:11181170</ref> <ref>PMID:11950885</ref> <ref>PMID:23620051</ref> <ref>PMID:26085578</ref> <ref>PMID:28114303</ref>	+	[https://www.uniprot.org/uniprot/MFN2_HUMAN MFN2_HUMAN] Mitochondrial outer membrane GTPase that mediates mitochondrial clustering and fusion (PubMed:11181170, PubMed:11950885, PubMed:28114303). Mitochondria are highly dynamic organelles, and their morphology is determined by the equilibrium between mitochondrial fusion and fission events (PubMed:28114303). Overexpression induces the formation of mitochondrial networks (PubMed:28114303). Membrane clustering requires GTPase activity and may involve a major rearrangement of the coiled coil domains (Probable). Plays a central role in mitochondrial metabolism and may be associated with obesity and/or apoptosis processes (By similarity). Plays an important role in the regulation of vascular smooth muscle cell proliferation (By similarity). Involved in the clearance of damaged mitochondria via selective autophagy (mitophagy) (PubMed:23620051). Is required for PRKN recruitment to dysfunctional mitochondria (PubMed:23620051). Involved in the control of unfolded protein response (UPR) upon ER stress including activation of apoptosis and autophagy during ER stress (By similarity). Acts as an upstream regulator of EIF2AK3 and suppresses EIF2AK3 activation under basal conditions (By similarity).[UniProtKB:Q80U63][UniProtKB:Q8R500]<ref>PMID:11181170</ref> <ref>PMID:11950885</ref> <ref>PMID:23620051</ref> <ref>PMID:26085578</ref> <ref>PMID:28114303</ref>
	<div style="background-color:#fffaf0;">		<div style="background-color:#fffaf0;">
	== Publication Abstract from PubMed ==		== Publication Abstract from PubMed ==
Line 25:		Line 25:
	__TOC__		__TOC__
	</StructureSection>		</StructureSection>
-	[[Category: ~~Human~~]]	+	[[Category: Homo sapiens]]
	[[Category: Large Structures]]		[[Category: Large Structures]]
-	[[Category: Cao~~, Y L~~]]	+	[[Category: Cao YL]]
-	[[Category: Chan~~, D C~~]]	+	[[Category: Chan DC]]
-	[[Category: Chen~~, S D~~]]	+	[[Category: Chen SD]]
-	[[Category: Chen~~, X X~~]]	+	[[Category: Chen XX]]
-	[[Category: Feng~~, J X~~]]	+	[[Category: Feng JX]]
-	[[Category: Gao, S]]	+	[[Category: Gao S]]
-	[[Category: Hu~~, J J~~]]	+	[[Category: Hu JJ]]
-	[[Category: Kang~~, S S~~]]	+	[[Category: Kang SS]]
-	[[Category: Lan, L]]	+	[[Category: Lan L]]
-	[[Category: Li~~, Y J~~]]	+	[[Category: Li YJ]]
-	[[Category: Luo, L]]	+	[[Category: Luo L]]
-	[[Category: Meng~~, S X~~]]	+	[[Category: Meng SX]]
-	[[Category: Qi~~, Y B~~]]	+	[[Category: Qi YB]]
-	[[Category: Yang~~, J F~~]]	+	[[Category: Yang JF]]
-	[[Category: Yu, B]]	+	[[Category: Yu B]]
-	[[Category: Zhong~~, Y T]]~~	+	[[Category: Zhong YT]]
-	~~[[Category: Cmt2a]]~~	+
-	~~[[Category: Gtpase activity]]~~	+
-	~~[[Category: Membrane protein]]~~	+
-	~~[[Category: Mitochondriral fusion~~]]	+

