3qwz - Revision history

OCA at 12:01, 14 March 2024

OCA — Thu, 14 Mar 2024 12:01:39 GMT

←Older revision		Revision as of 12:01, 14 March 2024
Line 3:		Line 3:
	<StructureSection load='3qwz' size='340' side='right'caption='[[3qwz]], [[Resolution\|resolution]] 2.00Å' scene=''>		<StructureSection load='3qwz' size='340' side='right'caption='[[3qwz]], [[Resolution\|resolution]] 2.00Å' scene=''>
	== Structural highlights ==		== Structural highlights ==
-	<table><tr><td colspan='2'>[[3qwz]] is a 2 chain structure with sequence from [https://en.wikipedia.org/wiki/~~Human Human~~]. Full crystallographic information is available from [http://oca.weizmann.ac.il/oca-bin/ocashort?id=3QWZ OCA]. For a <b>guided tour on the structure components</b> use [https://proteopedia.org/fgij/fg.htm?mol=3QWZ FirstGlance]. <br>	+	<table><tr><td colspan='2'>[[3qwz]] 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=3QWZ OCA]. For a <b>guided tour on the structure components</b> use [https://proteopedia.org/fgij/fg.htm?mol=3QWZ FirstGlance]. <br>
-	</td></tr><tr id='~~NonStdRes~~'><td class="sblockLbl"><b>[[~~Non-Standard_Residue~~\|~~NonStd Res~~:]]</b></td><td class="sblockDat"~~><scene name='pdbligand=MLY:N-DIMETHYL-LYSINE'>MLY</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]] 2Å</td></tr>
-	~~<tr~~ id~~='related'><td class~~="~~sblockLbl~~">~~<b>~~[[~~Related_structure~~\|~~Related:~~]]~~</b></td><td class="sblockDat"><div style='overflow: auto~~; ~~max-height: 3em;'>[[3qx1\|3qx1]]</div>~~</td></tr>	+	<tr id='ligand'><td class="sblockLbl"><b>[[Ligand\|Ligands:]]</b></td><td class="sblockDat" id="ligandDat"><scene name='pdbligand=MLY:N-DIMETHYL-LYSINE'>MLY</scene></td></tr>
-	<tr id='~~gene~~'><td class="sblockLbl"><b>[[~~Gene~~\|~~Gene~~:]]</b></td><td class="sblockDat">~~VCP ([https://www.ncbi.nlm.nih.gov/Taxonomy/Browser/wwwtax.cgi?mode~~=~~Info&srchmode~~=~~5&id=9606 HUMAN]), FAF1, UBXD12, UBXN3A, CGI~~-~~03 ([https:~~/~~/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'>[https://proteopedia.org/fgij/fg.htm?mol=3qwz FirstGlance], [http://oca.weizmann.ac.il/oca-bin/ocaids?id=3qwz OCA], [https://pdbe.org/3qwz PDBe], [https://www.rcsb.org/pdb/explore.do?structureId=3qwz RCSB], [https://www.ebi.ac.uk/pdbsum/3qwz PDBsum], [https://prosat.h-its.org/prosat/prosatexe?pdbcode=3qwz 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=3qwz FirstGlance], [http://oca.weizmann.ac.il/oca-bin/ocaids?id=3qwz OCA], [https://pdbe.org/3qwz PDBe], [https://www.rcsb.org/pdb/explore.do?structureId=3qwz RCSB], [https://www.ebi.ac.uk/pdbsum/3qwz PDBsum], [https://prosat.h-its.org/prosat/prosatexe?pdbcode=3qwz ProSAT]</span></td></tr>
	</table>		</table>
	== Disease ==		== Disease ==
-	[[https://www.uniprot.org/uniprot/TERA_HUMAN TERA_HUMAN]] Defects in VCP are the cause of inclusion body myopathy with early-onset Paget disease and frontotemporal dementia (IBMPFD) [MIM:[https://omim.org/entry/167320 167320]]; also known as muscular dystrophy, limb-girdle, with Paget disease of bone or pagetoid amyotrophic lateral sclerosis or pagetoid neuroskeletal syndrome or lower motor neuron degeneration with Paget-like bone disease. IBMPFD features adult-onset proximal and distal muscle weakness (clinically resembling limb girdle muscular dystrophy), early-onset Paget disease of bone in most cases and premature frontotemporal dementia.<ref>PMID:20512113</ref> <ref>PMID:15034582</ref> <ref>PMID:15732117</ref> <ref>PMID:16247064</ref> <ref>PMID:16321991</ref> Defects in VCP are the cause of amyotrophic lateral sclerosis type 14 with or without frontotemporal dementia (ALS14) [MIM:[https://omim.org/entry/613954 613954]]. ALS14 is a neurodegenerative disorder affecting upper motor neurons in the brain and lower motor neurons in the brain stem and spinal cord, resulting in fatal paralysis. Sensory abnormalities are absent. The pathologic hallmarks of the disease include pallor of the corticospinal tract due to loss of motor neurons, presence of ubiquitin-positive inclusions within surviving motor neurons, and deposition of pathologic aggregates. The etiology of amyotrophic lateral sclerosis is likely to be multifactorial, involving both genetic and environmental factors. The disease is inherited in 5-10% of the cases. Patients with ALS14 may develop frontotemporal dementia.<ref>PMID:21145000</ref>	+	[https://www.uniprot.org/uniprot/TERA_HUMAN TERA_HUMAN] Defects in VCP are the cause of inclusion body myopathy with early-onset Paget disease and frontotemporal dementia (IBMPFD) [MIM:[https://omim.org/entry/167320 167320]; also known as muscular dystrophy, limb-girdle, with Paget disease of bone or pagetoid amyotrophic lateral sclerosis or pagetoid neuroskeletal syndrome or lower motor neuron degeneration with Paget-like bone disease. IBMPFD features adult-onset proximal and distal muscle weakness (clinically resembling limb girdle muscular dystrophy), early-onset Paget disease of bone in most cases and premature frontotemporal dementia.