2yhy - Revision history

OCA at 10:52, 20 December 2023

OCA — Wed, 20 Dec 2023 10:52:57 GMT

←Older revision		Revision as of 10:52, 20 December 2023
Line 3:		Line 3:
	<StructureSection load='2yhy' size='340' side='right'caption='[[2yhy]], [[Resolution\|resolution]] 1.82Å' scene=''>		<StructureSection load='2yhy' size='340' side='right'caption='[[2yhy]], [[Resolution\|resolution]] 1.82Å' scene=''>
	== Structural highlights ==		== Structural highlights ==
-	<table><tr><td colspan='2'>[[2yhy]] is a 1 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=2YHY OCA]. For a <b>guided tour on the structure components</b> use [https://proteopedia.org/fgij/fg.htm?mol=2YHY FirstGlance]. <br>	+	<table><tr><td colspan='2'>[[2yhy]] 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=2YHY OCA]. For a <b>guided tour on the structure components</b> use [https://proteopedia.org/fgij/fg.htm?mol=2YHY FirstGlance]. <br>
-	</td></tr><tr id='ligand'><td class="sblockLbl"><b>[[Ligand\|Ligands:]]</b></td><td class="sblockDat" id="ligandDat"><scene name='pdbligand=2PE:NONAETHYLENE+GLYCOL'>2PE</scene>, <scene name='pdbligand=ADP:ADENOSINE-5-DIPHOSPHATE'>ADP</scene>, <scene name='pdbligand=BM3:2-(ACETYLAMINO)-2-DEOXY-ALPHA-D-MANNOPYRANOSE'>BM3</scene>, <scene name='pdbligand=CA:CALCIUM+ION'>CA</scene>, <scene name='pdbligand=CL:CHLORIDE+ION'>CL</scene>, <scene name='pdbligand=EDO:1,2-ETHANEDIOL'>EDO</scene>, <scene name='pdbligand=MG:MAGNESIUM+ION'>MG</scene>, <scene name='pdbligand=PG4:TETRAETHYLENE+GLYCOL'>PG4</scene>, <scene name='pdbligand=PGE:TRIETHYLENE+GLYCOL'>PGE</scene>, <scene name='pdbligand=ZN:ZINC+ION'>ZN</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]] 1.82Å</td></tr>
-	~~<tr id='related'><td class="sblockLbl"><b>[[Related_structure\|Related:]]</b></td><td class="sblockDat"><div style='overflow: auto; max-height: 3em;'>[[2yi1\|2yi1]], [[2yhw\|2yhw]]</div></td></tr>~~	+	<tr id='ligand'><td class="sblockLbl"><b>[[Ligand\|Ligands:]]</b></td><td class="sblockDat" id="ligandDat"><scene name='pdbligand=2PE:NONAETHYLENE+GLYCOL'>2PE</scene>, <scene name='pdbligand=ADP:ADENOSINE-5-DIPHOSPHATE'>ADP</scene>, <scene name='pdbligand=BM3:2-(ACETYLAMINO)-2-DEOXY-ALPHA-D-MANNOPYRANOSE'>BM3</scene>, <scene name='pdbligand=CA:CALCIUM+ION'>CA</scene>, <scene name='pdbligand=CL:CHLORIDE+ION'>CL</scene>, <scene name='pdbligand=EDO:1,2-ETHANEDIOL'>EDO</scene>, <scene name='pdbligand=MG:MAGNESIUM+ION'>MG</scene>, <scene name='pdbligand=PG4:TETRAETHYLENE+GLYCOL'>PG4</scene>, <scene name='pdbligand=PGE:TRIETHYLENE+GLYCOL'>PGE</scene>, <scene name='pdbligand=ZN:ZINC+ION'>ZN</scene></td></tr>
-	<tr id='activity'><td class="sblockLbl"><b>Activity:</b></td><td class="sblockDat"><span class='plainlinks'>[https://en.wikipedia.org/wiki/N-acylmannosamine_kinase N-acylmannosamine kinase], with EC number [https://www.brenda-enzymes.info/php/result_flat.php4?ecno=2.7.1.60 2.7.1.60] </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=2yhy FirstGlance], [http://oca.weizmann.ac.il/oca-bin/ocaids?id=2yhy OCA], [https://pdbe.org/2yhy PDBe], [https://www.rcsb.org/pdb/explore.do?structureId=2yhy RCSB], [https://www.ebi.ac.uk/pdbsum/2yhy PDBsum], [https://prosat.h-its.org/prosat/prosatexe?pdbcode=2yhy 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=2yhy FirstGlance], [http://oca.weizmann.ac.il/oca-bin/ocaids?id=2yhy OCA], [https://pdbe.org/2yhy PDBe], [https://www.rcsb.org/pdb/explore.do?structureId=2yhy RCSB], [https://www.ebi.ac.uk/pdbsum/2yhy PDBsum], [https://prosat.h-its.org/prosat/prosatexe?pdbcode=2yhy ProSAT]</span></td></tr>
	</table>		</table>
	== Disease ==		== Disease ==
-	[[https://www.uniprot.org/uniprot/GLCNE_HUMAN GLCNE_HUMAN]] Defects in GNE are a cause of sialuria (SIALURIA) [MIM:[https://omim.org/entry/269921 269921]]; also known as sialuria French type. In sialuria, free sialic acid accumulates in the cytoplasm and gram quantities of neuraminic acid are secreted in the urine. The metabolic defect involves lack of feedback inhibition of UDP-GlcNAc 2-epimerase by CMP-Neu5Ac, resulting in constitutive overproduction of free Neu5Ac. Clinical features include variable degrees of developmental delay, coarse facial features and hepatomegaly. Sialuria inheritance is autosomal dominant.<ref>PMID:2808337</ref> <ref>PMID:10330343</ref> <ref>PMID:10356312</ref> <ref>PMID:11326336</ref> Defects in GNE are the cause of inclusion body myopathy type 2 (IBM2) [MIM:[https://omim.org/entry/600737 600737]]. Hereditary inclusion body myopathies are a group of neuromuscular disorders characterized by adult onset, slowly progressive distal and proximal weakness and a typical muscle pathology including rimmed vacuoles and filamentous inclusions. IBM2 is an autosomal recessive disorder affecting mainly leg muscles, but with an unusual distribution that spares the quadriceps as also observed in Nonaka myopathy.<ref>PMID:11528398</ref> <ref>PMID:12409274</ref> <ref>PMID:12473769</ref> <ref>PMID:12473780</ref> <ref>PMID:12497639</ref> <ref>PMID:12811782</ref> <ref>PMID:15146476</ref> Defects in GNE are the cause of Nonaka myopathy (NM) [MIM:[https://omim.org/entry/605820 605820]]; also known as distal myopathy with rimmed vacuoles (DMRV). NM is an autosomal recessive muscular disorder, allelic to inclusion body myopathy 2. It is characterized by weakness of the anterior compartment of the lower limbs with onset in early adulthood, and sparing of the quadriceps muscles. As the inclusion body myopathy, NM is histologically characterized by the presence of numerous rimmed vacuoles without inflammatory changes in muscle specimens.<ref>PMID:12325084</ref> <ref>PMID:11916006</ref> <ref>PMID:12177386</ref> <ref>PMID:12473753</ref> <ref>PMID:12913203</ref>	+	[https://www.uniprot.org/uniprot/GLCNE_HUMAN GLCNE_HUMAN] Defects in GNE are a cause of sialuria (SIALURIA) [MIM:[https://omim.org/entry/269921 269921]; also known as sialuria French type. In sialuria, free sialic acid accumulates in the cytoplasm and gram quantities of neuraminic acid are secreted in the urine. The metabolic defect involves lack of feedback inhibition of UDP-GlcNAc 2-epimerase by CMP-Neu5Ac, resulting in constitutive overproduction of free Neu5Ac. Clinical features include variable degrees of developmental delay, coarse facial features and hepatomegaly. Sialuria inheritance is autosomal dominant.<ref>PMID:2808337</ref> <ref>PMID:10330343</ref> <ref>PMID:10356312</ref> <ref>PMID:11326336</ref> Defects in GNE are the cause of inclusion body myopathy type 2 (IBM2) [MIM:[https://omim.org/entry/600737 600737]. Hereditary inclusion body myopathies are a group of neuromuscular disorders characterized by adult onset, slowly progressive distal and proximal weakness and a typical muscle pathology including rimmed vacuoles and filamentous inclusions. IBM2 is an autosomal recessive disorder affecting mainly leg muscles, but with an unusual distribution that spares the quadriceps as also observed in Nonaka myopathy.<ref>PMID:11528398</ref> <ref>PMID:12409274</ref> <ref>PMID:12473769</ref> <ref>PMID:12473780</ref> <ref>PMID:12497639</ref> <ref>PMID:12811782</ref> <ref>PMID:15146476</ref> Defects in GNE are the cause of Nonaka myopathy (NM) [MIM:[https://omim.org/entry/605820 605820]; also known as distal myopathy with rimmed vacuoles (DMRV). NM is an autosomal recessive muscular disorder, allelic to inclusion body myopathy 2. It is characterized by weakness of the anterior compartment of the lower limbs with onset in early adulthood, and sparing of the quadriceps muscles. As the inclusion body myopathy, NM is histologically characterized by the presence of numerous rimmed vacuoles without inflammatory changes in muscle specimens.<ref>PMID:12325084</ref> <ref>PMID:11916006</ref> <ref>PMID:12177386</ref> <ref>PMID:12473753</ref> <ref>PMID:12913203</ref>
	== Function ==		== Function ==
-	[[https://www.uniprot.org/uniprot/GLCNE_HUMAN GLCNE_HUMAN]] Regulates and initiates biosynthesis of N-acetylneuraminic acid (NeuAc), a precursor of sialic acids. Plays an essential role in early development (By similarity). Required for normal sialylation in hematopoietic cells. Sialylation is implicated in cell adhesion, signal transduction, tumorigenicity and metastatic behavior of malignant cells.<ref>PMID:10334995</ref>	+	[https://www.uniprot.org/uniprot/GLCNE_HUMAN GLCNE_HUMAN] Regulates and initiates biosynthesis of N-acetylneuraminic acid (NeuAc), a precursor of sialic acids. Plays an essential role in early development (By similarity). Required for normal sialylation in hematopoietic cells. Sialylation is implicated in cell adhesion, signal transduction, tumorigenicity and metastatic behavior of malignant cells.<ref>PMID:10334995</ref>
	<div style="background-color:#fffaf0;">		<div style="background-color:#fffaf0;">
	== Publication Abstract from PubMed ==		== Publication Abstract from PubMed ==
Line 26:		Line 25:
	__TOC__		__TOC__
	</StructureSection>		</StructureSection>
-	[[Category: ~~Human~~]]	+	[[Category: Homo sapiens]]
	[[Category: Large Structures]]		[[Category: Large Structures]]
-	~~[[Category: N-acylmannosamine kinase]]~~	+	[[Category: Fan H]]
-	[[Category: Fan, H]]	+	[[Category: Hinderlich S]]
-	[[Category: Hinderlich, S]]	+	[[Category: Martinez J]]
-	[[Category: Martinez, J]]	+	[[Category: Moniot S]]
-	[[Category: Moniot, S]]	+	[[Category: Nguyen LD]]
-	[[Category: Nguyen~~, L D~~]]	+	[[Category: Reutter W]]
-	[[Category: Reutter, W]]	+	[[Category: Saenger W]]
-	[[Category: Saenger, W]]	+	[[Category: Tauberger E]]
-	[[Category: Tauberger, E]]	+
-	~~[[Category: Rok family]]~~	+
-	~~[[Category: Sialic acid]]~~	+
-	~~[[Category: Sugar kinase]]~~	+
-	~~[[Category: Transferase~~]]	+

