7jif - Revision history

OCA at 15:03, 18 October 2023

OCA — Wed, 18 Oct 2023 15:03:34 GMT

←Older revision		Revision as of 15:03, 18 October 2023
Line 3:		Line 3:
	<StructureSection load='7jif' size='340' side='right'caption='[[7jif]], [[Resolution\|resolution]] 1.76Å' scene=''>		<StructureSection load='7jif' size='340' side='right'caption='[[7jif]], [[Resolution\|resolution]] 1.76Å' scene=''>
	== Structural highlights ==		== Structural highlights ==
-	<table><tr><td colspan='2'>[[7jif]] is a 1 chain structure. Full crystallographic information is available from [http://oca.weizmann.ac.il/oca-bin/ocashort?id=7JIF OCA]. For a <b>guided tour on the structure components</b> use [https://proteopedia.org/fgij/fg.htm?mol=7JIF FirstGlance]. <br>	+	<table><tr><td colspan='2'>[[7jif]] 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=7JIF OCA]. For a <b>guided tour on the structure components</b> use [https://proteopedia.org/fgij/fg.htm?mol=7JIF FirstGlance]. <br>
-	</td></tr><tr id='ligand'><td class="sblockLbl"><b>[[Ligand\|Ligands:]]</b></td><td class="sblockDat" id="ligandDat"><scene name='pdbligand=GNP:PHOSPHOAMINOPHOSPHONIC+ACID-GUANYLATE+ESTER'>GNP</scene>, <scene name='pdbligand=GOL:GLYCEROL'>GOL</scene>, <scene name='pdbligand=MG:MAGNESIUM+ION'>MG</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]] 1.757Å</td></tr>
		+	<tr id='ligand'><td class="sblockLbl"><b>[[Ligand\|Ligands:]]</b></td><td class="sblockDat" id="ligandDat"><scene name='pdbligand=GNP:PHOSPHOAMINOPHOSPHONIC+ACID-GUANYLATE+ESTER'>GNP</scene>, <scene name='pdbligand=GOL:GLYCEROL'>GOL</scene>, <scene name='pdbligand=MG:MAGNESIUM+ION'>MG</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=7jif FirstGlance], [http://oca.weizmann.ac.il/oca-bin/ocaids?id=7jif OCA], [https://pdbe.org/7jif PDBe], [https://www.rcsb.org/pdb/explore.do?structureId=7jif RCSB], [https://www.ebi.ac.uk/pdbsum/7jif PDBsum], [https://prosat.h-its.org/prosat/prosatexe?pdbcode=7jif 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=7jif FirstGlance], [http://oca.weizmann.ac.il/oca-bin/ocaids?id=7jif OCA], [https://pdbe.org/7jif PDBe], [https://www.rcsb.org/pdb/explore.do?structureId=7jif RCSB], [https://www.ebi.ac.uk/pdbsum/7jif PDBsum], [https://prosat.h-its.org/prosat/prosatexe?pdbcode=7jif ProSAT]</span></td></tr>
	</table>		</table>
	== Disease ==		== Disease ==
-	[[https://www.uniprot.org/uniprot/RASH_HUMAN RASH_HUMAN]] Defects in HRAS are the cause of faciocutaneoskeletal syndrome (FCSS) [MIM:[https://omim.org/entry/218040 218040]]. A rare condition characterized by prenatally increased growth, postnatal growth deficiency, mental retardation, distinctive facial appearance, cardiovascular abnormalities (typically pulmonic stenosis, hypertrophic cardiomyopathy and/or atrial tachycardia), tumor predisposition, skin and musculoskeletal abnormalities.<ref>PMID:16170316</ref> <ref>PMID:16329078</ref> <ref>PMID:16443854</ref> <ref>PMID:17054105</ref> <ref>PMID:18247425</ref> <ref>PMID:18039947</ref> <ref>PMID:19995790</ref> Defects in HRAS are the cause of congenital myopathy with excess of muscle spindles (CMEMS) [MIM:[https://omim.org/entry/218040 218040]]. CMEMS is a variant of Costello syndrome.<ref>PMID:17412879</ref> Defects in HRAS may be a cause of susceptibility to Hurthle cell thyroid carcinoma (HCTC) [MIM:[https://omim.org/entry/607464 607464]]. Hurthle cell thyroid carcinoma accounts for approximately 3% of all thyroid cancers. Although they are classified as variants of follicular neoplasms, they are more often multifocal and somewhat more aggressive and are less likely to take up iodine than are other follicular neoplasms. Note=Mutations which change positions 12, 13 or 61 activate the potential of HRAS to transform cultured cells and are implicated in a variety of human tumors. Defects in HRAS are a cause of susceptibility to bladder cancer (BLC) [MIM:[https://omim.org/entry/109800 109800]]. A malignancy originating in tissues of the urinary bladder. It often presents with multiple tumors appearing at different times and at different sites in the bladder. Most bladder cancers are transitional cell carcinomas. They begin in cells that normally make up the inner lining of the bladder. Other types of bladder cancer include squamous cell carcinoma (cancer that begins in thin, flat cells) and adenocarcinoma (cancer that begins in cells that make and release mucus and other fluids). Bladder cancer is a complex disorder with both genetic and environmental influences. Note=Defects in HRAS are the cause of oral squamous cell carcinoma (OSCC).