<ref>PMID:20512113</ref> <ref>PMID:15034582</ref> <ref>PMID:15732117</ref> <ref>PMID:16247064</ref> <ref>PMID:16321991</ref> Defects in VCP are the cause of amyotrophic lateral sclerosis type 14 with or without frontotemporal dementia (ALS14) [MIM:[https://omim.org/entry/613954 613954]. ALS14 is a neurodegenerative disorder affecting upper motor neurons in the brain and lower motor neurons in the brain stem and spinal cord, resulting in fatal paralysis. Sensory abnormalities are absent. The pathologic hallmarks of the disease include pallor of the corticospinal tract due to loss of motor neurons, presence of ubiquitin-positive inclusions within surviving motor neurons, and deposition of pathologic aggregates. The etiology of amyotrophic lateral sclerosis is likely to be multifactorial, involving both genetic and environmental factors. The disease is inherited in 5-10% of the cases. Patients with ALS14 may develop frontotemporal dementia.<ref>PMID:21145000</ref>
	== Function ==		== Function ==
-	[[https://www.uniprot.org/uniprot/TERA_HUMAN TERA_HUMAN]] Necessary for the fragmentation of Golgi stacks during mitosis and for their reassembly after mitosis. Involved in the formation of the transitional endoplasmic reticulum (tER). The transfer of membranes from the endoplasmic reticulum to the Golgi apparatus occurs via 50-70 nm transition vesicles which derive from part-rough, part-smooth transitional elements of the endoplasmic reticulum (tER). Vesicle budding from the tER is an ATP-dependent process. The ternary complex containing UFD1L, VCP and NPLOC4 binds ubiquitinated proteins and is necessary for the export of misfolded proteins from the ER to the cytoplasm, where they are degraded by the proteasome. The NPLOC4-UFD1L-VCP complex regulates spindle disassembly at the end of mitosis and is necessary for the formation of a closed nuclear envelope. Regulates E3 ubiquitin-protein ligase activity of RNF19A (By similarity). Component of the VCP/p97-AMFR/gp78 complex that participates in the final step of the sterol-mediated ubiquitination and endoplasmic reticulum-associated degradation (ERAD) of HMGCR. Also involved in DNA damage response: recruited to double-strand breaks (DSBs) sites in a RNF8- and RNF168-dependent manner and promotes the recruitment of TP53BP1 at DNA damage sites. Recruited to stalled replication forks by SPRTN: may act by mediating extraction of DNA polymerase eta (POLH) to prevent excessive translesion DNA synthesis and limit the incidence of mutations induced by DNA damage.<ref>PMID:15456787</ref> <ref>PMID:16168377</ref> <ref>PMID:22020440</ref> <ref>PMID:22120668</ref> <ref>PMID:22607976</ref> <ref>PMID:23042607</ref> <ref>PMID:23042605</ref> ~~[[https://www.uniprot.org/uniprot/FAF1_HUMAN FAF1_HUMAN]] Potentiates but cannot initiate FAS-induced apoptosis.~~	+	[https://www.uniprot.org/uniprot/TERA_HUMAN TERA_HUMAN] Necessary for the fragmentation of Golgi stacks during mitosis and for their reassembly after mitosis. Involved in the formation of the transitional endoplasmic reticulum (tER). The transfer of membranes from the endoplasmic reticulum to the Golgi apparatus occurs via 50-70 nm transition vesicles which derive from part-rough, part-smooth transitional elements of the endoplasmic reticulum (tER). Vesicle budding from the tER is an ATP-dependent process. The ternary complex containing UFD1L, VCP and NPLOC4 binds ubiquitinated proteins and is necessary for the export of misfolded proteins from the ER to the cytoplasm, where they are degraded by the proteasome. The NPLOC4-UFD1L-VCP complex regulates spindle disassembly at the end of mitosis and is necessary for the formation of a closed nuclear envelope. Regulates E3 ubiquitin-protein ligase activity of RNF19A (By similarity). Component of the VCP/p97-AMFR/gp78 complex that participates in the final step of the sterol-mediated ubiquitination and endoplasmic reticulum-associated degradation (ERAD) of HMGCR. Also involved in DNA damage response: recruited to double-strand breaks (DSBs) sites in a RNF8- and RNF168-dependent manner and promotes the recruitment of TP53BP1 at DNA damage sites. Recruited to stalled replication forks by SPRTN: may act by mediating extraction of DNA polymerase eta (POLH) to prevent excessive translesion DNA synthesis and limit the incidence of mutations induced by DNA damage.<ref>PMID:15456787</ref> <ref>PMID:16168377</ref> <ref>PMID:22020440</ref> <ref>PMID:22120668</ref> <ref>PMID:22607976</ref> <ref>PMID:23042607</ref> <ref>PMID:23042605</ref>