OCA at 08:43, 27 November 2019

OCA — Wed, 27 Nov 2019 08:43:31 GMT

←Older revision		Revision as of 08:43, 27 November 2019
Line 3:		Line 3:
	<StructureSection load='6jfk' size='340' side='right'caption='[[6jfk]], [[Resolution\|resolution]] 2.00Å' scene=''>		<StructureSection load='6jfk' size='340' side='right'caption='[[6jfk]], [[Resolution\|resolution]] 2.00Å' scene=''>
	== Structural highlights ==		== Structural highlights ==
-	<table><tr><td colspan='2'>[[6jfk]] is a 1 chain structure. Full crystallographic information is available from [http://oca.weizmann.ac.il/oca-bin/ocashort?id=6JFK OCA]. For a <b>guided tour on the structure components</b> use [http://oca.weizmann.ac.il/oca-docs/fgij/fg.htm?mol=6JFK FirstGlance]. <br>	+	<table><tr><td colspan='2'>[[6jfk]] is a 1 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=6JFK OCA]. For a <b>guided tour on the structure components</b> use [http://oca.weizmann.ac.il/oca-docs/fgij/fg.htm?mol=6JFK FirstGlance]. <br>
	</td></tr><tr id='ligand'><td class="sblockLbl"><b>[[Ligand\|Ligands:]]</b></td><td class="sblockDat"><scene name='pdbligand=CIT:CITRIC+ACID'>CIT</scene>, <scene name='pdbligand=GDP:GUANOSINE-5-DIPHOSPHATE'>GDP</scene>, <scene name='pdbligand=GOL:GLYCEROL'>GOL</scene></td></tr>		</td></tr><tr id='ligand'><td class="sblockLbl"><b>[[Ligand\|Ligands:]]</b></td><td class="sblockDat"><scene name='pdbligand=CIT:CITRIC+ACID'>CIT</scene>, <scene name='pdbligand=GDP:GUANOSINE-5-DIPHOSPHATE'>GDP</scene>, <scene name='pdbligand=GOL:GLYCEROL'>GOL</scene></td></tr>
		+	<tr id='gene'><td class="sblockLbl"><b>[[Gene\|Gene:]]</b></td><td class="sblockDat">MFN2, CPRP1, KIAA0214 ([http://www.ncbi.nlm.nih.gov/Taxonomy/Browser/wwwtax.cgi?mode=Info&srchmode=5&id=9606 HUMAN])</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=6jfk FirstGlance], [http://oca.weizmann.ac.il/oca-bin/ocaids?id=6jfk OCA], [http://pdbe.org/6jfk PDBe], [http://www.rcsb.org/pdb/explore.do?structureId=6jfk RCSB], [http://www.ebi.ac.uk/pdbsum/6jfk PDBsum], [http://prosat.h-its.org/prosat/prosatexe?pdbcode=6jfk 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=6jfk FirstGlance], [http://oca.weizmann.ac.il/oca-bin/ocaids?id=6jfk OCA], [http://pdbe.org/6jfk PDBe], [http://www.rcsb.org/pdb/explore.do?structureId=6jfk RCSB], [http://www.ebi.ac.uk/pdbsum/6jfk PDBsum], [http://prosat.h-its.org/prosat/prosatexe?pdbcode=6jfk ProSAT]</span></td></tr>
	</table>		</table>
Line 24:		Line 25:
	__TOC__		__TOC__
	</StructureSection>		</StructureSection>
		+	[[Category: Human]]
	[[Category: Large Structures]]		[[Category: Large Structures]]
	[[Category: Cao, Y L]]		[[Category: Cao, Y L]]

OCA at 10:59, 13 November 2019

OCA — Wed, 13 Nov 2019 10:59:03 GMT

←Older revision		Revision as of 10:59, 13 November 2019
Line 1:		Line 1:
-	'''Unreleased structure'''

-	The entry ~~6jfk~~ is ~~ON HOLD~~ ~~until Paper~~ Publication	+	==GDP bound Mitofusin2 (MFN2)==
		+	<StructureSection load='6jfk' size='340' side='right'caption='[[6jfk]], [[Resolution\|resolution]] 2.00Å' scene=''>
		+	== Structural highlights ==
		+	<table><tr><td colspan='2'>[[6jfk]] is a 1 chain structure. Full crystallographic information is available from [http://oca.weizmann.ac.il/oca-bin/ocashort?id=6JFK OCA]. For a <b>guided tour on the structure components</b> use [http://oca.weizmann.ac.il/oca-docs/fgij/fg.htm?mol=6JFK FirstGlance]. <br>
		+	</td></tr><tr id='ligand'><td class="sblockLbl"><b>[[Ligand\|Ligands:]]</b></td><td class="sblockDat"><scene name='pdbligand=CIT:CITRIC+ACID'>CIT</scene>, <scene name='pdbligand=GDP:GUANOSINE-5-DIPHOSPHATE'>GDP</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'>[http://oca.weizmann.ac.il/oca-docs/fgij/fg.htm?mol=6jfk FirstGlance], [http://oca.weizmann.ac.il/oca-bin/ocaids?id=6jfk OCA], [http://pdbe.org/6jfk PDBe], [http://www.rcsb.org/pdb/explore.do?structureId=6jfk RCSB], [http://www.ebi.ac.uk/pdbsum/6jfk PDBsum], [http://prosat.h-its.org/prosat/prosatexe?pdbcode=6jfk ProSAT]</span></td></tr>
		+	</table>
		+	== Disease ==
		+	[[http://www.uniprot.org/uniprot/MFN2_HUMAN MFN2_HUMAN]] Multiple symmetric lipomatosis;Autosomal dominant Charcot-Marie-Tooth disease type 2A2;Severe early-onset axonal neuropathy due to MFN2 deficiency;Hereditary motor and sensory neuropathy type 5;Hereditary motor and sensory neuropathy type 6. The disease is caused by mutations affecting the gene represented in this entry. The disease is caused by mutations affecting the gene represented in this entry. The disease is caused by mutations affecting the gene represented in this entry.
		+	== Function ==
		+	[[http://www.uniprot.org/uniprot/MFN2_HUMAN MFN2_HUMAN]] Mitochondrial outer membrane GTPase that mediates mitochondrial clustering and fusion (PubMed:11181170, PubMed:11950885, PubMed:28114303). Mitochondria are highly dynamic organelles, and their morphology is determined by the equilibrium between mitochondrial fusion and fission events (PubMed:28114303). Overexpression induces the formation of mitochondrial networks (PubMed:28114303). Membrane clustering requires GTPase activity and may involve a major rearrangement of the coiled coil domains (Probable). Plays a central role in mitochondrial metabolism and may be associated with obesity and/or apoptosis processes (By similarity). Plays an important role in the regulation of vascular smooth muscle cell proliferation (By similarity). Involved in the clearance of damaged mitochondria via selective autophagy (mitophagy) (PubMed:23620051). Is required for PRKN recruitment to dysfunctional mitochondria (PubMed:23620051). Involved in the control of unfolded protein response (UPR) upon ER stress including activation of apoptosis and autophagy during ER stress (By similarity). Acts as an upstream regulator of EIF2AK3 and suppresses EIF2AK3 activation under basal conditions (By similarity).[UniProtKB:Q80U63][UniProtKB:Q8R500]<ref>PMID:11181170</ref> <ref>PMID:11950885</ref> <ref>PMID:23620051</ref> <ref>PMID:26085578</ref> <ref>PMID:28114303</ref>
		+	<div style="background-color:#fffaf0;">
		+	== Publication Abstract from PubMed ==
		+	Mitofusin-2 (MFN2) is a dynamin-like GTPase that plays a central role in regulating mitochondrial fusion and cell metabolism. Mutations in MFN2 cause the neurodegenerative disease Charcot-Marie-Tooth type 2A (CMT2A). The molecular basis underlying the physiological and pathological relevance of MFN2 is unclear. Here, we present crystal structures of truncated human MFN2 in different nucleotide-loading states. Unlike other dynamin superfamily members including MFN1, MFN2 forms sustained dimers even after GTP hydrolysis via the GTPase domain (G) interface, which accounts for its high membrane-tethering efficiency. The biochemical discrepancy between human MFN2 and MFN1 largely derives from a primate-only single amino acid variance. MFN2 and MFN1 can form heterodimers via the G interface in a nucleotide-dependent manner. CMT2A-related mutations, mapping to different functional zones of MFN2, lead to changes in GTP hydrolysis and homo/hetero-association ability. Our study provides fundamental insight into how mitofusins mediate mitochondrial fusion and the ways their disruptions cause disease.

