3m1n - Revision history

OCA at 08:47, 6 September 2023

OCA — Wed, 06 Sep 2023 08:47:17 GMT

←Older revision		Revision as of 08:47, 6 September 2023
Line 3:		Line 3:
	<StructureSection load='3m1n' size='340' side='right'caption='[[3m1n]], [[Resolution\|resolution]] 1.85Å' scene=''>		<StructureSection load='3m1n' size='340' side='right'caption='[[3m1n]], [[Resolution\|resolution]] 1.85Å' scene=''>
	== Structural highlights ==		== Structural highlights ==
-	<table><tr><td colspan='2'>[[3m1n]] 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=3M1N OCA]. For a <b>guided tour on the structure components</b> use [https://proteopedia.org/fgij/fg.htm?mol=3M1N FirstGlance]. <br>	+	<table><tr><td colspan='2'>[[3m1n]] 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=3M1N OCA]. For a <b>guided tour on the structure components</b> use [https://proteopedia.org/fgij/fg.htm?mol=3M1N FirstGlance]. <br>
-	</td></tr><tr id='~~ligand~~'><td class="sblockLbl"><b>[[~~Ligand~~\|~~Ligands~~:]]</b></td><td class="sblockDat" id="~~ligandDat~~">~~<scene name='pdbligand=SO4:SULFATE+ION'>SO4</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]] 1.85Å</td></tr>
-	<tr id='~~gene~~'><td class="sblockLbl"><b>[[~~Gene~~\|~~Gene~~:]]</b></td><td class="sblockDat">~~SHH ([https~~:/~~/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=SO4:SULFATE+ION'>SO4</scene>, <scene name='pdbligand=ZN:ZINC+ION'>ZN</scene></td></tr>
	<tr id='resources'><td class="sblockLbl"><b>Resources:</b></td><td class="sblockDat"><span class='plainlinks'>[https://proteopedia.org/fgij/fg.htm?mol=3m1n FirstGlance], [http://oca.weizmann.ac.il/oca-bin/ocaids?id=3m1n OCA], [https://pdbe.org/3m1n PDBe], [https://www.rcsb.org/pdb/explore.do?structureId=3m1n RCSB], [https://www.ebi.ac.uk/pdbsum/3m1n PDBsum], [https://prosat.h-its.org/prosat/prosatexe?pdbcode=3m1n 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=3m1n FirstGlance], [http://oca.weizmann.ac.il/oca-bin/ocaids?id=3m1n OCA], [https://pdbe.org/3m1n PDBe], [https://www.rcsb.org/pdb/explore.do?structureId=3m1n RCSB], [https://www.ebi.ac.uk/pdbsum/3m1n PDBsum], [https://prosat.h-its.org/prosat/prosatexe?pdbcode=3m1n ProSAT]</span></td></tr>
	</table>		</table>
	== Disease ==		== Disease ==
-	[[https://www.uniprot.org/uniprot/SHH_HUMAN SHH_HUMAN]] Defects in SHH are the cause of microphthalmia isolated with coloboma type 5 (MCOPCB5) [MIM:[https://omim.org/entry/611638 611638]]. Microphthalmia is a clinically heterogeneous disorder of eye formation, ranging from small size of a single eye to complete bilateral absence of ocular tissues. Ocular abnormalities like opacities of the cornea and lens, scaring of the retina and choroid, cataract and other abnormalities like cataract may also be present. Ocular colobomas are a set of malformations resulting from abnormal morphogenesis of the optic cup and stalk, and the fusion of the fetal fissure (optic fissure).<ref>PMID:12503095</ref> Defects in SHH are the cause of holoprosencephaly type 3 (HPE3) [MIM:[https://omim.org/entry/142945 142945]]. Holoprosencephaly (HPE) [MIM:[https://omim.org/entry/236100 236100]] is the most common structural anomaly of the brain, in which the developing forebrain fails to correctly separate into right and left hemispheres. Holoprosencephaly is genetically heterogeneous and associated with several distinct facies and phenotypic variability. The majority of HPE3 cases are apparently sporadic, although clear examples of autosomal dominant inheritance have been described. Interestingly, up to 30% of obligate carriers of HPE3 gene in autosomal dominant pedigrees are clinically unaffected.<ref>PMID:8896572</ref> <ref>PMID:9302262</ref> <ref>PMID:10441331</ref> <ref>PMID:10556296</ref> <ref>PMID:11479728</ref> <ref>PMID:15107988</ref> <ref>PMID:15221788</ref> <ref>PMID:15942952</ref> <ref>PMID:15942953</ref> <ref>PMID:16282375</ref> <ref>PMID:17001669</ref> <ref>PMID:19603532</ref> Defects in SHH are a cause of solitary median maxillary central incisor (SMMCI) [MIM:[https://omim.org/entry/147250 147250]]. SMMCI is a rare dental anomaly characterized by the congenital absence of one maxillary central incisor.<ref>PMID:11471164</ref> <ref>PMID:15103725</ref> Defects in SHH are the cause of triphalangeal thumb-polysyndactyly syndrome (TPTPS) [MIM:[https://omim.org/entry/174500 174500]]. TPTPS is an autosomal dominant syndrome characterized by a wide spectrum of pre- and post-axial abnormalities due to altered SHH expression pattern during limb development. TPTPS mutations have been mapped to the 7q36 locus in the LMBR1 gene which contains in its intron 5 a long-range cis-regulatory element of SHH expression.<ref>PMID:12837695</ref>	+	[https://www.uniprot.org/uniprot/SHH_HUMAN SHH_HUMAN] Defects in SHH are the cause of microphthalmia isolated with coloboma type 5 (MCOPCB5) [MIM:[https://omim.org/entry/611638 611638]. Microphthalmia is a clinically heterogeneous disorder of eye formation, ranging from small size of a single eye to complete bilateral absence of ocular tissues. Ocular abnormalities like opacities of the cornea and lens, scaring of the retina and choroid, cataract and other abnormalities like cataract may also be present. Ocular colobomas are a set of malformations resulting from abnormal morphogenesis of the optic cup and stalk, and the fusion of the fetal fissure (optic fissure).<ref>PMID:12503095</ref> Defects in SHH are the cause of holoprosencephaly type 3 (HPE3) [MIM:[https://omim.org/entry/142945 142945]. Holoprosencephaly (HPE) [MIM:[https://omim.org/entry/236100 236100] is the most common structural anomaly of the brain, in which the developing forebrain fails to correctly separate into right and left hemispheres. Holoprosencephaly is genetically heterogeneous and associated with several distinct facies and phenotypic variability. The majority of HPE3 cases are apparently sporadic, although clear examples of autosomal dominant inheritance have been described. Interestingly, up to 30% of obligate carriers of HPE3 gene in autosomal dominant pedigrees are clinically unaffected.<ref>PMID:8896572</ref> <ref>PMID:9302262</ref> <ref>PMID:10441331</ref> <ref>PMID:10556296</ref> <ref>PMID:11479728</ref> <ref>PMID:15107988</ref> <ref>PMID:15221788</ref> <ref>PMID:15942952</ref> <ref>PMID:15942953</ref> <ref>PMID:16282375</ref> <ref>PMID:17001669</ref> <ref>PMID:19603532</ref> Defects in SHH are a cause of solitary median maxillary central incisor (SMMCI) [MIM:[https://omim.org/entry/147250 147250]. SMMCI is a rare dental anomaly characterized by the congenital absence of one maxillary central incisor.<ref>PMID:11471164</ref> <ref>PMID:15103725</ref> Defects in SHH are the cause of triphalangeal thumb-polysyndactyly syndrome (TPTPS) [MIM:[https://omim.org/entry/174500 174500]. TPTPS is an autosomal dominant syndrome characterized by a wide spectrum of pre- and post-axial abnormalities due to altered SHH expression pattern during limb development. TPTPS mutations have been mapped to the 7q36 locus in the LMBR1 gene which contains in its intron 5 a long-range cis-regulatory element of SHH expression.<ref>PMID:12837695</ref>
	== Function ==		== Function ==
-	[[https://www.uniprot.org/uniprot/SHH_HUMAN SHH_HUMAN]] Binds to the patched (PTC) receptor, which functions in association with smoothened (SMO), to activate the transcription of target genes. In the absence of SHH, PTC represses the constitutive signaling activity of SMO. Also regulates another target, the gli oncogene. Intercellular signal essential for a variety of patterning events during development: signal produced by the notochord that induces ventral cell fate in the neural tube and somites, and the polarizing signal for patterning of the anterior-posterior axis of the developing limb bud. Displays both floor plate- and motor neuron-inducing activity. The threshold concentration of N-product required for motor neuron induction is 5-fold lower than that required for floor plate induction (By similarity).	+	[https://www.uniprot.org/uniprot/SHH_HUMAN SHH_HUMAN] Binds to the patched (PTC) receptor, which functions in association with smoothened (SMO), to activate the transcription of target genes. In the absence of SHH, PTC represses the constitutive signaling activity of SMO. Also regulates another target, the gli oncogene. Intercellular signal essential for a variety of patterning events during development: signal produced by the notochord that induces ventral cell fate in the neural tube and somites, and the polarizing signal for patterning of the anterior-posterior axis of the developing limb bud. Displays both floor plate- and motor neuron-inducing activity. The threshold concentration of N-product required for motor neuron induction is 5-fold lower than that required for floor plate induction (By similarity).
	== Evolutionary Conservation ==		== Evolutionary Conservation ==
	[[Image:Consurf_key_small.gif\|200px\|right]]		[[Image:Consurf_key_small.gif\|200px\|right]]
Line 33:		Line 33:

