6p7j - Revision history

OCA at 07:24, 11 October 2023

OCA — Wed, 11 Oct 2023 07:24:21 GMT

←Older revision		Revision as of 07:24, 11 October 2023
Line 3:		Line 3:
	<StructureSection load='6p7j' size='340' side='right'caption='[[6p7j]], [[Resolution\|resolution]] 3.50Å' scene=''>		<StructureSection load='6p7j' size='340' side='right'caption='[[6p7j]], [[Resolution\|resolution]] 3.50Å' scene=''>
	== Structural highlights ==		== Structural highlights ==
-	<table><tr><td colspan='2'>[[6p7j]] is a 1 chain structure. Full crystallographic information is available from [http://oca.weizmann.ac.il/oca-bin/ocashort?id=6P7J OCA]. For a <b>guided tour on the structure components</b> use [~~http~~://~~oca~~.~~weizmann.ac.il/oca-docs~~/fgij/fg.htm?mol=6P7J FirstGlance]. <br>	+	<table><tr><td colspan='2'>[[6p7j]] 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=6P7J OCA]. For a <b>guided tour on the structure components</b> use [https://proteopedia.org/fgij/fg.htm?mol=6P7J FirstGlance]. <br>
-	</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=6p7j FirstGlance], [http://oca.weizmann.ac.il/oca-bin/ocaids?id=6p7j OCA], [~~http~~://pdbe.org/6p7j PDBe], [~~http~~://www.rcsb.org/pdb/explore.do?structureId=6p7j RCSB], [~~http~~://www.ebi.ac.uk/pdbsum/6p7j PDBsum], [~~http~~://prosat.h-its.org/prosat/prosatexe?pdbcode=6p7j ProSAT]</span></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]] 3.501Å</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=6p7j FirstGlance], [http://oca.weizmann.ac.il/oca-bin/ocaids?id=6p7j OCA], [https://pdbe.org/6p7j PDBe], [https://www.rcsb.org/pdb/explore.do?structureId=6p7j RCSB], [https://www.ebi.ac.uk/pdbsum/6p7j PDBsum], [https://prosat.h-its.org/prosat/prosatexe?pdbcode=6p7j ProSAT]</span></td></tr>
	</table>		</table>
	== Disease ==		== Disease ==
-	[~~[http~~://www.uniprot.org/uniprot/TGFB1_HUMAN TGFB1_HUMAN]] Defects in TGFB1 are the cause of Camurati-Engelmann disease (CE) [MIM:[~~http~~://omim.org/entry/131300 131300]]; also known as progressive diaphyseal dysplasia 1 (DPD1). CE is an autosomal dominant disorder characterized by hyperostosis and sclerosis of the diaphyses of long bones. The disease typically presents in early childhood with pain, muscular weakness and waddling gait, and in some cases other features such as exophthalmos, facial paralysis, hearing difficulties and loss of vision.<ref>PMID:10973241</ref> <ref>PMID:11062463</ref> <ref>PMID:12493741</ref> <ref>PMID:12843182</ref> <ref>PMID:15103729</ref>	+	[https://www.uniprot.org/uniprot/TGFB1_HUMAN TGFB1_HUMAN] Defects in TGFB1 are the cause of Camurati-Engelmann disease (CE) [MIM:[https://omim.org/entry/131300 131300]; also known as progressive diaphyseal dysplasia 1 (DPD1). CE is an autosomal dominant disorder characterized by hyperostosis and sclerosis of the diaphyses of long bones. The disease typically presents in early childhood with pain, muscular weakness and waddling gait, and in some cases other features such as exophthalmos, facial paralysis, hearing difficulties and loss of vision.<ref>PMID:10973241</ref> <ref>PMID:11062463</ref> <ref>PMID:12493741</ref> <ref>PMID:12843182</ref> <ref>PMID:15103729</ref>
	== Function ==		== Function ==
-	[~~[http~~://www.uniprot.org/uniprot/TGFB1_HUMAN TGFB1_HUMAN]] Multifunctional protein that controls proliferation, differentiation and other functions in many cell types. Many cells synthesize TGFB1 and have specific receptors for it. It positively and negatively regulates many other growth factors. It plays an important role in bone remodeling as it is a potent stimulator of osteoblastic bone formation, causing chemotaxis, proliferation and differentiation in committed osteoblasts.	+	[https://www.uniprot.org/uniprot/TGFB1_HUMAN TGFB1_HUMAN] Multifunctional protein that controls proliferation, differentiation and other functions in many cell types. Many cells synthesize TGFB1 and have specific receptors for it. It positively and negatively regulates many other growth factors. It plays an important role in bone remodeling as it is a potent stimulator of osteoblastic bone formation, causing chemotaxis, proliferation and differentiation in committed osteoblasts.
-		+
-	~~==See Also==~~	+
-	*[[Journal:IUCrJ:S205225251901707X\|Journal:IUCrJ:S205225251901707X]]	+
	== References ==		== References ==
	<references/>		<references/>
	__TOC__		__TOC__
	</StructureSection>		</StructureSection>
		+	[[Category: Homo sapiens]]
	[[Category: Large Structures]]		[[Category: Large Structures]]
-	[[Category: Snell~~, E H~~]]	+	[[Category: Snell EH]]
-	[[Category: Snell~~, M E~~]]	+	[[Category: Snell ME]]
-	[[Category: Stachowski~~, T R]]~~	+	[[Category: Stachowski TR]]
-	~~[[Category: Cancer]]~~	+
-	~~[[Category: Cytokine]]~~	+
-	~~[[Category: Latency]]~~	+
-	~~[[Category: Pro-domain]]~~	+
-	~~[[Category: Transforming~~]]	+