OCA at 12:30, 27 April 2022

OCA — Wed, 27 Apr 2022 12:30:24 GMT

OCA at 12:51, 22 July 2020

OCA — Wed, 22 Jul 2020 12:51:49 GMT

←Older revision		Revision as of 12:51, 22 July 2020
Line 1:		Line 1:

	==Structure of N-Acetylmannosamine kinase in complex with N- acetylmannosamine and ADP==		==Structure of N-Acetylmannosamine kinase in complex with N- acetylmannosamine and ADP==
-	<StructureSection load='2yhy' size='340' side='right' caption='[[2yhy]], [[Resolution\|resolution]] 1.82Å' scene=''>	+	<StructureSection load='2yhy' size='340' side='right'caption='[[2yhy]], [[Resolution\|resolution]] 1.82Å' scene=''>
	== Structural highlights ==		== Structural highlights ==
-	<table><tr><td colspan='2'>[[2yhy]] 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=2YHY OCA]. For a <b>guided tour on the structure components</b> use [http://~~oca~~.~~weizmann.ac.il/oca-docs~~/fgij/fg.htm?mol=2YHY FirstGlance]. <br>	+	<table><tr><td colspan='2'>[[2yhy]] 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=2YHY OCA]. For a <b>guided tour on the structure components</b> use [http://proteopedia.org/fgij/fg.htm?mol=2YHY FirstGlance]. <br>
-	</td></tr><tr id='ligand'><td class="sblockLbl"><b>[[Ligand\|Ligands:]]</b></td><td class="sblockDat"><scene name='pdbligand=2PE:NONAETHYLENE+GLYCOL'>2PE</scene>, <scene name='pdbligand=ADP:ADENOSINE-5-DIPHOSPHATE'>ADP</scene>, <scene name='pdbligand=BM3:2-(ACETYLAMINO)-2-DEOXY-ALPHA-D-MANNOPYRANOSE'>BM3</scene>, <scene name='pdbligand=CA:CALCIUM+ION'>CA</scene>, <scene name='pdbligand=CL:CHLORIDE+ION'>CL</scene>, <scene name='pdbligand=EDO:1,2-ETHANEDIOL'>EDO</scene>, <scene name='pdbligand=MG:MAGNESIUM+ION'>MG</scene>, <scene name='pdbligand=PG4:TETRAETHYLENE+GLYCOL'>PG4</scene>, <scene name='pdbligand=PGE:TRIETHYLENE+GLYCOL'>PGE</scene>, <scene name='pdbligand=ZN:ZINC+ION'>ZN</scene></td></tr>	+	</td></tr><tr id='ligand'><td class="sblockLbl"><b>[[Ligand\|Ligands:]]</b></td><td class="sblockDat" id="ligandDat"><scene name='pdbligand=2PE:NONAETHYLENE+GLYCOL'>2PE</scene>, <scene name='pdbligand=ADP:ADENOSINE-5-DIPHOSPHATE'>ADP</scene>, <scene name='pdbligand=BM3:2-(ACETYLAMINO)-2-DEOXY-ALPHA-D-MANNOPYRANOSE'>BM3</scene>, <scene name='pdbligand=CA:CALCIUM+ION'>CA</scene>, <scene name='pdbligand=CL:CHLORIDE+ION'>CL</scene>, <scene name='pdbligand=EDO:1,2-ETHANEDIOL'>EDO</scene>, <scene name='pdbligand=MG:MAGNESIUM+ION'>MG</scene>, <scene name='pdbligand=PG4:TETRAETHYLENE+GLYCOL'>PG4</scene>, <scene name='pdbligand=PGE:TRIETHYLENE+GLYCOL'>PGE</scene>, <scene name='pdbligand=ZN:ZINC+ION'>ZN</scene></td></tr>
	<tr id='related'><td class="sblockLbl"><b>[[Related_structure\|Related:]]</b></td><td class="sblockDat">[[2yi1\|2yi1]], [[2yhw\|2yhw]]</td></tr>		<tr id='related'><td class="sblockLbl"><b>[[Related_structure\|Related:]]</b></td><td class="sblockDat">[[2yi1\|2yi1]], [[2yhw\|2yhw]]</td></tr>
	<tr id='activity'><td class="sblockLbl"><b>Activity:</b></td><td class="sblockDat"><span class='plainlinks'>[http://en.wikipedia.org/wiki/N-acylmannosamine_kinase N-acylmannosamine kinase], with EC number [http://www.brenda-enzymes.info/php/result_flat.php4?ecno=2.7.1.60 2.7.1.60] </span></td></tr>		<tr id='activity'><td class="sblockLbl"><b>Activity:</b></td><td class="sblockDat"><span class='plainlinks'>[http://en.wikipedia.org/wiki/N-acylmannosamine_kinase N-acylmannosamine kinase], with EC number [http://www.brenda-enzymes.info/php/result_flat.php4?ecno=2.7.1.60 2.7.1.60] </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=2yhy FirstGlance], [http://oca.weizmann.ac.il/oca-bin/ocaids?id=2yhy OCA], [http://pdbe.org/2yhy PDBe], [http://www.rcsb.org/pdb/explore.do?structureId=2yhy RCSB], [http://www.ebi.ac.uk/pdbsum/2yhy PDBsum], [http://prosat.h-its.org/prosat/prosatexe?pdbcode=2yhy ProSAT]</span></td></tr>	+	<tr id='resources'><td class="sblockLbl"><b>Resources:</b></td><td class="sblockDat"><span class='plainlinks'>[http://proteopedia.org/fgij/fg.htm?mol=2yhy FirstGlance], [http://oca.weizmann.ac.il/oca-bin/ocaids?id=2yhy OCA], [http://pdbe.org/2yhy PDBe], [http://www.rcsb.org/pdb/explore.do?structureId=2yhy RCSB], [http://www.ebi.ac.uk/pdbsum/2yhy PDBsum], [http://prosat.h-its.org/prosat/prosatexe?pdbcode=2yhy ProSAT]</span></td></tr>
	</table>		</table>
	== Disease ==		== Disease ==
Line 27:		Line 27:
	</StructureSection>		</StructureSection>
	[[Category: Human]]		[[Category: Human]]
		+	[[Category: Large Structures]]
	[[Category: N-acylmannosamine kinase]]		[[Category: N-acylmannosamine kinase]]
	[[Category: Fan, H]]		[[Category: Fan, H]]