	==See Also==		==See Also==
-	*[[Sonic ~~Hedgehog~~\|Sonic ~~Hedgehog~~]]	+	*[[Sonic hedgehog 3D structures\|Sonic hedgehog 3D structures]]
	== References ==		== References ==
	<references/>		<references/>
	__TOC__		__TOC__
	</StructureSection>		</StructureSection>
-	[[Category: ~~Human~~]]	+	[[Category: Homo sapiens]]
	[[Category: Large Structures]]		[[Category: Large Structures]]
-	[[Category: Boriack-Sjodin~~, P A~~]]	+	[[Category: Boriack-Sjodin PA]]
-	[[Category: Garber~~, E A~~]]	+	[[Category: Garber EA]]
-	[[Category: Pepinsky~~, R B~~]]	+	[[Category: Pepinsky RB]]
-	[[Category: Silvian~~, L F]]~~	+	[[Category: Silvian LF]]
-	~~[[Category: Autocatalytic cleavage]]~~	+
-	~~[[Category: Cell membrane]]~~	+
-	~~[[Category: Developmental protein]]~~	+
-	~~[[Category: Glycoprotein]]~~	+
-	~~[[Category: Hedgehog protein]]~~	+
-	~~[[Category: Holoprosencephaly]]~~	+
-	~~[[Category: Hydrolase]]~~	+
-	~~[[Category: Lipoprotein]]~~	+
-	~~[[Category: Membrane]]~~	+
-	~~[[Category: Microphthalmia]]~~	+
-	~~[[Category: Palmitate]]~~	+
-	~~[[Category: Protease]]~~	+
-	~~[[Category: Secreted]]~~	+
-	~~[[Category: Signaling]]~~	+
-	~~[[Category: Signaling protein]]~~	+
-	~~[[Category: Sulfate ion]]~~	+
-	~~[[Category: Zinc ion~~]]	+