	==See Also==		==See Also==
Line 20:		Line 19:
	__TOC__		__TOC__
	</StructureSection>		</StructureSection>
-	[[Category: ~~Human~~]]	+	[[Category: Homo sapiens]]
	[[Category: Large Structures]]		[[Category: Large Structures]]
-	[[Category: Jeon, H]]	+	[[Category: Jeon H]]
-	[[Category: Kim~~, E E~~]]	+	[[Category: Kim EE]]
-	[[Category: Kim~~, K H~~]]	+	[[Category: Kim KH]]
-	[[Category: Lee~~, J J~~]]	+	[[Category: Lee JJ]]
-	[[Category: Lee~~, K J~~]]	+	[[Category: Lee KJ]]
-	[[Category: Park~~, J K]]~~	+	[[Category: Park JK]]
-	~~[[Category: P97 binding]]~~	+
-	~~[[Category: Transport protein]]~~	+
-	~~[[Category: Ubx~~]]	+

OCA at 05:39, 15 June 2022

OCA — Wed, 15 Jun 2022 05:39:58 GMT

←Older revision		Revision as of 05:39, 15 June 2022
Line 1:		Line 1:

	==Crystal structure of FAF1 UBX-p97N-domain complex==		==Crystal structure of FAF1 UBX-p97N-domain complex==
-	<StructureSection load='3qwz' size='340' side='right' caption='[[3qwz]], [[Resolution\|resolution]] 2.00Å' scene=''>	+	<StructureSection load='3qwz' size='340' side='right'caption='[[3qwz]], [[Resolution\|resolution]] 2.00Å' scene=''>
	== Structural highlights ==		== Structural highlights ==
-	<table><tr><td colspan='2'>[[3qwz]] 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=3QWZ OCA]. For a <b>guided tour on the structure components</b> use [~~http~~://~~oca~~.~~weizmann.ac.il/oca-docs~~/fgij/fg.htm?mol=3QWZ FirstGlance]. <br>	+	<table><tr><td colspan='2'>[[3qwz]] is a 2 chain structure with sequence from [https://en.wikipedia.org/wiki/Human Human]. Full crystallographic information is available from [http://oca.weizmann.ac.il/oca-bin/ocashort?id=3QWZ OCA]. For a <b>guided tour on the structure components</b> use [https://proteopedia.org/fgij/fg.htm?mol=3QWZ FirstGlance]. <br>
	</td></tr><tr id='NonStdRes'><td class="sblockLbl"><b>[[Non-Standard_Residue\|NonStd Res:]]</b></td><td class="sblockDat"><scene name='pdbligand=MLY:N-DIMETHYL-LYSINE'>MLY</scene></td></tr>		</td></tr><tr id='NonStdRes'><td class="sblockLbl"><b>[[Non-Standard_Residue\|NonStd Res:]]</b></td><td class="sblockDat"><scene name='pdbligand=MLY:N-DIMETHYL-LYSINE'>MLY</scene></td></tr>
-	<tr id='related'><td class="sblockLbl"><b>[[Related_structure\|Related:]]</b></td><td class="sblockDat">[[3qx1\|3qx1]]</td></tr>	+	<tr id='related'><td class="sblockLbl"><b>[[Related_structure\|Related:]]</b></td><td class="sblockDat"><div style='overflow: auto; max-height: 3em;'>[[3qx1\|3qx1]]</div></td></tr>
-	<tr id='gene'><td class="sblockLbl"><b>[[Gene\|Gene:]]</b></td><td class="sblockDat">VCP ([~~http~~://www.ncbi.nlm.nih.gov/Taxonomy/Browser/wwwtax.cgi?mode=Info&srchmode=5&id=9606 HUMAN]), FAF1, UBXD12, UBXN3A, CGI-03 ([~~http~~://www.ncbi.nlm.nih.gov/Taxonomy/Browser/wwwtax.cgi?mode=Info&srchmode=5&id=9606 HUMAN])</td></tr>	+	<tr id='gene'><td class="sblockLbl"><b>[[Gene\|Gene:]]</b></td><td class="sblockDat">VCP ([https://www.ncbi.nlm.nih.gov/Taxonomy/Browser/wwwtax.cgi?mode=Info&srchmode=5&id=9606 HUMAN]), FAF1, UBXD12, UBXN3A, CGI-03 ([https://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=3qwz FirstGlance], [http://oca.weizmann.ac.il/oca-bin/ocaids?id=3qwz OCA], [~~http~~://pdbe.org/3qwz PDBe], [~~http~~://www.rcsb.org/pdb/explore.do?structureId=3qwz RCSB], [~~http~~://www.ebi.ac.uk/pdbsum/3qwz PDBsum], [~~http~~://prosat.h-its.org/prosat/prosatexe?pdbcode=3qwz 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=3qwz FirstGlance], [http://oca.weizmann.ac.il/oca-bin/ocaids?id=3qwz OCA], [https://pdbe.org/3qwz PDBe], [https://www.rcsb.org/pdb/explore.do?structureId=3qwz RCSB], [https://www.ebi.ac.uk/pdbsum/3qwz PDBsum], [https://prosat.h-its.org/prosat/prosatexe?pdbcode=3qwz ProSAT]</span></td></tr>
	</table>		</table>
	== Disease ==		== Disease ==
-	[[~~http~~://www.uniprot.org/uniprot/TERA_HUMAN TERA_HUMAN]] Defects in VCP are the cause of inclusion body myopathy with early-onset Paget disease and frontotemporal dementia (IBMPFD) [MIM:[~~http~~://omim.org/entry/167320 167320]]; also known as muscular dystrophy, limb-girdle, with Paget disease of bone or pagetoid amyotrophic lateral sclerosis or pagetoid neuroskeletal syndrome or lower motor neuron degeneration with Paget-like bone disease. IBMPFD features adult-onset proximal and distal muscle weakness (clinically resembling limb girdle muscular dystrophy), early-onset Paget disease of bone in most cases and premature frontotemporal dementia.<ref>PMID:20512113</ref> <ref>PMID:15034582</ref> <ref>PMID:15732117</ref> <ref>PMID:16247064</ref> <ref>PMID:16321991</ref> Defects in VCP are the cause of amyotrophic lateral sclerosis type 14 with or without frontotemporal dementia (ALS14) [MIM:[~~http~~://omim.org/entry/613954 613954]]. ALS14 is a neurodegenerative disorder affecting upper motor neurons in the brain and lower motor neurons in the brain stem and spinal cord, resulting in fatal paralysis. Sensory abnormalities are absent. The pathologic hallmarks of the disease include pallor of the corticospinal tract due to loss of motor neurons, presence of ubiquitin-positive inclusions within surviving motor neurons, and deposition of pathologic aggregates. The etiology of amyotrophic lateral sclerosis is likely to be multifactorial, involving both genetic and environmental factors. The disease is inherited in 5-10% of the cases. Patients with ALS14 may develop frontotemporal dementia.