OCA at 19:34, 4 August 2016

OCA — Thu, 04 Aug 2016 19:34:05 GMT

←Older revision		Revision as of 19:34, 4 August 2016
Line 1:		Line 1:
		+
	==Structure of N-Acetylmannosamine kinase in complex with N- acetylmannosamine and ADP==		==Structure of N-Acetylmannosamine kinase in complex with N- acetylmannosamine and ADP==
	<StructureSection load='2yhy' size='340' side='right' caption='[[2yhy]], [[Resolution\|resolution]] 1.82Å' scene=''>		<StructureSection load='2yhy' size='340' side='right' caption='[[2yhy]], [[Resolution\|resolution]] 1.82Å' scene=''>
	== Structural highlights ==		== Structural highlights ==
-	<table><tr><td colspan='2'>[[2yhy]] is a 1 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=2YHY OCA]. For a <b>guided tour on the structure components</b> use [http://oca.weizmann.ac.il/oca-docs/fgij/fg.htm?mol=2YHY FirstGlance]. <br>	+	<table><tr><td colspan='2'>[[2yhy]] 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=2YHY OCA]. For a <b>guided tour on the structure components</b> use [http://oca.weizmann.ac.il/oca-docs/fgij/fg.htm?mol=2YHY FirstGlance]. <br>
	</td></tr><tr id='ligand'><td class="sblockLbl"><b>[[Ligand\|Ligands:]]</b></td><td class="sblockDat"><scene name='pdbligand=2PE:NONAETHYLENE+GLYCOL'>2PE</scene>, <scene name='pdbligand=ADP:ADENOSINE-5-DIPHOSPHATE'>ADP</scene>, <scene name='pdbligand=BM3:2-(ACETYLAMINO)-2-DEOXY-ALPHA-D-MANNOPYRANOSE'>BM3</scene>, <scene name='pdbligand=CA:CALCIUM+ION'>CA</scene>, <scene name='pdbligand=CL:CHLORIDE+ION'>CL</scene>, <scene name='pdbligand=EDO:1,2-ETHANEDIOL'>EDO</scene>, <scene name='pdbligand=MG:MAGNESIUM+ION'>MG</scene>, <scene name='pdbligand=PG4:TETRAETHYLENE+GLYCOL'>PG4</scene>, <scene name='pdbligand=PGE:TRIETHYLENE+GLYCOL'>PGE</scene>, <scene name='pdbligand=ZN:ZINC+ION'>ZN</scene></td></tr>		</td></tr><tr id='ligand'><td class="sblockLbl"><b>[[Ligand\|Ligands:]]</b></td><td class="sblockDat"><scene name='pdbligand=2PE:NONAETHYLENE+GLYCOL'>2PE</scene>, <scene name='pdbligand=ADP:ADENOSINE-5-DIPHOSPHATE'>ADP</scene>, <scene name='pdbligand=BM3:2-(ACETYLAMINO)-2-DEOXY-ALPHA-D-MANNOPYRANOSE'>BM3</scene>, <scene name='pdbligand=CA:CALCIUM+ION'>CA</scene>, <scene name='pdbligand=CL:CHLORIDE+ION'>CL</scene>, <scene name='pdbligand=EDO:1,2-ETHANEDIOL'>EDO</scene>, <scene name='pdbligand=MG:MAGNESIUM+ION'>MG</scene>, <scene name='pdbligand=PG4:TETRAETHYLENE+GLYCOL'>PG4</scene>, <scene name='pdbligand=PGE:TRIETHYLENE+GLYCOL'>PGE</scene>, <scene name='pdbligand=ZN:ZINC+ION'>ZN</scene></td></tr>
	<tr id='related'><td class="sblockLbl"><b>[[Related_structure\|Related:]]</b></td><td class="sblockDat">[[2yi1\|2yi1]], [[2yhw\|2yhw]]</td></tr>		<tr id='related'><td class="sblockLbl"><b>[[Related_structure\|Related:]]</b></td><td class="sblockDat">[[2yi1\|2yi1]], [[2yhw\|2yhw]]</td></tr>
	<tr id='activity'><td class="sblockLbl"><b>Activity:</b></td><td class="sblockDat"><span class='plainlinks'>[http://en.wikipedia.org/wiki/N-acylmannosamine_kinase N-acylmannosamine kinase], with EC number [http://www.brenda-enzymes.info/php/result_flat.php4?ecno=2.7.1.60 2.7.1.60] </span></td></tr>		<tr id='activity'><td class="sblockLbl"><b>Activity:</b></td><td class="sblockDat"><span class='plainlinks'>[http://en.wikipedia.org/wiki/N-acylmannosamine_kinase N-acylmannosamine kinase], with EC number [http://www.brenda-enzymes.info/php/result_flat.php4?ecno=2.7.1.60 2.7.1.60] </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=2yhy FirstGlance], [http://oca.weizmann.ac.il/oca-bin/ocaids?id=2yhy OCA], [http://www.rcsb.org/pdb/explore.do?structureId=2yhy RCSB], [http://www.ebi.ac.uk/pdbsum/2yhy 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=2yhy FirstGlance], [http://oca.weizmann.ac.il/oca-bin/ocaids?id=2yhy OCA], [http://pdbe.org/2yhy PDBe], [http://www.rcsb.org/pdb/explore.do?structureId=2yhy RCSB], [http://www.ebi.ac.uk/pdbsum/2yhy PDBsum], [http://prosat.h-its.org/prosat/prosatexe?pdbcode=2yhy ProSAT]</span></td></tr>
	</table>		</table>
	== Disease ==		== Disease ==
Line 20:		Line 21:
	From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine.<br>		From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine.<br>
	</div>		</div>
		+	<div class="pdbe-citations 2yhy" style="background-color:#fffaf0;"></div>
	== References ==		== References ==
	<references/>		<references/>
	__TOC__		__TOC__
	</StructureSection>		</StructureSection>
-	[[Category: ~~Homo sapiens~~]]	+	[[Category: Human]]
	[[Category: N-acylmannosamine kinase]]		[[Category: N-acylmannosamine kinase]]
	[[Category: Fan, H]]		[[Category: Fan, H]]

OCA at 13:53, 18 December 2014

OCA — Thu, 18 Dec 2014 13:53:23 GMT

←Older revision		Revision as of 13:53, 18 December 2014
Line 1:		Line 1:
-	~~{{STRUCTURE_2yhy~~\| ~~PDB~~=2yhy \| ~~SCENE~~= }}	+	==Structure of N-Acetylmannosamine kinase in complex with N- acetylmannosamine and ADP==
-	===~~Structure of~~ N-~~Acetylmannosamine~~ kinase in ~~complex~~ with N- ~~acetylmannosamine~~ and ~~ADP~~===	+	<StructureSection load='2yhy' size='340' side='right' caption='[[2yhy]], [[Resolution\|resolution]] 1.82Å' scene=''>
-	~~{{ABSTRACT_PUBMED_22343627}}~~	+	== Structural highlights ==
		+	<table><tr><td colspan='2'>[[2yhy]] is a 1 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=2YHY OCA]. For a <b>guided tour on the structure components</b> use [http://oca.weizmann.ac.il/oca-docs/fgij/fg.htm?mol=2YHY FirstGlance]. <br>