OCA at 12:41, 13 October 2021

OCA — Wed, 13 Oct 2021 12:41:23 GMT

←Older revision		Revision as of 12:41, 13 October 2021
Line 1:		Line 1:

	==Crystal structure of Human Sonic Hedgehog N-terminal domain==		==Crystal structure of Human Sonic Hedgehog N-terminal domain==
-	<StructureSection load='3m1n' size='340' side='right' caption='[[3m1n]], [[Resolution\|resolution]] 1.85Å' scene=''>	+	<StructureSection load='3m1n' size='340' side='right'caption='[[3m1n]], [[Resolution\|resolution]] 1.85Å' scene=''>
	== Structural highlights ==		== Structural highlights ==
-	<table><tr><td colspan='2'>[[3m1n]] 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=3M1N OCA]. For a <b>guided tour on the structure components</b> use [~~http~~://~~oca~~.~~weizmann.ac.il/oca-docs~~/fgij/fg.htm?mol=3M1N FirstGlance]. <br>	+	<table><tr><td colspan='2'>[[3m1n]] 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=3M1N OCA]. For a <b>guided tour on the structure components</b> use [https://proteopedia.org/fgij/fg.htm?mol=3M1N FirstGlance]. <br>
-	</td></tr><tr id='ligand'><td class="sblockLbl"><b>[[Ligand\|Ligands:]]</b></td><td class="sblockDat"><scene name='pdbligand=SO4:SULFATE+ION'>SO4</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=SO4:SULFATE+ION'>SO4</scene>, <scene name='pdbligand=ZN:ZINC+ION'>ZN</scene></td></tr>
-	<tr id='gene'><td class="sblockLbl"><b>[[Gene\|Gene:]]</b></td><td class="sblockDat">SHH ([~~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">SHH ([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=3m1n FirstGlance], [http://oca.weizmann.ac.il/oca-bin/ocaids?id=3m1n OCA], [~~http~~://pdbe.org/3m1n PDBe], [~~http~~://www.rcsb.org/pdb/explore.do?structureId=3m1n RCSB], [~~http~~://www.ebi.ac.uk/pdbsum/3m1n PDBsum], [~~http~~://prosat.h-its.org/prosat/prosatexe?pdbcode=3m1n 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=3m1n FirstGlance], [http://oca.weizmann.ac.il/oca-bin/ocaids?id=3m1n OCA], [https://pdbe.org/3m1n PDBe], [https://www.rcsb.org/pdb/explore.do?structureId=3m1n RCSB], [https://www.ebi.ac.uk/pdbsum/3m1n PDBsum], [https://prosat.h-its.org/prosat/prosatexe?pdbcode=3m1n ProSAT]</span></td></tr>
	</table>		</table>
	== Disease ==		== Disease ==
-	[[~~http~~://www.uniprot.org/uniprot/SHH_HUMAN SHH_HUMAN]] Defects in SHH are the cause of microphthalmia isolated with coloboma type 5 (MCOPCB5) [MIM:[~~http~~://omim.org/entry/611638 611638]]. Microphthalmia is a clinically heterogeneous disorder of eye formation, ranging from small size of a single eye to complete bilateral absence of ocular tissues. Ocular abnormalities like opacities of the cornea and lens, scaring of the retina and choroid, cataract and other abnormalities like cataract may also be present. Ocular colobomas are a set of malformations resulting from abnormal morphogenesis of the optic cup and stalk, and the fusion of the fetal fissure (optic fissure).<ref>PMID:12503095</ref> Defects in SHH are the cause of holoprosencephaly type 3 (HPE3) [MIM:[~~http~~://omim.org/entry/142945 142945]]. Holoprosencephaly (HPE) [MIM:[~~http~~://omim.org/entry/236100 236100]] is the most common structural anomaly of the brain, in which the developing forebrain fails to correctly separate into right and left hemispheres. Holoprosencephaly is genetically heterogeneous and associated with several distinct facies and phenotypic variability. The majority of HPE3 cases are apparently sporadic, although clear examples of autosomal dominant inheritance have been described. Interestingly, up to 30% of obligate carriers of HPE3 gene in autosomal dominant pedigrees are clinically unaffected.<ref>PMID:8896572</ref> <ref>PMID:9302262</ref> <ref>PMID:10441331</ref> <ref>PMID:10556296</ref> <ref>PMID:11479728</ref> <ref>PMID:15107988</ref> <ref>PMID:15221788</ref> <ref>PMID:15942952</ref> <ref>PMID:15942953</ref> <ref>PMID:16282375</ref> <ref>PMID:17001669</ref> <ref>PMID:19603532</ref> Defects in SHH are a cause of solitary median maxillary central incisor (SMMCI) [MIM:[~~http~~://omim.org/entry/147250 147250]]. SMMCI is a rare dental anomaly characterized by the congenital absence of one maxillary central incisor.<ref>PMID:11471164</ref> <ref>PMID:15103725</ref> Defects in SHH are the cause of triphalangeal thumb-polysyndactyly syndrome (TPTPS) [MIM:[~~http~~://omim.org/entry/174500 174500]]. TPTPS is an autosomal dominant syndrome characterized by a wide spectrum of pre- and post-axial abnormalities due to altered SHH expression pattern during limb development. TPTPS mutations have been mapped to the 7q36 locus in the LMBR1 gene which contains in its intron 5 a long-range cis-regulatory element of SHH expression.<ref>PMID:12837695</ref>	+	[[https://www.uniprot.org/uniprot/SHH_HUMAN SHH_HUMAN]] Defects in SHH are the cause of microphthalmia isolated with coloboma type 5 (MCOPCB5) [MIM:[https://omim.org/entry/611638 611638]]. Microphthalmia is a clinically heterogeneous disorder of eye formation, ranging from small size of a single eye to complete bilateral absence of ocular tissues. Ocular abnormalities like opacities of the cornea and lens, scaring of the retina and choroid, cataract and other abnormalities like cataract may also be present. Ocular colobomas are a set of malformations resulting from abnormal morphogenesis of the optic cup and stalk, and the fusion of the fetal fissure (optic fissure).<ref>PMID:12503095</ref> Defects in SHH are the cause of holoprosencephaly type 3 (HPE3) [MIM:[https://omim.org/entry/142945 142945]]. Holoprosencephaly (HPE) [MIM:[https://omim.org/entry/236100 236100]] is the most common structural anomaly of the brain, in which the developing forebrain fails to correctly separate into right and left hemispheres. Holoprosencephaly is genetically heterogeneous and associated with several distinct facies and phenotypic variability. The majority of HPE3 cases are apparently sporadic, although clear examples of autosomal dominant inheritance have been described. Interestingly, up to 30% of obligate carriers of HPE3 gene in autosomal dominant pedigrees are clinically unaffected.<ref>PMID:8896572</ref> <ref>PMID:9302262</ref> <ref>PMID:10441331</ref> <ref>PMID:10556296</ref> <ref>PMID:11479728</ref> <ref>PMID:15107988</ref> <ref>PMID:15221788</ref> <ref>PMID:15942952</ref> <ref>PMID:15942953</ref> <ref>PMID:16282375</ref> <ref>PMID:17001669</ref> <ref>PMID:19603532</ref> Defects in SHH are a cause of solitary median maxillary central incisor (SMMCI) [MIM:[https://omim.org/entry/147250 147250]]. SMMCI is a rare dental anomaly characterized by the congenital absence of one maxillary central incisor.<ref>PMID:11471164</ref> <ref>PMID:15103725</ref> Defects in SHH are the cause of triphalangeal thumb-polysyndactyly syndrome (TPTPS) [MIM:[https://omim.org/entry/174500 174500]]. TPTPS is an autosomal dominant syndrome characterized by a wide spectrum of pre- and post-axial abnormalities due to altered SHH expression pattern during limb development. TPTPS mutations have been mapped to the 7q36 locus in the LMBR1 gene which contains in its intron 5 a long-range cis-regulatory element of SHH expression.<ref>PMID:12837695</ref>
	== Function ==		== Function ==
-	[[~~http~~://www.uniprot.org/uniprot/SHH_HUMAN SHH_HUMAN]] Binds to the patched (PTC) receptor, which functions in association with smoothened (SMO), to activate the transcription of target genes. In the absence of SHH, PTC represses the constitutive signaling activity of SMO. Also regulates another target, the gli oncogene. Intercellular signal essential for a variety of patterning events during development: signal produced by the notochord that induces ventral cell fate in the neural tube and somites, and the polarizing signal for patterning of the anterior-posterior axis of the developing limb bud. Displays both floor plate- and motor neuron-inducing activity. The threshold concentration of N-product required for motor neuron induction is 5-fold lower than that required for floor plate induction (By similarity).	+	[[https://www.uniprot.org/uniprot/SHH_HUMAN SHH_HUMAN]] Binds to the patched (PTC) receptor, which functions in association with smoothened (SMO), to activate the transcription of target genes. In the absence of SHH, PTC represses the constitutive signaling activity of SMO. Also regulates another target, the gli oncogene. Intercellular signal essential for a variety of patterning events during development: signal produced by the notochord that induces ventral cell fate in the neural tube and somites, and the polarizing signal for patterning of the anterior-posterior axis of the developing limb bud. Displays both floor plate- and motor neuron-inducing activity. The threshold concentration of N-product required for motor neuron induction is 5-fold lower than that required for floor plate induction (By similarity).
	== Evolutionary Conservation ==		== Evolutionary Conservation ==
	[[Image:Consurf_key_small.gif\|200px\|right]]		[[Image:Consurf_key_small.gif\|200px\|right]]
Line 39:		Line 39:
	</StructureSection>		</StructureSection>
	[[Category: Human]]		[[Category: Human]]
		+	[[Category: Large Structures]]
	[[Category: Boriack-Sjodin, P A]]		[[Category: Boriack-Sjodin, P A]]
	[[Category: Garber, E A]]		[[Category: Garber, E A]]