<ref>PMID:21145000</ref>	+	[[https://www.uniprot.org/uniprot/TERA_HUMAN TERA_HUMAN]] Defects in VCP are the cause of inclusion body myopathy with early-onset Paget disease and frontotemporal dementia (IBMPFD) [MIM:[https://omim.org/entry/167320 167320]]; also known as muscular dystrophy, limb-girdle, with Paget disease of bone or pagetoid amyotrophic lateral sclerosis or pagetoid neuroskeletal syndrome or lower motor neuron degeneration with Paget-like bone disease. IBMPFD features adult-onset proximal and distal muscle weakness (clinically resembling limb girdle muscular dystrophy), early-onset Paget disease of bone in most cases and premature frontotemporal dementia.<ref>PMID:20512113</ref> <ref>PMID:15034582</ref> <ref>PMID:15732117</ref> <ref>PMID:16247064</ref> <ref>PMID:16321991</ref> Defects in VCP are the cause of amyotrophic lateral sclerosis type 14 with or without frontotemporal dementia (ALS14) [MIM:[https://omim.org/entry/613954 613954]]. ALS14 is a neurodegenerative disorder affecting upper motor neurons in the brain and lower motor neurons in the brain stem and spinal cord, resulting in fatal paralysis. Sensory abnormalities are absent. The pathologic hallmarks of the disease include pallor of the corticospinal tract due to loss of motor neurons, presence of ubiquitin-positive inclusions within surviving motor neurons, and deposition of pathologic aggregates. The etiology of amyotrophic lateral sclerosis is likely to be multifactorial, involving both genetic and environmental factors. The disease is inherited in 5-10% of the cases. Patients with ALS14 may develop frontotemporal dementia.<ref>PMID:21145000</ref>
	== Function ==		== Function ==
-	[[~~http~~://www.uniprot.org/uniprot/TERA_HUMAN TERA_HUMAN]] Necessary for the fragmentation of Golgi stacks during mitosis and for their reassembly after mitosis. Involved in the formation of the transitional endoplasmic reticulum (tER). The transfer of membranes from the endoplasmic reticulum to the Golgi apparatus occurs via 50-70 nm transition vesicles which derive from part-rough, part-smooth transitional elements of the endoplasmic reticulum (tER). Vesicle budding from the tER is an ATP-dependent process. The ternary complex containing UFD1L, VCP and NPLOC4 binds ubiquitinated proteins and is necessary for the export of misfolded proteins from the ER to the cytoplasm, where they are degraded by the proteasome. The NPLOC4-UFD1L-VCP complex regulates spindle disassembly at the end of mitosis and is necessary for the formation of a closed nuclear envelope. Regulates E3 ubiquitin-protein ligase activity of RNF19A (By similarity). Component of the VCP/p97-AMFR/gp78 complex that participates in the final step of the sterol-mediated ubiquitination and endoplasmic reticulum-associated degradation (ERAD) of HMGCR. Also involved in DNA damage response: recruited to double-strand breaks (DSBs) sites in a RNF8- and RNF168-dependent manner and promotes the recruitment of TP53BP1 at DNA damage sites. Recruited to stalled replication forks by SPRTN: may act by mediating extraction of DNA polymerase eta (POLH) to prevent excessive translesion DNA synthesis and limit the incidence of mutations induced by DNA damage.<ref>PMID:15456787</ref> <ref>PMID:16168377</ref> <ref>PMID:22020440</ref> <ref>PMID:22120668</ref> <ref>PMID:22607976</ref> <ref>PMID:23042607</ref> <ref>PMID:23042605</ref> [[~~http~~://www.uniprot.org/uniprot/FAF1_HUMAN FAF1_HUMAN]] Potentiates but cannot initiate FAS-induced apoptosis.	+	[[https://www.uniprot.org/uniprot/TERA_HUMAN TERA_HUMAN]] Necessary for the fragmentation of Golgi stacks during mitosis and for their reassembly after mitosis. Involved in the formation of the transitional endoplasmic reticulum (tER). The transfer of membranes from the endoplasmic reticulum to the Golgi apparatus occurs via 50-70 nm transition vesicles which derive from part-rough, part-smooth transitional elements of the endoplasmic reticulum (tER). Vesicle budding from the tER is an ATP-dependent process. The ternary complex containing UFD1L, VCP and NPLOC4 binds ubiquitinated proteins and is necessary for the export of misfolded proteins from the ER to the cytoplasm, where they are degraded by the proteasome. The NPLOC4-UFD1L-VCP complex regulates spindle disassembly at the end of mitosis and is necessary for the formation of a closed nuclear envelope. Regulates E3 ubiquitin-protein ligase activity of RNF19A (By similarity). Component of the VCP/p97-AMFR/gp78 complex that participates in the final step of the sterol-mediated ubiquitination and endoplasmic reticulum-associated degradation (ERAD) of HMGCR. Also involved in DNA damage response: recruited to double-strand breaks (DSBs) sites in a RNF8- and RNF168-dependent manner and promotes the recruitment of TP53BP1 at DNA damage sites. Recruited to stalled replication forks by SPRTN: may act by mediating extraction of DNA polymerase eta (POLH) to prevent excessive translesion DNA synthesis and limit the incidence of mutations induced by DNA damage.<ref>PMID:15456787</ref> <ref>PMID:16168377</ref> <ref>PMID:22020440</ref> <ref>PMID:22120668</ref> <ref>PMID:22607976</ref> <ref>PMID:23042607</ref> <ref>PMID:23042605</ref> [[https://www.uniprot.org/uniprot/FAF1_HUMAN FAF1_HUMAN]] Potentiates but cannot initiate FAS-induced apoptosis.