		+	</td></tr><tr id='ligand'><td class="sblockLbl"><b>[[Ligand\|Ligands:]]</b></td><td class="sblockDat"><scene name='pdbligand=2PE:NONAETHYLENE+GLYCOL'>2PE</scene>, <scene name='pdbligand=ADP:ADENOSINE-5-DIPHOSPHATE'>ADP</scene>, <scene name='pdbligand=BM3:2-(ACETYLAMINO)-2-DEOXY-ALPHA-D-MANNOPYRANOSE'>BM3</scene>, <scene name='pdbligand=CA:CALCIUM+ION'>CA</scene>, <scene name='pdbligand=CL:CHLORIDE+ION'>CL</scene>, <scene name='pdbligand=EDO:1,2-ETHANEDIOL'>EDO</scene>, <scene name='pdbligand=MG:MAGNESIUM+ION'>MG</scene>, <scene name='pdbligand=PG4:TETRAETHYLENE+GLYCOL'>PG4</scene>, <scene name='pdbligand=PGE:TRIETHYLENE+GLYCOL'>PGE</scene>, <scene name='pdbligand=ZN:ZINC+ION'>ZN</scene></td></tr>
		+	<tr id='related'><td class="sblockLbl"><b>[[Related_structure\|Related:]]</b></td><td class="sblockDat">[[2yi1\|2yi1]], [[2yhw\|2yhw]]</td></tr>
		+	<tr id='activity'><td class="sblockLbl"><b>Activity:</b></td><td class="sblockDat"><span class='plainlinks'>[http://en.wikipedia.org/wiki/N-acylmannosamine_kinase N-acylmannosamine kinase], with EC number [http://www.brenda-enzymes.info/php/result_flat.php4?ecno=2.7.1.60 2.7.1.60] </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=2yhy FirstGlance], [http://oca.weizmann.ac.il/oca-bin/ocaids?id=2yhy OCA], [http://www.rcsb.org/pdb/explore.do?structureId=2yhy RCSB], [http://www.ebi.ac.uk/pdbsum/2yhy PDBsum]</span></td></tr>
		+	</table>
		+	== Disease ==
		+	[[http://www.uniprot.org/uniprot/GLCNE_HUMAN GLCNE_HUMAN]] Defects in GNE are a cause of sialuria (SIALURIA) [MIM:[http://omim.org/entry/269921 269921]]; also known as sialuria French type. In sialuria, free sialic acid accumulates in the cytoplasm and gram quantities of neuraminic acid are secreted in the urine. The metabolic defect involves lack of feedback inhibition of UDP-GlcNAc 2-epimerase by CMP-Neu5Ac, resulting in constitutive overproduction of free Neu5Ac. Clinical features include variable degrees of developmental delay, coarse facial features and hepatomegaly. Sialuria inheritance is autosomal dominant.<ref>PMID:2808337</ref> <ref>PMID:10330343</ref> <ref>PMID:10356312</ref> <ref>PMID:11326336</ref> Defects in GNE are the cause of inclusion body myopathy type 2 (IBM2) [MIM:[http://omim.org/entry/600737 600737]]. Hereditary inclusion body myopathies are a group of neuromuscular disorders characterized by adult onset, slowly progressive distal and proximal weakness and a typical muscle pathology including rimmed vacuoles and filamentous inclusions. IBM2 is an autosomal recessive disorder affecting mainly leg muscles, but with an unusual distribution that spares the quadriceps as also observed in Nonaka myopathy.<ref>PMID:11528398</ref> <ref>PMID:12409274</ref> <ref>PMID:12473769</ref> <ref>PMID:12473780</ref> <ref>PMID:12497639</ref> <ref>PMID:12811782</ref> <ref>PMID:15146476</ref> Defects in GNE are the cause of Nonaka myopathy (NM) [MIM:[http://omim.org/entry/605820 605820]]; also known as distal myopathy with rimmed vacuoles (DMRV). NM is an autosomal recessive muscular disorder, allelic to inclusion body myopathy 2. It is characterized by weakness of the anterior compartment of the lower limbs with onset in early adulthood, and sparing of the quadriceps muscles. As the inclusion body myopathy, NM is histologically characterized by the presence of numerous rimmed vacuoles without inflammatory changes in muscle specimens.<ref>PMID:12325084</ref> <ref>PMID:11916006</ref> <ref>PMID:12177386</ref> <ref>PMID:12473753</ref> <ref>PMID:12913203</ref>
		+	== Function ==
		+	[[http://www.uniprot.org/uniprot/GLCNE_HUMAN GLCNE_HUMAN]] Regulates and initiates biosynthesis of N-acetylneuraminic acid (NeuAc), a precursor of sialic acids. Plays an essential role in early development (By similarity). Required for normal sialylation in hematopoietic cells. Sialylation is implicated in cell adhesion, signal transduction, tumorigenicity and metastatic behavior of malignant cells.<ref>PMID:10334995</ref>
		+	<div style="background-color:#fffaf0;">
		+	== Publication Abstract from PubMed ==
		+	Sialic acids are essential components of membrane glycoconjugates. They are responsible for the interaction, structure, and functionality of all deuterostome cells and have major functions in cellular processes in health and diseases. The key enzyme of the biosynthesis of sialic acid is the bifunctional UDP-N-acetylglucosamine-2-epimerase/N-acetylmannosamine kinase that transforms UDP-N-acetylglucosamine to N-acetylmannosamine (ManNAc) followed by its phosphorylation to ManNAc 6-phosphate and has a direct impact on the sialylation of cell surface components. Here, we present the crystal structures of the human N-acetylmannosamine kinase (MNK) domain of UDP-N-acetylglucosamine-2-epimerase/N-acetylmannosamine kinase in complexes with ManNAc at 1.64 A resolution, MNK.ManNAc.ADP (1.82 A) and MNK.ManNAc 6-phosphate.ADP (2.10 A). Our findings offer detailed insights in the active center of MNK and serve as a structural basis to design inhibitors. We synthesized a novel inhibitor, 6-O-acetyl-ManNAc, which is more potent than those previously tested. Specific inhibitors of sialic acid biosynthesis may serve to further study biological functions of sialic acid.