OCA at 07:42, 9 January 2019

OCA — Wed, 09 Jan 2019 07:42:28 GMT

←Older revision		Revision as of 07:42, 9 January 2019
Line 16:		Line 16:
	Check<jmol>		Check<jmol>
	<jmolCheckbox>		<jmolCheckbox>
-	<scriptWhenChecked>select protein; define ~consurf_to_do selected; consurf_initial_scene = true; script "/wiki/ConSurf/m1/3m1n_consurf.spt"</scriptWhenChecked>	+	<scriptWhenChecked>; select protein; define ~consurf_to_do selected; consurf_initial_scene = true; script "/wiki/ConSurf/m1/3m1n_consurf.spt"</scriptWhenChecked>
	<scriptWhenUnchecked>script /wiki/extensions/Proteopedia/spt/initialview01.spt</scriptWhenUnchecked>		<scriptWhenUnchecked>script /wiki/extensions/Proteopedia/spt/initialview01.spt</scriptWhenUnchecked>
	<text>to colour the structure by Evolutionary Conservation</text>		<text>to colour the structure by Evolutionary Conservation</text>

OCA at 15:26, 4 August 2016

OCA — Thu, 04 Aug 2016 15:26:20 GMT

←Older revision		Revision as of 15:26, 4 August 2016
Line 1:		Line 1:
		+
	==Crystal structure of Human Sonic Hedgehog N-terminal domain==		==Crystal structure of Human Sonic Hedgehog N-terminal domain==
	<StructureSection load='3m1n' size='340' side='right' caption='[[3m1n]], [[Resolution\|resolution]] 1.85Å' scene=''>		<StructureSection load='3m1n' size='340' side='right' caption='[[3m1n]], [[Resolution\|resolution]] 1.85Å' scene=''>
	== Structural highlights ==		== Structural highlights ==
-	<table><tr><td colspan='2'>[[3m1n]] 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=3M1N OCA]. For a <b>guided tour on the structure components</b> use [http://oca.weizmann.ac.il/oca-docs/fgij/fg.htm?mol=3M1N FirstGlance]. <br>	+	<table><tr><td colspan='2'>[[3m1n]] 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=3M1N OCA]. For a <b>guided tour on the structure components</b> use [http://oca.weizmann.ac.il/oca-docs/fgij/fg.htm?mol=3M1N FirstGlance]. <br>
	</td></tr><tr id='ligand'><td class="sblockLbl"><b>[[Ligand\|Ligands:]]</b></td><td class="sblockDat"><scene name='pdbligand=SO4:SULFATE+ION'>SO4</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=SO4:SULFATE+ION'>SO4</scene>, <scene name='pdbligand=ZN:ZINC+ION'>ZN</scene></td></tr>
-	<tr id='gene'><td class="sblockLbl"><b>[[Gene\|Gene:]]</b></td><td class="sblockDat">SHH ([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">SHH ([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=3m1n FirstGlance], [http://oca.weizmann.ac.il/oca-bin/ocaids?id=3m1n OCA], [http://www.rcsb.org/pdb/explore.do?structureId=3m1n RCSB], [http://www.ebi.ac.uk/pdbsum/3m1n 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=3m1n FirstGlance], [http://oca.weizmann.ac.il/oca-bin/ocaids?id=3m1n OCA], [http://pdbe.org/3m1n PDBe], [http://www.rcsb.org/pdb/explore.do?structureId=3m1n RCSB], [http://www.ebi.ac.uk/pdbsum/3m1n PDBsum], [http://prosat.h-its.org/prosat/prosatexe?pdbcode=3m1n ProSAT]</span></td></tr>
	</table>		</table>
	== Disease ==		== Disease ==
Line 19:		Line 20:
	<text>to colour the structure by Evolutionary Conservation</text>		<text>to colour the structure by Evolutionary Conservation</text>
	</jmolCheckbox>		</jmolCheckbox>
-	</jmol>, as determined by [http://consurfdb.tau.ac.il/ ConSurfDB]. You may read the [[Conservation%2C_Evolutionary\|explanation]] of the method and the full data available from [http://bental.tau.ac.il/new_ConSurfDB/~~chain_selection~~.php?pdb_ID=~~2ata~~ ConSurf].	+	</jmol>, as determined by [http://consurfdb.tau.ac.il/ ConSurfDB]. You may read the [[Conservation%2C_Evolutionary\|explanation]] of the method and the full data available from [http://bental.tau.ac.il/new_ConSurfDB/main_output.php?pdb_ID=3m1n ConSurf].
	<div style="clear:both"></div>		<div style="clear:both"></div>
	<div style="background-color:#fffaf0;">		<div style="background-color:#fffaf0;">
Line 29:		Line 30:
	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 3m1n" style="background-color:#fffaf0;"></div>
		+
		+	==See Also==
		+	*[[Sonic Hedgehog\|Sonic Hedgehog]]
	== References ==		== References ==
	<references/>		<references/>
	__TOC__		__TOC__
	</StructureSection>		</StructureSection>
-	[[Category: ~~Homo sapiens~~]]	+	[[Category: Human]]
	[[Category: Boriack-Sjodin, P A]]		[[Category: Boriack-Sjodin, P A]]
	[[Category: Garber, E A]]		[[Category: Garber, E A]]