-	~~Authors~~:	+	Structural insights of human mitofusin-2 into mitochondrial fusion and CMT2A onset.,Li YJ, Cao YL, Feng JX, Qi Y, Meng S, Yang JF, Zhong YT, Kang S, Chen X, Lan L, Luo L, Yu B, Chen S, Chan DC, Hu J, Gao S Nat Commun. 2019 Oct 29;10(1):4914. doi: 10.1038/s41467-019-12912-0. PMID:31664033<ref>PMID:31664033</ref>

-	~~Description~~:	+	From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine.<br>
-	[[Category: ~~Unreleased~~ Structures]]	+	</div>
		+	<div class="pdbe-citations 6jfk" style="background-color:#fffaf0;"></div>
		+	== References ==
		+	<references/>
		+	__TOC__
		+	</StructureSection>
		+	[[Category: Large Structures]]
		+	[[Category: Cao, Y L]]
		+	[[Category: Chan, D C]]
		+	[[Category: Chen, S D]]
		+	[[Category: Chen, X X]]
		+	[[Category: Feng, J X]]
		+	[[Category: Gao, S]]
		+	[[Category: Hu, J J]]
		+	[[Category: Kang, S S]]
		+	[[Category: Lan, L]]
		+	[[Category: Li, Y J]]
		+	[[Category: Luo, L]]
		+	[[Category: Meng, S X]]
		+	[[Category: Qi, Y B]]
		+	[[Category: Yang, J F]]
		+	[[Category: Yu, B]]
		+	[[Category: Zhong, Y T]]
		+	[[Category: Cmt2a]]
		+	[[Category: Gtpase activity]]
		+	[[Category: Membrane protein]]
		+	[[Category: Mitochondriral fusion]]

OCA at 05:48, 20 March 2019

OCA — Wed, 20 Mar 2019 05:48:23 GMT

←Older revision		Revision as of 05:48, 20 March 2019
Line 1:		Line 1:
	'''Unreleased structure'''		'''Unreleased structure'''

-	The entry 6jfk is ON HOLD	+	The entry 6jfk is ON HOLD until Paper Publication

	Authors:		Authors:

OCA: Protected "6jfk" [edit=sysop:move=sysop]

OCA — Thu, 21 Feb 2019 04:58:45 GMT

Protected "6jfk" [edit=sysop:move=sysop]

←Older revision

Revision as of 04:58, 21 February 2019

OCA: New page: '''Unreleased structure''' The entry 6jfk is ON HOLD Authors: Description: Category: Unreleased Structures

OCA — Thu, 21 Feb 2019 04:58:43 GMT

New page: '''Unreleased structure''' The entry 6jfk is ON HOLD Authors: Description: Category: Unreleased Structures

New page

'''Unreleased structure'''

The entry 6jfk is ON HOLD

Authors:

Description:
[[Category: Unreleased Structures]]