-	~~==Disease==~~	+	Crystal structures of N-acetylmannosamine kinase provide insights into enzyme activity and inhibition.,Martinez J, Nguyen LD, Hinderlich S, Zimmer R, Tauberger E, Reutter W, Saenger W, Fan H, Moniot S J Biol Chem. 2012 Apr 20;287(17):13656-65. Epub 2012 Feb 16. PMID:22343627<ref>PMID:22343627</ref>
-	~~[[http://www.uniprot.org/uniprot/GLCNE_HUMAN GLCNE_HUMAN]] Defects in GNE are a cause~~ of ~~sialuria (SIALURIA) [MIM:[http://omim.org/entry/269921 269921]]; also known as sialuria French type. In sialuria, free sialic acid accumulates in the cytoplasm~~ and ~~gram quantities of neuraminic acid are secreted in the urine. The metabolic defect involves lack of feedback~~ inhibition ~~of UDP-GlcNAc 2-epimerase by CMP-Neu5Ac, resulting in constitutive overproduction of free Neu5Ac~~. ~~Clinical features include variable degrees of developmental delay~~, coarse facial features and hepatomegaly. Sialuria inheritance is autosomal dominant.<ref>PMID:2808337</ref><ref>PMID:10330343</ref><ref>PMID:10356312</ref><ref>PMID:11326336</ref> Defects in GNE are the cause of inclusion body myopathy type 2 (IBM2) [MIM:[http://omim.org/entry/600737 600737]]. Hereditary inclusion body myopathies are a group of neuromuscular disorders characterized by adult onset, slowly progressive distal and proximal weakness and a typical muscle pathology including rimmed vacuoles and filamentous inclusions. IBM2 is an autosomal recessive disorder affecting mainly leg muscles, ~~but with an unusual distribution that spares the quadriceps as also observed in Nonaka myopathy~~.<ref>PMID:11528398</ref><ref>PMID:12409274</ref><ref>PMID:12473769</ref><ref>PMID:12473780</ref><ref>PMID:12497639</ref><ref>PMID:12811782</ref><ref>PMID:15146476</ref> Defects in GNE are the cause of Nonaka myopathy (NM) ~~[MIM~~:~~[http://omim~~.~~org/entry/605820 605820]]; also known as distal myopathy with rimmed vacuoles (DMRV)~~. NM is an autosomal recessive muscular disorder, allelic to inclusion body myopathy 2. It is characterized by weakness of the anterior compartment of the lower limbs with onset in early adulthood, and sparing of the quadriceps muscles. As the inclusion body myopathy, NM is histologically characterized by the presence of numerous rimmed vacuoles without inflammatory changes in muscle specimens.<ref>PMID:~~12325084</ref><ref>PMID:11916006</ref><ref>PMID:12177386</ref><ref>PMID:12473753</ref>~~<ref>PMID:~~12913203~~</ref>	+