	==See Also==		==See Also==
-	*[[ATPase\|ATPase]]	+	*[[ATPase 3D structures\|ATPase 3D structures]]
	== References ==		== References ==
	<references/>		<references/>
Line 21:		Line 21:
	</StructureSection>		</StructureSection>
	[[Category: Human]]		[[Category: Human]]
		+	[[Category: Large Structures]]
	[[Category: Jeon, H]]		[[Category: Jeon, H]]
	[[Category: Kim, E E]]		[[Category: Kim, E E]]

OCA at 02:02, 5 August 2016

OCA — Fri, 05 Aug 2016 02:02:12 GMT

←Older revision		Revision as of 02:02, 5 August 2016
Line 1:		Line 1:
		+
	==Crystal structure of FAF1 UBX-p97N-domain complex==		==Crystal structure of FAF1 UBX-p97N-domain complex==
	<StructureSection load='3qwz' size='340' side='right' caption='[[3qwz]], [[Resolution\|resolution]] 2.00Å' scene=''>		<StructureSection load='3qwz' size='340' side='right' caption='[[3qwz]], [[Resolution\|resolution]] 2.00Å' scene=''>
	== Structural highlights ==		== Structural highlights ==
-	<table><tr><td colspan='2'>[[3qwz]] is a 2 chain structure with sequence from [http://en.wikipedia.org/wiki/~~Homo_sapiens Homo sapiens~~]. Full crystallographic information is available from [http://oca.weizmann.ac.il/oca-bin/ocashort?id=3QWZ OCA]. For a <b>guided tour on the structure components</b> use [http://oca.weizmann.ac.il/oca-docs/fgij/fg.htm?mol=3QWZ FirstGlance]. <br>	+	<table><tr><td colspan='2'>[[3qwz]] 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=3QWZ OCA]. For a <b>guided tour on the structure components</b> use [http://oca.weizmann.ac.il/oca-docs/fgij/fg.htm?mol=3QWZ FirstGlance]. <br>
	</td></tr><tr id='NonStdRes'><td class="sblockLbl"><b>[[Non-Standard_Residue\|NonStd Res:]]</b></td><td class="sblockDat"><scene name='pdbligand=MLY:N-DIMETHYL-LYSINE'>MLY</scene></td></tr>		</td></tr><tr id='NonStdRes'><td class="sblockLbl"><b>[[Non-Standard_Residue\|NonStd Res:]]</b></td><td class="sblockDat"><scene name='pdbligand=MLY:N-DIMETHYL-LYSINE'>MLY</scene></td></tr>
	<tr id='related'><td class="sblockLbl"><b>[[Related_structure\|Related:]]</b></td><td class="sblockDat">[[3qx1\|3qx1]]</td></tr>		<tr id='related'><td class="sblockLbl"><b>[[Related_structure\|Related:]]</b></td><td class="sblockDat">[[3qx1\|3qx1]]</td></tr>
-	<tr id='gene'><td class="sblockLbl"><b>[[Gene\|Gene:]]</b></td><td class="sblockDat">VCP ([http://www.ncbi.nlm.nih.gov/Taxonomy/Browser/wwwtax.cgi?mode=Info&srchmode=5&id=9606 ~~Homo sapiens~~]), FAF1, UBXD12, UBXN3A, CGI-03 ([http://www.ncbi.nlm.nih.gov/Taxonomy/Browser/wwwtax.cgi?mode=Info&srchmode=5&id=9606 ~~Homo sapiens~~])</td></tr>	+	<tr id='gene'><td class="sblockLbl"><b>[[Gene\|Gene:]]</b></td><td class="sblockDat">VCP ([http://www.ncbi.nlm.nih.gov/Taxonomy/Browser/wwwtax.cgi?mode=Info&srchmode=5&id=9606 HUMAN]), FAF1, UBXD12, UBXN3A, CGI-03 ([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=3qwz FirstGlance], [http://oca.weizmann.ac.il/oca-bin/ocaids?id=3qwz OCA], [http://www.rcsb.org/pdb/explore.do?structureId=3qwz RCSB], [http://www.ebi.ac.uk/pdbsum/3qwz 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=3qwz FirstGlance], [http://oca.weizmann.ac.il/oca-bin/ocaids?id=3qwz OCA], [http://pdbe.org/3qwz PDBe], [http://www.rcsb.org/pdb/explore.do?structureId=3qwz RCSB], [http://www.ebi.ac.uk/pdbsum/3qwz PDBsum], [http://prosat.h-its.org/prosat/prosatexe?pdbcode=3qwz ProSAT]</span></td></tr>
	</table>		</table>
	== Disease ==		== Disease ==
Line 19:		Line 20:
	__TOC__		__TOC__
	</StructureSection>		</StructureSection>
-	[[Category: ~~Homo sapiens~~]]	+	[[Category: Human]]
	[[Category: Jeon, H]]		[[Category: Jeon, H]]
	[[Category: Kim, E E]]		[[Category: Kim, E E]]