OCA at 07:22, 11 March 2020

OCA — Wed, 11 Mar 2020 07:22:26 GMT

←Older revision		Revision as of 07:22, 11 March 2020
Line 1:		Line 1:
-	'''Unreleased structure'''

-	~~The entry~~ 6p7j is ~~ON HOLD~~ ~~until Paper Publication~~	+	==Crystal structure of Latency Associated Peptide unbound to TGF-beta1==
		+	<StructureSection load='6p7j' size='340' side='right'caption='[[6p7j]], [[Resolution\|resolution]] 3.50Å' scene=''>
		+	== Structural highlights ==
		+	<table><tr><td colspan='2'>[[6p7j]] is a 1 chain structure. Full crystallographic information is available from [http://oca.weizmann.ac.il/oca-bin/ocashort?id=6P7J OCA]. For a <b>guided tour on the structure components</b> use [http://oca.weizmann.ac.il/oca-docs/fgij/fg.htm?mol=6P7J FirstGlance]. <br>
		+	</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=6p7j FirstGlance], [http://oca.weizmann.ac.il/oca-bin/ocaids?id=6p7j OCA], [http://pdbe.org/6p7j PDBe], [http://www.rcsb.org/pdb/explore.do?structureId=6p7j RCSB], [http://www.ebi.ac.uk/pdbsum/6p7j PDBsum], [http://prosat.h-its.org/prosat/prosatexe?pdbcode=6p7j ProSAT]</span></td></tr>
		+	</table>
		+	== Disease ==
		+	[[http://www.uniprot.org/uniprot/TGFB1_HUMAN TGFB1_HUMAN]] Defects in TGFB1 are the cause of Camurati-Engelmann disease (CE) [MIM:[http://omim.org/entry/131300 131300]]; also known as progressive diaphyseal dysplasia 1 (DPD1). CE is an autosomal dominant disorder characterized by hyperostosis and sclerosis of the diaphyses of long bones. The disease typically presents in early childhood with pain, muscular weakness and waddling gait, and in some cases other features such as exophthalmos, facial paralysis, hearing difficulties and loss of vision.<ref>PMID:10973241</ref> <ref>PMID:11062463</ref> <ref>PMID:12493741</ref> <ref>PMID:12843182</ref> <ref>PMID:15103729</ref>
		+	== Function ==
		+	[[http://www.uniprot.org/uniprot/TGFB1_HUMAN TGFB1_HUMAN]] Multifunctional protein that controls proliferation, differentiation and other functions in many cell types. Many cells synthesize TGFB1 and have specific receptors for it. It positively and negatively regulates many other growth factors. It plays an important role in bone remodeling as it is a potent stimulator of osteoblastic bone formation, causing chemotaxis, proliferation and differentiation in committed osteoblasts.

-	~~Authors~~:	+	==See Also==
-		+	*[[Journal:IUCrJ:S205225251901707X\|Journal:IUCrJ:S205225251901707X]]
-	~~Description:~~	+	== References ==
-	[[Category: ~~Unreleased~~ Structures]]	+	<references/>
		+	__TOC__
		+	</StructureSection>
		+	[[Category: Large Structures]]
		+	[[Category: Snell, E H]]
		+	[[Category: Snell, M E]]
		+	[[Category: Stachowski, T R]]
		+	[[Category: Cancer]]
		+	[[Category: Cytokine]]
		+	[[Category: Latency]]
		+	[[Category: Pro-domain]]
		+	[[Category: Transforming]]

OCA at 04:15, 19 June 2019

OCA — Wed, 19 Jun 2019 04:15:06 GMT

←Older revision		Revision as of 04:15, 19 June 2019
Line 1:		Line 1:
	'''Unreleased structure'''		'''Unreleased structure'''

-	The entry 6p7j is ON HOLD	+	The entry 6p7j is ON HOLD until Paper Publication

	Authors:		Authors:

OCA: Protected "6p7j" [edit=sysop:move=sysop]

OCA — Wed, 12 Jun 2019 04:07:13 GMT

Protected "6p7j" [edit=sysop:move=sysop]

←Older revision

Revision as of 04:07, 12 June 2019

OCA: New page: '''Unreleased structure''' The entry 6p7j is ON HOLD Authors: Description: Category: Unreleased Structures

OCA — Wed, 12 Jun 2019 04:07:10 GMT

New page: '''Unreleased structure''' The entry 6p7j is ON HOLD Authors: Description: Category: Unreleased Structures

New page

'''Unreleased structure'''

The entry 6p7j is ON HOLD

Authors:

Description:
[[Category: Unreleased Structures]]