-	~~==Function==~~	+	From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine.<br>
-	~~[[http:~~/~~/www.uniprot.org/uniprot/GLCNE_HUMAN GLCNE_HUMAN]] Regulates and initiates biosynthesis of N-acetylneuraminic acid (NeuAc)~~, a ~~precursor~~ of ~~sialic acids~~. ~~Plays an essential role in early development (By similarity)~~. ~~Required for normal sialylation in hematopoietic cells. Sialylation is implicated in cell adhesion, signal transduction, tumorigenicity and metastatic behavior~~ of ~~malignant cells~~.<~~ref~~>~~PMID:10334995~~</~~ref~~>	+	</div>
-		+	== References ==
-	==~~About this Structure==~~	+	<references/>
-	[[2yhy]] is a 1 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=2YHY OCA].	+	__TOC__
-		+	</StructureSection>
-	~~==Reference~~==	+
-	~~<ref group="xtra">PMID:022343627</ref>~~<references ~~group="xtra"~~/><~~references~~/>	+
	[[Category: Homo sapiens]]		[[Category: Homo sapiens]]
	[[Category: N-acylmannosamine kinase]]		[[Category: N-acylmannosamine kinase]]
-	[[Category: Fan, H.]]	+	[[Category: Fan, H]]
-	[[Category: Hinderlich, S.]]	+	[[Category: Hinderlich, S]]
-	[[Category: Martinez, J.]]	+	[[Category: Martinez, J]]
-	[[Category: Moniot, S.]]	+	[[Category: Moniot, S]]
-	[[Category: Nguyen, L D.]]	+	[[Category: Nguyen, L D]]
-	[[Category: Reutter, W.]]	+	[[Category: Reutter, W]]
-	[[Category: Saenger, W.]]	+	[[Category: Saenger, W]]
-	[[Category: Tauberger, E.]]	+	[[Category: Tauberger, E]]
	[[Category: Rok family]]		[[Category: Rok family]]
	[[Category: Sialic acid]]		[[Category: Sialic acid]]
	[[Category: Sugar kinase]]		[[Category: Sugar kinase]]
	[[Category: Transferase]]		[[Category: Transferase]]

OCA at 01:29, 25 March 2013

OCA — Mon, 25 Mar 2013 01:29:25 GMT

←Older revision		Revision as of 01:29, 25 March 2013
Line 1:		Line 1:
-	[[Image:2yhy.png\|left\|200px]]
-
-	<!--
-	The line below this paragraph, containing "STRUCTURE_2yhy", 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_2yhy\| PDB=2yhy \| SCENE= }}		{{STRUCTURE_2yhy\| PDB=2yhy \| SCENE= }}
-
	===Structure of N-Acetylmannosamine kinase in complex with N- acetylmannosamine and ADP===		===Structure of N-Acetylmannosamine kinase in complex with N- acetylmannosamine and ADP===
		+	{{ABSTRACT_PUBMED_22343627}}

		+	==Disease==
		+	[[http://www.uniprot.org/uniprot/GLCNE_HUMAN GLCNE_HUMAN]] Defects in GNE are a cause of sialuria (SIALURIA) [MIM:[http://omim.org/entry/269921 269921]]; also known as sialuria French type. In sialuria, free sialic acid accumulates in the cytoplasm and gram quantities of neuraminic acid are secreted in the urine. The metabolic defect involves lack of feedback inhibition of UDP-GlcNAc 2-epimerase by CMP-Neu5Ac, resulting in constitutive overproduction of free Neu5Ac. Clinical features include variable degrees of developmental delay, coarse facial features and hepatomegaly. Sialuria inheritance is autosomal dominant.<ref>PMID:2808337</ref><ref>PMID:10330343</ref><ref>PMID:10356312</ref><ref>PMID:11326336</ref> Defects in GNE are the cause of inclusion body myopathy type 2 (IBM2) [MIM:[http://omim.org/entry/600737 600737]]. Hereditary inclusion body myopathies are a group of neuromuscular disorders characterized by adult onset, slowly progressive distal and proximal weakness and a typical muscle pathology including rimmed vacuoles and filamentous inclusions. IBM2 is an autosomal recessive disorder affecting mainly leg muscles, but with an unusual distribution that spares the quadriceps as also observed in Nonaka myopathy.<ref>PMID:11528398</ref><ref>PMID:12409274</ref><ref>PMID:12473769</ref><ref>PMID:12473780</ref><ref>PMID:12497639</ref><ref>PMID:12811782</ref><ref>PMID:15146476</ref> Defects in GNE are the cause of Nonaka myopathy (NM) [MIM:[http://omim.org/entry/605820 605820]]; also known as distal myopathy with rimmed vacuoles (DMRV). NM is an autosomal recessive muscular disorder, allelic to inclusion body myopathy 2. It is characterized by weakness of the anterior compartment of the lower limbs with onset in early adulthood, and sparing of the quadriceps muscles. As the inclusion body myopathy, NM is histologically characterized by the presence of numerous rimmed vacuoles without inflammatory changes in muscle specimens.<ref>PMID:12325084</ref><ref>PMID:11916006</ref><ref>PMID:12177386</ref><ref>PMID:12473753</ref><ref>PMID:12913203</ref>

-	~~<!--~~	+	==Function==
-	~~The line below this paragraph, {{ABSTRACT_PUBMED_22343627}}, adds the Publication Abstract to the page~~	+	[[http://www.uniprot.org/uniprot/GLCNE_HUMAN GLCNE_HUMAN]] Regulates and initiates biosynthesis of N-acetylneuraminic acid (NeuAc), a precursor of sialic acids. Plays an essential role in early development (By similarity). Required for normal sialylation in hematopoietic cells. Sialylation is implicated in cell adhesion, signal transduction, tumorigenicity and metastatic behavior of malignant cells.<ref>PMID:10334995</ref>
-	~~(as it appears on PubMed at~~ http://www.~~pubmed~~.~~gov~~), ~~where 22343627~~ is ~~the PubMed ID number~~.	+
-	-->	+
-	~~{{ABSTRACT_PUBMED_22343627}}~~	+

	==About this Structure==		==About this Structure==
Line 22:		Line 13:

	==Reference==		==Reference==
-	<ref group="xtra">PMID:022343627</ref><references group="xtra"/>	+	<ref group="xtra">PMID:022343627</ref><references group="xtra"/><references/>
	[[Category: Homo sapiens]]		[[Category: Homo sapiens]]
	[[Category: N-acylmannosamine kinase]]		[[Category: N-acylmannosamine kinase]]

OCA at 18:17, 2 May 2012

OCA — Wed, 02 May 2012 18:17:13 GMT

←Older revision		Revision as of 18:17, 2 May 2012
Line 1:		Line 1:
-	[[Image:2yhy.~~jpg~~\|left\|200px]]	+	[[Image:2yhy.png\|left\|200px]]

	<!--		<!--
Line 11:		Line 11:
	===Structure of N-Acetylmannosamine kinase in complex with N- acetylmannosamine and ADP===		===Structure of N-Acetylmannosamine kinase in complex with N- acetylmannosamine and ADP===

		+
		+	<!--
		+	The line below this paragraph, {{ABSTRACT_PUBMED_22343627}}, adds the Publication Abstract to the page
		+	(as it appears on PubMed at http://www.pubmed.gov), where 22343627 is the PubMed ID number.
		+	-->
		+	{{ABSTRACT_PUBMED_22343627}}

	==About this Structure==		==About this Structure==
	[[2yhy]] is a 1 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=2YHY OCA].		[[2yhy]] is a 1 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=2YHY OCA].
		+
		+	==Reference==
		+	<ref group="xtra">PMID:022343627</ref><references group="xtra"/>
	[[Category: Homo sapiens]]		[[Category: Homo sapiens]]
	[[Category: N-acylmannosamine kinase]]		[[Category: N-acylmannosamine kinase]]

OCA at 08:54, 29 February 2012

OCA — Wed, 29 Feb 2012 08:54:53 GMT

←Older revision		Revision as of 08:54, 29 February 2012
Line 1:		Line 1:
-	~~'''Unreleased structure'''~~	+	[[Image:2yhy.jpg\|left\|200px]]