OCA at 23:07, 3 January 2015

OCA — Sat, 03 Jan 2015 23:07:58 GMT

←Older revision		Revision as of 23:07, 3 January 2015
Line 1:		Line 1:
-	~~{{STRUCTURE_3qwz\| PDB=3qwz \| SCENE= }}~~	+	==Crystal structure of FAF1 UBX-p97N-domain complex==
-	===Crystal structure of FAF1 UBX-p97N-domain complex===	+	<StructureSection load='3qwz' size='340' side='right' caption='[[3qwz]], [[Resolution\|resolution]] 2.00Å' scene=''>
-		+	== Structural highlights ==
-	==Disease==	+	<table><tr><td colspan='2'>[[3qwz]] is a 2 chain structure with sequence from [http://en.wikipedia.org/wiki/Homo_sapiens Homo sapiens]. Full crystallographic information is available from [http://oca.weizmann.ac.il/oca-bin/ocashort?id=3QWZ OCA]. For a <b>guided tour on the structure components</b> use [http://oca.weizmann.ac.il/oca-docs/fgij/fg.htm?mol=3QWZ FirstGlance]. <br>
-	[[http://www.uniprot.org/uniprot/TERA_HUMAN TERA_HUMAN]] Defects in VCP are the cause of inclusion body myopathy with early-onset Paget disease and frontotemporal dementia (IBMPFD) [MIM:[http://omim.org/entry/167320 167320]]; also known as muscular dystrophy, limb-girdle, with Paget disease of bone or pagetoid amyotrophic lateral sclerosis or pagetoid neuroskeletal syndrome or lower motor neuron degeneration with Paget-like bone disease. IBMPFD features adult-onset proximal and distal muscle weakness (clinically resembling limb girdle muscular dystrophy), early-onset Paget disease of bone in most cases and premature frontotemporal dementia.<ref>PMID:20512113</ref><ref>PMID:15034582</ref><ref>PMID:15732117</ref><ref>PMID:16247064</ref><ref>PMID:16321991</ref> Defects in VCP are the cause of amyotrophic lateral sclerosis type 14 with or without frontotemporal dementia (ALS14) [MIM:[http://omim.org/entry/613954 613954]]. ALS14 is a neurodegenerative disorder affecting upper motor neurons in the brain and lower motor neurons in the brain stem and spinal cord, resulting in fatal paralysis. Sensory abnormalities are absent. The pathologic hallmarks of the disease include pallor of the corticospinal tract due to loss of motor neurons, presence of ubiquitin-positive inclusions within surviving motor neurons, and deposition of pathologic aggregates. The etiology of amyotrophic lateral sclerosis is likely to be multifactorial, involving both genetic and environmental factors. The disease is inherited in 5-10% of the cases. Patients with ALS14 may develop frontotemporal dementia.<ref>PMID:21145000</ref>	+	</td></tr><tr id='NonStdRes'><td class="sblockLbl"><b>[[Non-Standard_Residue\|NonStd Res:]]</b></td><td class="sblockDat"><scene name='pdbligand=MLY:N-DIMETHYL-LYSINE'>MLY</scene></td></tr>
-		+	<tr id='related'><td class="sblockLbl"><b>[[Related_structure\|Related:]]</b></td><td class="sblockDat">[[3qx1\|3qx1]]</td></tr>
-	==Function==	+	<tr id='gene'><td class="sblockLbl"><b>[[Gene\|Gene:]]</b></td><td class="sblockDat">VCP ([http://www.ncbi.nlm.nih.gov/Taxonomy/Browser/wwwtax.cgi?mode=Info&srchmode=5&id=9606 Homo sapiens]), FAF1, UBXD12, UBXN3A, CGI-03 ([http://www.ncbi.nlm.nih.gov/Taxonomy/Browser/wwwtax.cgi?mode=Info&srchmode=5&id=9606 Homo sapiens])</td></tr>
-	[[http://www.uniprot.org/uniprot/TERA_HUMAN TERA_HUMAN]] Necessary for the fragmentation of Golgi stacks during mitosis and for their reassembly after mitosis. Involved in the formation of the transitional endoplasmic reticulum (tER). The transfer of membranes from the endoplasmic reticulum to the Golgi apparatus occurs via 50-70 nm transition vesicles which derive from part-rough, part-smooth transitional elements of the endoplasmic reticulum (tER). Vesicle budding from the tER is an ATP-dependent process. The ternary complex containing UFD1L, VCP and NPLOC4 binds ubiquitinated proteins and is necessary for the export of misfolded proteins from the ER to the cytoplasm, where they are degraded by the proteasome. The NPLOC4-UFD1L-VCP complex regulates spindle disassembly at the end of mitosis and is necessary for the formation of a closed nuclear envelope. Regulates E3 ubiquitin-protein ligase activity of RNF19A (By similarity). Component of the VCP/p97-AMFR/gp78 complex that participates in the final step of the sterol-mediated ubiquitination and endoplasmic reticulum-associated degradation (ERAD) of HMGCR. Also involved in DNA damage response: recruited to double-strand breaks (DSBs) sites in a RNF8- and RNF168-dependent manner and promotes the recruitment of TP53BP1 at DNA damage sites. Recruited to stalled replication forks by SPRTN: may act by mediating extraction of DNA polymerase eta (POLH) to prevent excessive translesion DNA synthesis and limit the incidence of mutations induced by DNA damage.<ref>PMID:15456787</ref><ref>PMID:16168377</ref><ref>PMID:22020440</ref><ref>PMID:22120668</ref><ref>PMID:22607976</ref><ref>PMID:23042607</ref><ref>PMID:23042605</ref> [[http://www.uniprot.org/uniprot/FAF1_HUMAN FAF1_HUMAN]] Potentiates but cannot initiate FAS-induced apoptosis.	+	<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=3qwz FirstGlance], [http://oca.weizmann.ac.il/oca-bin/ocaids?id=3qwz OCA], [http://www.rcsb.org/pdb/explore.do?structureId=3qwz RCSB], [http://www.ebi.ac.uk/pdbsum/3qwz PDBsum]</span></td></tr>
-		+	</table>
-	~~==About this Structure==~~	+	== Disease ==
-	[[3qwz]] is a 2 chain structure with sequence from [http://en.wikipedia.org/wiki/Homo_sapiens Homo sapiens]. Full crystallographic information is available from [http://oca.weizmann.ac.il/oca-bin/ocashort?id=3QWZ OCA].	+	[[http://www.uniprot.org/uniprot/TERA_HUMAN TERA_HUMAN]] Defects in VCP are the cause of inclusion body myopathy with early-onset Paget disease and frontotemporal dementia (IBMPFD) [MIM:[http://omim.org/entry/167320 167320]]; also known as muscular dystrophy, limb-girdle, with Paget disease of bone or pagetoid amyotrophic lateral sclerosis or pagetoid neuroskeletal syndrome or lower motor neuron degeneration with Paget-like bone disease. IBMPFD features adult-onset proximal and distal muscle weakness (clinically resembling limb girdle muscular dystrophy), early-onset Paget disease of bone in most cases and premature frontotemporal dementia.<ref>PMID:20512113</ref> <ref>PMID:15034582</ref> <ref>PMID:15732117</ref> <ref>PMID:16247064</ref> <ref>PMID:16321991</ref> Defects in VCP are the cause of amyotrophic lateral sclerosis type 14 with or without frontotemporal dementia (ALS14) [MIM:[http://omim.org/entry/613954 613954]]. ALS14 is a neurodegenerative disorder affecting upper motor neurons in the brain and lower motor neurons in the brain stem and spinal cord, resulting in fatal paralysis. Sensory abnormalities are absent. The pathologic hallmarks of the disease include pallor of the corticospinal tract due to loss of motor neurons, presence of ubiquitin-positive inclusions within surviving motor neurons, and deposition of pathologic aggregates. The etiology of amyotrophic lateral sclerosis is likely to be multifactorial, involving both genetic and environmental factors. The disease is inherited in 5-10% of the cases. Patients with ALS14 may develop frontotemporal dementia.<ref>PMID:21145000</ref>
		+	== Function ==
		+	[[http://www.uniprot.org/uniprot/TERA_HUMAN TERA_HUMAN]] Necessary for the fragmentation of Golgi stacks during mitosis and for their reassembly after mitosis. Involved in the formation of the transitional endoplasmic reticulum (tER). The transfer of membranes from the endoplasmic reticulum to the Golgi apparatus occurs via 50-70 nm transition vesicles which derive from part-rough, part-smooth transitional elements of the endoplasmic reticulum (tER). Vesicle budding from the tER is an ATP-dependent process. The ternary complex containing UFD1L, VCP and NPLOC4 binds ubiquitinated proteins and is necessary for the export of misfolded proteins from the ER to the cytoplasm, where they are degraded by the proteasome. The NPLOC4-UFD1L-VCP complex regulates spindle disassembly at the end of mitosis and is necessary for the formation of a closed nuclear envelope. Regulates E3 ubiquitin-protein ligase activity of RNF19A (By similarity). Component of the VCP/p97-AMFR/gp78 complex that participates in the final step of the sterol-mediated ubiquitination and endoplasmic reticulum-associated degradation (ERAD) of HMGCR. Also involved in DNA damage response: recruited to double-strand breaks (DSBs) sites in a RNF8- and RNF168-dependent manner and promotes the recruitment of TP53BP1 at DNA damage sites. Recruited to stalled replication forks by SPRTN: may act by mediating extraction of DNA polymerase eta (POLH) to prevent excessive translesion DNA synthesis and limit the incidence of mutations induced by DNA damage.<ref>PMID:15456787</ref> <ref>PMID:16168377</ref> <ref>PMID:22020440</ref> <ref>PMID:22120668</ref> <ref>PMID:22607976</ref> <ref>PMID:23042607</ref> <ref>PMID:23042605</ref> [[http://www.uniprot.org/uniprot/FAF1_HUMAN FAF1_HUMAN]] Potentiates but cannot initiate FAS-induced apoptosis.