OCA at 17:15, 18 December 2014

OCA — Thu, 18 Dec 2014 17:15:07 GMT

←Older revision		Revision as of 17:15, 18 December 2014
Line 1:		Line 1:
-	~~{{STRUCTURE_3m1n\| PDB=3m1n \| SCENE= }}~~	+	==Crystal structure of Human Sonic Hedgehog N-terminal domain==
-	===Crystal structure of Human Sonic Hedgehog N-terminal domain===	+	<StructureSection load='3m1n' size='340' side='right' caption='[[3m1n]], [[Resolution\|resolution]] 1.85Å' scene=''>
-	~~{{ABSTRACT_PUBMED_10753901}}~~	+	== Structural highlights ==
-		+	<table><tr><td colspan='2'>[[3m1n]] 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=3M1N OCA]. For a <b>guided tour on the structure components</b> use [http://oca.weizmann.ac.il/oca-docs/fgij/fg.htm?mol=3M1N FirstGlance]. <br>
-	==Disease==	+	</td></tr><tr id='ligand'><td class="sblockLbl"><b>[[Ligand\|Ligands:]]</b></td><td class="sblockDat"><scene name='pdbligand=SO4:SULFATE+ION'>SO4</scene>, <scene name='pdbligand=ZN:ZINC+ION'>ZN</scene></td></tr>
-	[[http://www.uniprot.org/uniprot/SHH_HUMAN SHH_HUMAN]] Defects in SHH are the cause of microphthalmia isolated with coloboma type 5 (MCOPCB5) [MIM:[http://omim.org/entry/611638 611638]]. Microphthalmia is a clinically heterogeneous disorder of eye formation, ranging from small size of a single eye to complete bilateral absence of ocular tissues. Ocular abnormalities like opacities of the cornea and lens, scaring of the retina and choroid, cataract and other abnormalities like cataract may also be present. Ocular colobomas are a set of malformations resulting from abnormal morphogenesis of the optic cup and stalk, and the fusion of the fetal fissure (optic fissure).<ref>PMID:12503095</ref> Defects in SHH are the cause of holoprosencephaly type 3 (HPE3) [MIM:[http://omim.org/entry/142945 142945]]. Holoprosencephaly (HPE) [MIM:[http://omim.org/entry/236100 236100]] is the most common structural anomaly of the brain, in which the developing forebrain fails to correctly separate into right and left hemispheres. Holoprosencephaly is genetically heterogeneous and associated with several distinct facies and phenotypic variability. The majority of HPE3 cases are apparently sporadic, although clear examples of autosomal dominant inheritance have been described. Interestingly, up to 30% of obligate carriers of HPE3 gene in autosomal dominant pedigrees are clinically unaffected.<ref>PMID:8896572</ref><ref>PMID:9302262</ref><ref>PMID:10441331</ref><ref>PMID:10556296</ref><ref>PMID:11479728</ref><ref>PMID:15107988</ref><ref>PMID:15221788</ref><ref>PMID:15942952</ref><ref>PMID:15942953</ref><ref>PMID:16282375</ref><ref>PMID:17001669</ref><ref>PMID:19603532</ref> Defects in SHH are a cause of solitary median maxillary central incisor (SMMCI) [MIM:[http://omim.org/entry/147250 147250]]. SMMCI is a rare dental anomaly characterized by the congenital absence of one maxillary central incisor.<ref>PMID:11471164</ref><ref>PMID:15103725</ref> Defects in SHH are the cause of triphalangeal thumb-polysyndactyly syndrome (TPTPS) [MIM:[http://omim.org/entry/174500 174500]]. TPTPS is an autosomal dominant syndrome characterized by a wide spectrum of pre- and post-axial abnormalities due to altered SHH expression pattern during limb development. TPTPS mutations have been mapped to the 7q36 locus in the LMBR1 gene which contains in its intron 5 a long-range cis-regulatory element of SHH expression.<ref>PMID:12837695</ref>	+	<tr id='gene'><td class="sblockLbl"><b>[[Gene\|Gene:]]</b></td><td class="sblockDat">SHH ([http://www.ncbi.nlm.nih.gov/Taxonomy/Browser/wwwtax.cgi?mode=Info&srchmode=5&id=9606 Homo sapiens])</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=3m1n FirstGlance], [http://oca.weizmann.ac.il/oca-bin/ocaids?id=3m1n OCA], [http://www.rcsb.org/pdb/explore.do?structureId=3m1n RCSB], [http://www.ebi.ac.uk/pdbsum/3m1n PDBsum]</span></td></tr>
-	==Function==	+	</table>
		+	== Disease ==
		+	[[http://www.uniprot.org/uniprot/SHH_HUMAN SHH_HUMAN]] Defects in SHH are the cause of microphthalmia isolated with coloboma type 5 (MCOPCB5) [MIM:[http://omim.org/entry/611638 611638]]. Microphthalmia is a clinically heterogeneous disorder of eye formation, ranging from small size of a single eye to complete bilateral absence of ocular tissues. Ocular abnormalities like opacities of the cornea and lens, scaring of the retina and choroid, cataract and other abnormalities like cataract may also be present. Ocular colobomas are a set of malformations resulting from abnormal morphogenesis of the optic cup and stalk, and the fusion of the fetal fissure (optic fissure).<ref>PMID:12503095</ref> Defects in SHH are the cause of holoprosencephaly type 3 (HPE3) [MIM:[http://omim.org/entry/142945 142945]]. Holoprosencephaly (HPE) [MIM:[http://omim.org/entry/236100 236100]] is the most common structural anomaly of the brain, in which the developing forebrain fails to correctly separate into right and left hemispheres. Holoprosencephaly is genetically heterogeneous and associated with several distinct facies and phenotypic variability. The majority of HPE3 cases are apparently sporadic, although clear examples of autosomal dominant inheritance have been described. Interestingly, up to 30% of obligate carriers of HPE3 gene in autosomal dominant pedigrees are clinically unaffected.