-	The ~~entry 2yhy~~ is ~~ON HOLD~~ ~~until Paper Publication~~	+	<!--
		+	The line below this paragraph, containing "STRUCTURE_2yhy", 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_2yhy\| PDB=2yhy \| SCENE= }}

-	~~Authors: Martinez, J., Nguyen, L.D., Tauberger, E., Hinderlich, S., Reutter, W., Fan, H., Saenger, W., Moniot, S.~~	+	===Structure of N-Acetylmannosamine kinase in complex with N- acetylmannosamine and ADP===

-	~~Description:~~ Structure ~~of N-Acetylmannosamine kinase in complex~~ with N-~~acetylmannosamine and ADP~~	+
		+	==About this Structure==
		+	[[2yhy]] is a 1 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=2YHY OCA].
		+	[[Category: Homo sapiens]]
		+	[[Category: N-acylmannosamine kinase]]
		+	[[Category: Fan, H.]]
		+	[[Category: Hinderlich, S.]]
		+	[[Category: Martinez, J.]]
		+	[[Category: Moniot, S.]]
		+	[[Category: Nguyen, L D.]]
		+	[[Category: Reutter, W.]]
		+	[[Category: Saenger, W.]]
		+	[[Category: Tauberger, E.]]
		+	[[Category: Rok family]]
		+	[[Category: Sialic acid]]
		+	[[Category: Sugar kinase]]
		+	[[Category: Transferase]]

OCA: Protected "2yhy" [edit=sysop:move=sysop]

OCA — Wed, 18 May 2011 05:03:22 GMT

Protected "2yhy" [edit=sysop:move=sysop]

←Older revision

Revision as of 05:03, 18 May 2011

OCA: New page: '''Unreleased structure''' The entry 2yhy is ON HOLD until Paper Publication Authors: Martinez, J., Nguyen, L.D., Tauberger, E., Hinderlich, S., Reutter, W., Fan, H., Saenger, W., Monio...

OCA — Wed, 18 May 2011 05:03:22 GMT

New page: '''Unreleased structure''' The entry 2yhy is ON HOLD until Paper Publication Authors: Martinez, J., Nguyen, L.D., Tauberger, E., Hinderlich, S., Reutter, W., Fan, H., Saenger, W., Monio...

New page

'''Unreleased structure'''

The entry 2yhy is ON HOLD until Paper Publication

Authors: Martinez, J., Nguyen, L.D., Tauberger, E., Hinderlich, S., Reutter, W., Fan, H., Saenger, W., Moniot, S.

Description: Structure of N-Acetylmannosamine kinase in complex with N-acetylmannosamine and ADP