	==See Also==		==See Also==
	*[[ATPase\|ATPase]]		*[[ATPase\|ATPase]]
-		+	== References ==
-	==~~Reference~~==	+	<references/>
-	<references ~~group="xtra"~~/><~~references~~/>	+	__TOC__
		+	</StructureSection>
	[[Category: Homo sapiens]]		[[Category: Homo sapiens]]
-	[[Category: Jeon, H.]]	+	[[Category: Jeon, H]]
-	[[Category: Kim, E E.]]	+	[[Category: Kim, E E]]
-	[[Category: Kim, K H.]]	+	[[Category: Kim, K H]]
-	[[Category: Lee, J J.]]	+	[[Category: Lee, J J]]
-	[[Category: Lee, K J.]]	+	[[Category: Lee, K J]]
-	[[Category: Park, J K.]]	+	[[Category: Park, J K]]
	[[Category: P97 binding]]		[[Category: P97 binding]]
	[[Category: Transport protein]]		[[Category: Transport protein]]
	[[Category: Ubx]]		[[Category: Ubx]]

OCA at 06:58, 25 March 2013

OCA — Mon, 25 Mar 2013 06:58:52 GMT

←Older revision		Revision as of 06:58, 25 March 2013
Line 1:		Line 1:
-	[[Image:3qwz.jpg\|left\|200px]]
-
-	<!--
-	The line below this paragraph, containing "STRUCTURE_3qwz", creates the "Structure Box" on the page.
-	You may change the PDB parameter (which sets the PDB file loaded into the applet)
-	or the SCENE parameter (which sets the initial scene displayed when the page is loaded),
-	or leave the SCENE parameter empty for the default display.
-	-->
	{{STRUCTURE_3qwz\| PDB=3qwz \| SCENE= }}		{{STRUCTURE_3qwz\| PDB=3qwz \| SCENE= }}
-
	===Crystal structure of FAF1 UBX-p97N-domain complex===		===Crystal structure of FAF1 UBX-p97N-domain complex===

		+	==Disease==
		+	[[http://www.uniprot.org/uniprot/TERA_HUMAN TERA_HUMAN]] Defects in VCP are the cause of inclusion body myopathy with early-onset Paget disease and frontotemporal dementia (IBMPFD) [MIM:[http://omim.org/entry/167320 167320]]; also known as muscular dystrophy, limb-girdle, with Paget disease of bone or pagetoid amyotrophic lateral sclerosis or pagetoid neuroskeletal syndrome or lower motor neuron degeneration with Paget-like bone disease. IBMPFD features adult-onset proximal and distal muscle weakness (clinically resembling limb girdle muscular dystrophy), early-onset Paget disease of bone in most cases and premature frontotemporal dementia.<ref>PMID:20512113</ref><ref>PMID:15034582</ref><ref>PMID:15732117</ref><ref>PMID:16247064</ref><ref>PMID:16321991</ref> Defects in VCP are the cause of amyotrophic lateral sclerosis type 14 with or without frontotemporal dementia (ALS14) [MIM:[http://omim.org/entry/613954 613954]]. ALS14 is a neurodegenerative disorder affecting upper motor neurons in the brain and lower motor neurons in the brain stem and spinal cord, resulting in fatal paralysis. Sensory abnormalities are absent. The pathologic hallmarks of the disease include pallor of the corticospinal tract due to loss of motor neurons, presence of ubiquitin-positive inclusions within surviving motor neurons, and deposition of pathologic aggregates. The etiology of amyotrophic lateral sclerosis is likely to be multifactorial, involving both genetic and environmental factors. The disease is inherited in 5-10% of the cases. Patients with ALS14 may develop frontotemporal dementia.<ref>PMID:21145000</ref>
		+
		+	==Function==
		+	[[http://www.uniprot.org/uniprot/TERA_HUMAN TERA_HUMAN]] Necessary for the fragmentation of Golgi stacks during mitosis and for their reassembly after mitosis. Involved in the formation of the transitional endoplasmic reticulum (tER). The transfer of membranes from the endoplasmic reticulum to the Golgi apparatus occurs via 50-70 nm transition vesicles which derive from part-rough, part-smooth transitional elements of the endoplasmic reticulum (tER). Vesicle budding from the tER is an ATP-dependent process. The ternary complex containing UFD1L, VCP and NPLOC4 binds ubiquitinated proteins and is necessary for the export of misfolded proteins from the ER to the cytoplasm, where they are degraded by the proteasome. The NPLOC4-UFD1L-VCP complex regulates spindle disassembly at the end of mitosis and is necessary for the formation of a closed nuclear envelope. Regulates E3 ubiquitin-protein ligase activity of RNF19A (By similarity). Component of the VCP/p97-AMFR/gp78 complex that participates in the final step of the sterol-mediated ubiquitination and endoplasmic reticulum-associated degradation (ERAD) of HMGCR. Also involved in DNA damage response: recruited to double-strand breaks (DSBs) sites in a RNF8- and RNF168-dependent manner and promotes the recruitment of TP53BP1 at DNA damage sites. Recruited to stalled replication forks by SPRTN: may act by mediating extraction of DNA polymerase eta (POLH) to prevent excessive translesion DNA synthesis and limit the incidence of mutations induced by DNA damage.<ref>PMID:15456787</ref><ref>PMID:16168377</ref><ref>PMID:22020440</ref><ref>PMID:22120668</ref><ref>PMID:22607976</ref><ref>PMID:23042607</ref><ref>PMID:23042605</ref> [[http://www.uniprot.org/uniprot/FAF1_HUMAN FAF1_HUMAN]] Potentiates but cannot initiate FAS-induced apoptosis.