<ref>PMID:8896572</ref> <ref>PMID:9302262</ref> <ref>PMID:10441331</ref> <ref>PMID:10556296</ref> <ref>PMID:11479728</ref> <ref>PMID:15107988</ref> <ref>PMID:15221788</ref> <ref>PMID:15942952</ref> <ref>PMID:15942953</ref> <ref>PMID:16282375</ref> <ref>PMID:17001669</ref> <ref>PMID:19603532</ref> Defects in SHH are a cause of solitary median maxillary central incisor (SMMCI) [MIM:[http://omim.org/entry/147250 147250]]. SMMCI is a rare dental anomaly characterized by the congenital absence of one maxillary central incisor.<ref>PMID:11471164</ref> <ref>PMID:15103725</ref> Defects in SHH are the cause of triphalangeal thumb-polysyndactyly syndrome (TPTPS) [MIM:[http://omim.org/entry/174500 174500]]. TPTPS is an autosomal dominant syndrome characterized by a wide spectrum of pre- and post-axial abnormalities due to altered SHH expression pattern during limb development. TPTPS mutations have been mapped to the 7q36 locus in the LMBR1 gene which contains in its intron 5 a long-range cis-regulatory element of SHH expression.<ref>PMID:12837695</ref>
		+	== Function ==
	[[http://www.uniprot.org/uniprot/SHH_HUMAN SHH_HUMAN]] Binds to the patched (PTC) receptor, which functions in association with smoothened (SMO), to activate the transcription of target genes. In the absence of SHH, PTC represses the constitutive signaling activity of SMO. Also regulates another target, the gli oncogene. Intercellular signal essential for a variety of patterning events during development: signal produced by the notochord that induces ventral cell fate in the neural tube and somites, and the polarizing signal for patterning of the anterior-posterior axis of the developing limb bud. Displays both floor plate- and motor neuron-inducing activity. The threshold concentration of N-product required for motor neuron induction is 5-fold lower than that required for floor plate induction (By similarity).		[[http://www.uniprot.org/uniprot/SHH_HUMAN SHH_HUMAN]] Binds to the patched (PTC) receptor, which functions in association with smoothened (SMO), to activate the transcription of target genes. In the absence of SHH, PTC represses the constitutive signaling activity of SMO. Also regulates another target, the gli oncogene. Intercellular signal essential for a variety of patterning events during development: signal produced by the notochord that induces ventral cell fate in the neural tube and somites, and the polarizing signal for patterning of the anterior-posterior axis of the developing limb bud. Displays both floor plate- and motor neuron-inducing activity. The threshold concentration of N-product required for motor neuron induction is 5-fold lower than that required for floor plate induction (By similarity).
		+	== Evolutionary Conservation ==
		+	[[Image:Consurf_key_small.gif\|200px\|right]]
		+	Check<jmol>
		+	<jmolCheckbox>
		+	<scriptWhenChecked>select protein; define ~consurf_to_do selected; consurf_initial_scene = true; script "/wiki/ConSurf/m1/3m1n_consurf.spt"</scriptWhenChecked>
		+	<scriptWhenUnchecked>script /wiki/extensions/Proteopedia/spt/initialview01.spt</scriptWhenUnchecked>
		+	<text>to colour the structure by Evolutionary Conservation</text>
		+	</jmolCheckbox>
		+	</jmol>, as determined by [http://consurfdb.tau.ac.il/ ConSurfDB]. You may read the [[Conservation%2C_Evolutionary\|explanation]] of the method and the full data available from [http://bental.tau.ac.il/new_ConSurfDB/chain_selection.php?pdb_ID=2ata ConSurf].
		+	<div style="clear:both"></div>
		+	<div style="background-color:#fffaf0;">
		+	== Publication Abstract from PubMed ==
		+	We have defined regions in the Sonic hedgehog (Shh) molecule that are important for Patched (Ptc) receptor binding by targeting selected surface amino acid residues with probes of diverse sizes and shapes and assessing the effects of these modifications on function. Eleven amino acid residues that surround the surface of the protein were chosen for these studies and mutated to cysteine residues. These cysteines were then selectively modified with thiol-specific probes, and the modified proteins were tested for hedgehog receptor binding activity and their ability to induce differentiation of C3H10T1/2 cells into osteoblasts. Based on these analyses, approximately one-third of the Shh surface can be modified without effect on function regardless of the size of the attachment. These sites are located near to where the C terminus protrudes from the surface of the protein. All other sites were sensitive to modification, indicating that the interaction of Shh with its primary receptor Ptc is mediated over a large surface of the Shh protein. For sites Asn-50 and Ser-156, function was lost with the smallest of the probes tested, indicating that these residues are in close proximity to the Ptc-binding site. The epitope for the neutralizing mAb 5E1 mapped to a close but distinct region of the structure. The structure-activity data provide a unique view of the interactions between Shh and Ptc that is not readily attainable by conventional mapping strategies.