←Older revision		Revision as of 12:30, 27 April 2022
Line 3:		Line 3:
	<StructureSection load='2yhy' size='340' side='right'caption='[[2yhy]], [[Resolution\|resolution]] 1.82Å' scene=''>		<StructureSection load='2yhy' size='340' side='right'caption='[[2yhy]], [[Resolution\|resolution]] 1.82Å' scene=''>
	== Structural highlights ==		== Structural highlights ==
-	<table><tr><td colspan='2'>[[2yhy]] 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=2YHY OCA]. For a <b>guided tour on the structure components</b> use [~~http~~://proteopedia.org/fgij/fg.htm?mol=2YHY FirstGlance]. <br>	+	<table><tr><td colspan='2'>[[2yhy]] is a 1 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=2YHY OCA]. For a <b>guided tour on the structure components</b> use [https://proteopedia.org/fgij/fg.htm?mol=2YHY FirstGlance]. <br>
	</td></tr><tr id='ligand'><td class="sblockLbl"><b>[[Ligand\|Ligands:]]</b></td><td class="sblockDat" id="ligandDat"><scene name='pdbligand=2PE:NONAETHYLENE+GLYCOL'>2PE</scene>, <scene name='pdbligand=ADP:ADENOSINE-5-DIPHOSPHATE'>ADP</scene>, <scene name='pdbligand=BM3:2-(ACETYLAMINO)-2-DEOXY-ALPHA-D-MANNOPYRANOSE'>BM3</scene>, <scene name='pdbligand=CA:CALCIUM+ION'>CA</scene>, <scene name='pdbligand=CL:CHLORIDE+ION'>CL</scene>, <scene name='pdbligand=EDO:1,2-ETHANEDIOL'>EDO</scene>, <scene name='pdbligand=MG:MAGNESIUM+ION'>MG</scene>, <scene name='pdbligand=PG4:TETRAETHYLENE+GLYCOL'>PG4</scene>, <scene name='pdbligand=PGE:TRIETHYLENE+GLYCOL'>PGE</scene>, <scene name='pdbligand=ZN:ZINC+ION'>ZN</scene></td></tr>		</td></tr><tr id='ligand'><td class="sblockLbl"><b>[[Ligand\|Ligands:]]</b></td><td class="sblockDat" id="ligandDat"><scene name='pdbligand=2PE:NONAETHYLENE+GLYCOL'>2PE</scene>, <scene name='pdbligand=ADP:ADENOSINE-5-DIPHOSPHATE'>ADP</scene>, <scene name='pdbligand=BM3:2-(ACETYLAMINO)-2-DEOXY-ALPHA-D-MANNOPYRANOSE'>BM3</scene>, <scene name='pdbligand=CA:CALCIUM+ION'>CA</scene>, <scene name='pdbligand=CL:CHLORIDE+ION'>CL</scene>, <scene name='pdbligand=EDO:1,2-ETHANEDIOL'>EDO</scene>, <scene name='pdbligand=MG:MAGNESIUM+ION'>MG</scene>, <scene name='pdbligand=PG4:TETRAETHYLENE+GLYCOL'>PG4</scene>, <scene name='pdbligand=PGE:TRIETHYLENE+GLYCOL'>PGE</scene>, <scene name='pdbligand=ZN:ZINC+ION'>ZN</scene></td></tr>
-	<tr id='related'><td class="sblockLbl"><b>[[Related_structure\|Related:]]</b></td><td class="sblockDat">[[2yi1\|2yi1]], [[2yhw\|2yhw]]</td></tr>	+	<tr id='related'><td class="sblockLbl"><b>[[Related_structure\|Related:]]</b></td><td class="sblockDat"><div style='overflow: auto; max-height: 3em;'>[[2yi1\|2yi1]], [[2yhw\|2yhw]]</div></td></tr>
-	<tr id='activity'><td class="sblockLbl"><b>Activity:</b></td><td class="sblockDat"><span class='plainlinks'>[~~http~~://en.wikipedia.org/wiki/N-acylmannosamine_kinase N-acylmannosamine kinase], with EC number [~~http~~://www.brenda-enzymes.info/php/result_flat.php4?ecno=2.7.1.60 2.7.1.60] </span></td></tr>	+	<tr id='activity'><td class="sblockLbl"><b>Activity:</b></td><td class="sblockDat"><span class='plainlinks'>[https://en.wikipedia.org/wiki/N-acylmannosamine_kinase N-acylmannosamine kinase], with EC number [https://www.brenda-enzymes.info/php/result_flat.php4?ecno=2.7.1.60 2.7.1.60] </span></td></tr>
-	<tr id='resources'><td class="sblockLbl"><b>Resources:</b></td><td class="sblockDat"><span class='plainlinks'>[~~http~~://proteopedia.org/fgij/fg.htm?mol=2yhy FirstGlance], [http://oca.weizmann.ac.il/oca-bin/ocaids?id=2yhy OCA], [~~http~~://pdbe.org/2yhy PDBe], [~~http~~://www.rcsb.org/pdb/explore.do?structureId=2yhy RCSB], [~~http~~://www.ebi.ac.uk/pdbsum/2yhy PDBsum], [~~http~~://prosat.h-its.org/prosat/prosatexe?pdbcode=2yhy 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=2yhy FirstGlance], [http://oca.weizmann.ac.il/oca-bin/ocaids?id=2yhy OCA], [https://pdbe.org/2yhy PDBe], [https://www.rcsb.org/pdb/explore.do?structureId=2yhy RCSB], [https://www.ebi.ac.uk/pdbsum/2yhy PDBsum], [https://prosat.h-its.org/prosat/prosatexe?pdbcode=2yhy ProSAT]</span></td></tr>
	</table>		</table>
	== Disease ==		== Disease ==
-	[[~~http~~://www.uniprot.org/uniprot/GLCNE_HUMAN GLCNE_HUMAN]] Defects in GNE are a cause of sialuria (SIALURIA) [MIM:[~~http~~://omim.org/entry/269921 269921]]; also known as sialuria French type. In sialuria, free sialic acid accumulates in the cytoplasm and gram quantities of neuraminic acid are secreted in the urine. The metabolic defect involves lack of feedback inhibition of UDP-GlcNAc 2-epimerase by CMP-Neu5Ac, resulting in constitutive overproduction of free Neu5Ac. Clinical features include variable degrees of developmental delay, coarse facial features and hepatomegaly. Sialuria inheritance is autosomal dominant.<ref>PMID:2808337</ref> <ref>PMID:10330343</ref> <ref>PMID:10356312</ref> <ref>PMID:11326336</ref> Defects in GNE are the cause of inclusion body myopathy type 2 (IBM2) [MIM:[~~http~~://omim.org/entry/600737 600737]]. Hereditary inclusion body myopathies are a group of neuromuscular disorders characterized by adult onset, slowly progressive distal and proximal weakness and a typical muscle pathology including rimmed vacuoles and filamentous inclusions. IBM2 is an autosomal recessive disorder affecting mainly leg muscles, but with an unusual distribution that spares the quadriceps as also observed in Nonaka myopathy.<ref>PMID:11528398</ref> <ref>PMID:12409274</ref> <ref>PMID:12473769</ref> <ref>PMID:12473780</ref> <ref>PMID:12497639</ref> <ref>PMID:12811782</ref> <ref>PMID:15146476</ref> Defects in GNE are the cause of Nonaka myopathy (NM) [MIM:[~~http~~://omim.org/entry/605820 605820]]; also known as distal myopathy with rimmed vacuoles (DMRV). NM is an autosomal recessive muscular disorder, allelic to inclusion body myopathy 2. It is characterized by weakness of the anterior compartment of the lower limbs with onset in early adulthood, and sparing of the quadriceps muscles. As the inclusion body myopathy, NM is histologically characterized by the presence of numerous rimmed vacuoles without inflammatory changes in muscle specimens.<ref>PMID:12325084</ref> <ref>PMID:11916006</ref> <ref>PMID:12177386</ref> <ref>PMID:12473753</ref> <ref>PMID:12913203</ref>	+	[[https://www.uniprot.org/uniprot/GLCNE_HUMAN GLCNE_HUMAN]] Defects in GNE are a cause of sialuria (SIALURIA) [MIM:[https://omim.org/entry/269921 269921]]; also known as sialuria French type. In sialuria, free sialic acid accumulates in the cytoplasm and gram quantities of neuraminic acid are secreted in the urine. The metabolic defect involves lack of feedback inhibition of UDP-GlcNAc 2-epimerase by CMP-Neu5Ac, resulting in constitutive overproduction of free Neu5Ac. Clinical features include variable degrees of developmental delay, coarse facial features and hepatomegaly. Sialuria inheritance is autosomal dominant.<ref>PMID:2808337</ref> <ref>PMID:10330343</ref> <ref>PMID:10356312</ref> <ref>PMID:11326336</ref> Defects in GNE are the cause of inclusion body myopathy type 2 (IBM2) [MIM:[https://omim.org/entry/600737 600737]]. Hereditary inclusion body myopathies are a group of neuromuscular disorders characterized by adult onset, slowly progressive distal and proximal weakness and a typical muscle pathology including rimmed vacuoles and filamentous inclusions. IBM2 is an autosomal recessive disorder affecting mainly leg muscles, but with an unusual distribution that spares the quadriceps as also observed in Nonaka myopathy.<ref>PMID:11528398</ref> <ref>PMID:12409274</ref> <ref>PMID:12473769</ref> <ref>PMID:12473780</ref> <ref>PMID:12497639</ref> <ref>PMID:12811782</ref> <ref>PMID:15146476</ref> Defects in GNE are the cause of Nonaka myopathy (NM) [MIM:[https://omim.org/entry/605820 605820]]; also known as distal myopathy with rimmed vacuoles (DMRV). NM is an autosomal recessive muscular disorder, allelic to inclusion body myopathy 2. It is characterized by weakness of the anterior compartment of the lower limbs with onset in early adulthood, and sparing of the quadriceps muscles. As the inclusion body myopathy, NM is histologically characterized by the presence of numerous rimmed vacuoles without inflammatory changes in muscle specimens.<ref>PMID:12325084</ref> <ref>PMID:11916006</ref> <ref>PMID:12177386</ref> <ref>PMID:12473753</ref> <ref>PMID:12913203</ref>
	== Function ==		== Function ==
-	[[~~http~~://www.uniprot.org/uniprot/GLCNE_HUMAN GLCNE_HUMAN]] Regulates and initiates biosynthesis of N-acetylneuraminic acid (NeuAc), a precursor of sialic acids. Plays an essential role in early development (By similarity). Required for normal sialylation in hematopoietic cells. Sialylation is implicated in cell adhesion, signal transduction, tumorigenicity and metastatic behavior of malignant cells.<ref>PMID:10334995</ref>	+	[[https://www.uniprot.org/uniprot/GLCNE_HUMAN GLCNE_HUMAN]] Regulates and initiates biosynthesis of N-acetylneuraminic acid (NeuAc), a precursor of sialic acids. Plays an essential role in early development (By similarity). Required for normal sialylation in hematopoietic cells. Sialylation is implicated in cell adhesion, signal transduction, tumorigenicity and metastatic behavior of malignant cells.<ref>PMID:10334995</ref>
	<div style="background-color:#fffaf0;">		<div style="background-color:#fffaf0;">
	== Publication Abstract from PubMed ==		== Publication Abstract from PubMed ==