	==About this Structure==		==About this Structure==
	[[3qwz]] is a 2 chain structure with sequence from [http://en.wikipedia.org/wiki/Homo_sapiens Homo sapiens]. Full crystallographic information is available from [http://oca.weizmann.ac.il/oca-bin/ocashort?id=3QWZ OCA].		[[3qwz]] is a 2 chain structure with sequence from [http://en.wikipedia.org/wiki/Homo_sapiens Homo sapiens]. Full crystallographic information is available from [http://oca.weizmann.ac.il/oca-bin/ocashort?id=3QWZ OCA].
		+
		+	==See Also==
		+	*[[ATPase\|ATPase]]
		+
		+	==Reference==
		+	<references group="xtra"/><references/>
	[[Category: Homo sapiens]]		[[Category: Homo sapiens]]
	[[Category: Jeon, H.]]		[[Category: Jeon, H.]]

OCA at 09:18, 9 May 2012

OCA — Wed, 09 May 2012 09:18:41 GMT

←Older revision		Revision as of 09:18, 9 May 2012
Line 1:		Line 1:
-	~~'''Unreleased structure'''~~	+	[[Image:3qwz.jpg\|left\|200px]]

-	The ~~entry 3qwz~~ is ~~ON HOLD~~ ~~until Paper Publication~~	+	<!--
		+	The line below this paragraph, containing "STRUCTURE_3qwz", creates the "Structure Box" on the page.
		+	You may change the PDB parameter (which sets the PDB file loaded into the applet)
		+	or the SCENE parameter (which sets the initial scene displayed when the page is loaded),
		+	or leave the SCENE parameter empty for the default display.
		+	-->
		+	{{STRUCTURE_3qwz\| PDB=3qwz \| SCENE= }}

-	~~Authors: Park, J.K., Jeon, H., Lee, J.J., Kim, K.H., Lee, K.J., Kim, E.E.~~	+	===Crystal structure of FAF1 UBX-p97N-domain complex===

-	~~Description: Crystal~~ structure ~~of FAF1 UBX~~-~~p97N-domain complex~~	+
		+	==About this Structure==
		+	[[3qwz]] is a 2 chain structure with sequence from [http://en.wikipedia.org/wiki/Homo_sapiens Homo sapiens]. Full crystallographic information is available from [http://oca.weizmann.ac.il/oca-bin/ocashort?id=3QWZ OCA].
		+	[[Category: Homo sapiens]]
		+	[[Category: Jeon, H.]]
		+	[[Category: Kim, E E.]]
		+	[[Category: Kim, K H.]]
		+	[[Category: Lee, J J.]]
		+	[[Category: Lee, K J.]]
		+	[[Category: Park, J K.]]
		+	[[Category: P97 binding]]
		+	[[Category: Transport protein]]
		+	[[Category: Ubx]]

OCA at 05:19, 1 June 2011

OCA — Wed, 01 Jun 2011 05:19:00 GMT

←Older revision		Revision as of 05:19, 1 June 2011
Line 1:		Line 1:
	'''Unreleased structure'''		'''Unreleased structure'''

-	The entry 3qwz is ON HOLD	+	The entry 3qwz is ON HOLD until Paper Publication

	Authors: Park, J.K., Jeon, H., Lee, J.J., Kim, K.H., Lee, K.J., Kim, E.E.		Authors: Park, J.K., Jeon, H., Lee, J.J., Kim, K.H., Lee, K.J., Kim, E.E.

	Description: Crystal structure of FAF1 UBX-p97N-domain complex		Description: Crystal structure of FAF1 UBX-p97N-domain complex

OCA: Protected "3qwz" [edit=sysop:move=sysop]

OCA — Wed, 09 Mar 2011 06:09:34 GMT

Protected "3qwz" [edit=sysop:move=sysop]

←Older revision

Revision as of 06:09, 9 March 2011

OCA: New page: '''Unreleased structure''' The entry 3qwz is ON HOLD Authors: Park, J.K., Jeon, H., Lee, J.J., Kim, K.H., Lee, K.J., Kim, E.E. Description: Crystal structure of FAF1 UBX-p97N-domain co...

OCA — Wed, 09 Mar 2011 06:09:33 GMT

New page: '''Unreleased structure''' The entry 3qwz is ON HOLD Authors: Park, J.K., Jeon, H., Lee, J.J., Kim, K.H., Lee, K.J., Kim, E.E. Description: Crystal structure of FAF1 UBX-p97N-domain co...

New page

'''Unreleased structure'''

The entry 3qwz is ON HOLD

Authors: Park, J.K., Jeon, H., Lee, J.J., Kim, K.H., Lee, K.J., Kim, E.E.

Description: Crystal structure of FAF1 UBX-p97N-domain complex