-	~~==About this Structure==~~	+	Mapping sonic hedgehog-receptor interactions by steric interference.,Pepinsky RB, Rayhorn P, Day ES, Dergay A, Williams KP, Galdes A, Taylor FR, Boriack-Sjodin PA, Garber EA J Biol Chem. 2000 Apr 14;275(15):10995-1001. PMID:10753901<ref>PMID:10753901</ref>
-	~~[[3m1n]] 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=3M1N OCA].~~	+

-	==~~Reference~~==	+	From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine.<br>
-	~~<ref group="xtra">PMID:010753901</ref>~~<references ~~group="xtra"~~/><~~references~~/>	+	</div>
		+	== References ==
		+	<references/>
		+	__TOC__
		+	</StructureSection>
	[[Category: Homo sapiens]]		[[Category: Homo sapiens]]
-	[[Category: Boriack-Sjodin, P A.]]	+	[[Category: Boriack-Sjodin, P A]]
-	[[Category: Garber, E A.]]	+	[[Category: Garber, E A]]
-	[[Category: Pepinsky, R B.]]	+	[[Category: Pepinsky, R B]]
-	[[Category: Silvian, L F.]]	+	[[Category: Silvian, L F]]
	[[Category: Autocatalytic cleavage]]		[[Category: Autocatalytic cleavage]]
	[[Category: Cell membrane]]		[[Category: Cell membrane]]

OCA: Protected "3m1n" [edit=sysop:move=sysop]

OCA — Sun, 24 Mar 2013 21:25:38 GMT

Protected "3m1n" [edit=sysop:move=sysop]

←Older revision

Revision as of 21:25, 24 March 2013

OCA at 21:25, 24 March 2013

OCA — Sun, 24 Mar 2013 21:25:36 GMT

←Older revision		Revision as of 21:25, 24 March 2013
Line 1:		Line 1:
-	{{Seed}}
-	[[Image:3m1n.jpg\|left\|200px]]
-
-	<!--
-	The line below this paragraph, containing "STRUCTURE_3m1n", 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_3m1n\| PDB=3m1n \| SCENE= }}		{{STRUCTURE_3m1n\| PDB=3m1n \| SCENE= }}
-
	===Crystal structure of Human Sonic Hedgehog N-terminal domain===		===Crystal structure of Human Sonic Hedgehog N-terminal domain===
-
-
-	<!--
-	The line below this paragraph, {{ABSTRACT_PUBMED_10753901}}, adds the Publication Abstract to the page
-	(as it appears on PubMed at http://www.pubmed.gov), where 10753901 is the PubMed ID number.
-	-->
	{{ABSTRACT_PUBMED_10753901}}		{{ABSTRACT_PUBMED_10753901}}