<ref>PMID:1459726</ref> Defects in HRAS are the cause of Schimmelpenning-Feuerstein-Mims syndrome (SFM) [MIM:[https://omim.org/entry/163200 163200]]. A disease characterized by sebaceous nevi, often on the face, associated with variable ipsilateral abnormalities of the central nervous system, ocular anomalies, and skeletal defects. Many oral manifestations have been reported, not only including hypoplastic and malformed teeth, and mucosal papillomatosis, but also ankyloglossia, hemihyperplastic tongue, intraoral nevus, giant cell granuloma, ameloblastoma, bone cysts, follicular cysts, oligodontia, and odontodysplasia. Sebaceous nevi follow the lines of Blaschko and these can continue as linear intraoral lesions, as in mucosal papillomatosis.<ref>PMID:22683711</ref>	+	[https://www.uniprot.org/uniprot/RASH_HUMAN RASH_HUMAN] Defects in HRAS are the cause of faciocutaneoskeletal syndrome (FCSS) [MIM:[https://omim.org/entry/218040 218040]. A rare condition characterized by prenatally increased growth, postnatal growth deficiency, mental retardation, distinctive facial appearance, cardiovascular abnormalities (typically pulmonic stenosis, hypertrophic cardiomyopathy and/or atrial tachycardia), tumor predisposition, skin and musculoskeletal abnormalities.<ref>PMID:16170316</ref> <ref>PMID:16329078</ref> <ref>PMID:16443854</ref> <ref>PMID:17054105</ref> <ref>PMID:18247425</ref> <ref>PMID:18039947</ref> <ref>PMID:19995790</ref> Defects in HRAS are the cause of congenital myopathy with excess of muscle spindles (CMEMS) [MIM:[https://omim.org/entry/218040 218040]. CMEMS is a variant of Costello syndrome.<ref>PMID:17412879</ref> Defects in HRAS may be a cause of susceptibility to Hurthle cell thyroid carcinoma (HCTC) [MIM:[https://omim.org/entry/607464 607464]. Hurthle cell thyroid carcinoma accounts for approximately 3% of all thyroid cancers. Although they are classified as variants of follicular neoplasms, they are more often multifocal and somewhat more aggressive and are less likely to take up iodine than are other follicular neoplasms. Note=Mutations which change positions 12, 13 or 61 activate the potential of HRAS to transform cultured cells and are implicated in a variety of human tumors. Defects in HRAS are a cause of susceptibility to bladder cancer (BLC) [MIM:[https://omim.org/entry/109800 109800]. A malignancy originating in tissues of the urinary bladder. It often presents with multiple tumors appearing at different times and at different sites in the bladder. Most bladder cancers are transitional cell carcinomas. They begin in cells that normally make up the inner lining of the bladder. Other types of bladder cancer include squamous cell carcinoma (cancer that begins in thin, flat cells) and adenocarcinoma (cancer that begins in cells that make and release mucus and other fluids). Bladder cancer is a complex disorder with both genetic and environmental influences. Note=Defects in HRAS are the cause of oral squamous cell carcinoma (OSCC).<ref>PMID:1459726</ref> Defects in HRAS are the cause of Schimmelpenning-Feuerstein-Mims syndrome (SFM) [MIM:[https://omim.org/entry/163200 163200]. A disease characterized by sebaceous nevi, often on the face, associated with variable ipsilateral abnormalities of the central nervous system, ocular anomalies, and skeletal defects. Many oral manifestations have been reported, not only including hypoplastic and malformed teeth, and mucosal papillomatosis, but also ankyloglossia, hemihyperplastic tongue, intraoral nevus, giant cell granuloma, ameloblastoma, bone cysts, follicular cysts, oligodontia, and odontodysplasia. Sebaceous nevi follow the lines of Blaschko and these can continue as linear intraoral lesions, as in mucosal papillomatosis.<ref>PMID:22683711</ref>
	== Function ==		== Function ==
-	[[https://www.uniprot.org/uniprot/RASH_HUMAN RASH_HUMAN]] Ras proteins bind GDP/GTP and possess intrinsic GTPase activity.<ref>PMID:14500341</ref> <ref>PMID:9020151</ref> <ref>PMID:12740440</ref>	+	[https://www.uniprot.org/uniprot/RASH_HUMAN RASH_HUMAN] Ras proteins bind GDP/GTP and possess intrinsic GTPase activity.<ref>PMID:14500341</ref> <ref>PMID:9020151</ref> <ref>PMID:12740440</ref>
	<div style="background-color:#fffaf0;">		<div style="background-color:#fffaf0;">
	== Publication Abstract from PubMed ==		== Publication Abstract from PubMed ==
Line 20:		Line 21:
	</div>		</div>
	<div class="pdbe-citations 7jif" style="background-color:#fffaf0;"></div>		<div class="pdbe-citations 7jif" style="background-color:#fffaf0;"></div>
		+
		+	==See Also==
		+	*[[GTPase Hras 3D structures\|GTPase Hras 3D structures]]
	== References ==		== References ==
	<references/>		<references/>
	__TOC__		__TOC__
	</StructureSection>		</StructureSection>
		+	[[Category: Homo sapiens]]
	[[Category: Large Structures]]		[[Category: Large Structures]]
-	[[Category: Haigis~~, K M~~]]	+	[[Category: Haigis KM]]
-	[[Category: Johnson~~, C W]]~~	+	[[Category: Johnson CW]]
-	~~[[Category: Mutant cancer gtpase]]~~	+
-	~~[[Category: Oncoprotein~~]]	+