	==Disease==		==Disease==
-	~~Known disease associated with this structure: Coloboma, ocular OMIM:~~[[http://www.~~ncbi~~.~~nlm.nih.gov~~/~~entrez~~/~~dispomim~~.~~cgi?id=600725 600725~~]], ~~Holoprosencephaly-~~3 ~~OMIM~~:[[http://~~www~~.~~ncbi.nlm~~.~~nih.gov~~/~~entrez~~/~~dispomim~~.~~cgi?id=600725 600725~~]], ~~Microphthalmia~~, ~~isolated~~, ~~with coloboma 5 OMIM~~:[[http://~~www~~.~~ncbi.nlm.nih.gov~~/~~entrez~~/~~dispomim.cgi?id=600725 600725~~]]~~, Solitary median~~ maxillary central incisor ~~OMIM~~:[[http://~~www~~.~~ncbi~~.~~nlm~~.~~nih~~.~~gov~~/~~entrez~~/~~dispomim~~.~~cgi?id=600725 600725~~]]	+	[[http://www.uniprot.org/uniprot/SHH_HUMAN SHH_HUMAN]] Defects in SHH are the cause of microphthalmia isolated with coloboma type 5 (MCOPCB5) [MIM:[http://omim.org/entry/611638 611638]]. Microphthalmia is a clinically heterogeneous disorder of eye formation, ranging from small size of a single eye to complete bilateral absence of ocular tissues. Ocular abnormalities like opacities of the cornea and lens, scaring of the retina and choroid, cataract and other abnormalities like cataract may also be present. Ocular colobomas are a set of malformations resulting from abnormal morphogenesis of the optic cup and stalk, and the fusion of the fetal fissure (optic fissure).<ref>PMID:12503095</ref> Defects in SHH are the cause of holoprosencephaly type 3 (HPE3) [MIM:[http://omim.org/entry/142945 142945]]. Holoprosencephaly (HPE) [MIM:[http://omim.org/entry/236100 236100]] is the most common structural anomaly of the brain, in which the developing forebrain fails to correctly separate into right and left hemispheres. Holoprosencephaly is genetically heterogeneous and associated with several distinct facies and phenotypic variability. The majority of HPE3 cases are apparently sporadic, although clear examples of autosomal dominant inheritance have been described. Interestingly, up to 30% of obligate carriers of HPE3 gene in autosomal dominant pedigrees are clinically unaffected.<ref>PMID:8896572</ref><ref>PMID:9302262</ref><ref>PMID:10441331</ref><ref>PMID:10556296</ref><ref>PMID:11479728</ref><ref>PMID:15107988</ref><ref>PMID:15221788</ref><ref>PMID:15942952</ref><ref>PMID:15942953</ref><ref>PMID:16282375</ref><ref>PMID:17001669</ref><ref>PMID:19603532</ref> Defects in SHH are a cause of solitary median maxillary central incisor (SMMCI) [MIM:[http://omim.org/entry/147250 147250]]. SMMCI is a rare dental anomaly characterized by the congenital absence of one maxillary central incisor.<ref>PMID:11471164</ref><ref>PMID:15103725</ref> Defects in SHH are the cause of triphalangeal thumb-polysyndactyly syndrome (TPTPS) [MIM:[http://omim.org/entry/174500 174500]]. TPTPS is an autosomal dominant syndrome characterized by a wide spectrum of pre- and post-axial abnormalities due to altered SHH expression pattern during limb development. TPTPS mutations have been mapped to the 7q36 locus in the LMBR1 gene which contains in its intron 5 a long-range cis-regulatory element of SHH expression.<ref>PMID:12837695</ref>
		+
		+	==Function==
		+	[[http://www.uniprot.org/uniprot/SHH_HUMAN SHH_HUMAN]] Binds to the patched (PTC) receptor, which functions in association with smoothened (SMO), to activate the transcription of target genes. In the absence of SHH, PTC represses the constitutive signaling activity of SMO. Also regulates another target, the gli oncogene. Intercellular signal essential for a variety of patterning events during development: signal produced by the notochord that induces ventral cell fate in the neural tube and somites, and the polarizing signal for patterning of the anterior-posterior axis of the developing limb bud. Displays both floor plate- and motor neuron-inducing activity. The threshold concentration of N-product required for motor neuron induction is 5-fold lower than that required for floor plate induction (By similarity).

	==About this Structure==		==About this Structure==
-	~~3M1N~~ is a 2 ~~chains~~ structure with ~~sequences~~ 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=3M1N OCA].	+	[[3m1n]] 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=3M1N OCA].

	==Reference==		==Reference==
-	<ref group="xtra">PMID:~~10753901~~</ref><references group="xtra"/>	+	<ref group="xtra">PMID:010753901</ref><references group="xtra"/><references/>
	[[Category: Homo sapiens]]		[[Category: Homo sapiens]]
	[[Category: Boriack-Sjodin, P A.]]		[[Category: Boriack-Sjodin, P A.]]
Line 49:		Line 36:
	[[Category: Sulfate ion]]		[[Category: Sulfate ion]]
	[[Category: Zinc ion]]		[[Category: Zinc ion]]
-
-	''Page seeded by [http://oca.weizmann.ac.il/oca OCA ] on Wed Mar 17 09:28:12 2010''

OCA: New page: {{Seed}} 200px