OCA at 07:18, 9 March 2022

OCA — Wed, 09 Mar 2022 07:18:28 GMT

←Older revision		Revision as of 07:18, 9 March 2022
Line 1:		Line 1:

	==HRAS A59T GppNHp==		==HRAS A59T GppNHp==
-	<StructureSection load='7jif' size='340' side='right'caption='[[7jif]]' scene=''>	+	<StructureSection load='7jif' size='340' side='right'caption='[[7jif]], [[Resolution\|resolution]] 1.76Å' scene=''>
	== Structural highlights ==		== Structural highlights ==
-	<table><tr><td colspan='2'>Full crystallographic information is available from [http://oca.weizmann.ac.il/oca-bin/ocashort?id=7JIF OCA]. For a <b>guided tour on the structure components</b> use [https://proteopedia.org/fgij/fg.htm?mol=7JIF FirstGlance]. <br>	+	<table><tr><td colspan='2'>[[7jif]] is a 1 chain structure. Full crystallographic information is available from [http://oca.weizmann.ac.il/oca-bin/ocashort?id=7JIF OCA]. For a <b>guided tour on the structure components</b> use [https://proteopedia.org/fgij/fg.htm?mol=7JIF FirstGlance]. <br>
-	</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=7jif FirstGlance], [http://oca.weizmann.ac.il/oca-bin/ocaids?id=7jif OCA], [https://pdbe.org/7jif PDBe], [https://www.rcsb.org/pdb/explore.do?structureId=7jif RCSB], [https://www.ebi.ac.uk/pdbsum/7jif PDBsum], [https://prosat.h-its.org/prosat/prosatexe?pdbcode=7jif ProSAT]</span></td></tr>	+	</td></tr><tr id='ligand'><td class="sblockLbl"><b>[[Ligand\|Ligands:]]</b></td><td class="sblockDat" id="ligandDat"><scene name='pdbligand=GNP:PHOSPHOAMINOPHOSPHONIC+ACID-GUANYLATE+ESTER'>GNP</scene>, <scene name='pdbligand=GOL:GLYCEROL'>GOL</scene>, <scene name='pdbligand=MG:MAGNESIUM+ION'>MG</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=7jif FirstGlance], [http://oca.weizmann.ac.il/oca-bin/ocaids?id=7jif OCA], [https://pdbe.org/7jif PDBe], [https://www.rcsb.org/pdb/explore.do?structureId=7jif RCSB], [https://www.ebi.ac.uk/pdbsum/7jif PDBsum], [https://prosat.h-its.org/prosat/prosatexe?pdbcode=7jif ProSAT]</span></td></tr>
	</table>		</table>
		+	== Disease ==
		+	[[https://www.uniprot.org/uniprot/RASH_HUMAN RASH_HUMAN]] Defects in HRAS are the cause of faciocutaneoskeletal syndrome (FCSS) [MIM:[https://omim.org/entry/218040 218040]]. A rare condition characterized by prenatally increased growth, postnatal growth deficiency, mental retardation, distinctive facial appearance, cardiovascular abnormalities (typically pulmonic stenosis, hypertrophic cardiomyopathy and/or atrial tachycardia), tumor predisposition, skin and musculoskeletal abnormalities.<ref>PMID:16170316</ref> <ref>PMID:16329078</ref> <ref>PMID:16443854</ref> <ref>PMID:17054105</ref> <ref>PMID:18247425</ref> <ref>PMID:18039947</ref> <ref>PMID:19995790</ref> Defects in HRAS are the cause of congenital myopathy with excess of muscle spindles (CMEMS) [MIM:[https://omim.org/entry/218040 218040]]. CMEMS is a variant of Costello syndrome.<ref>PMID:17412879</ref> Defects in HRAS may be a cause of susceptibility to Hurthle cell thyroid carcinoma (HCTC) [MIM:[https://omim.org/entry/607464 607464]]. Hurthle cell thyroid carcinoma accounts for approximately 3% of all thyroid cancers. Although they are classified as variants of follicular neoplasms, they are more often multifocal and somewhat more aggressive and are less likely to take up iodine than are other follicular neoplasms. Note=Mutations which change positions 12, 13 or 61 activate the potential of HRAS to transform cultured cells and are implicated in a variety of human tumors. Defects in HRAS are a cause of susceptibility to bladder cancer (BLC) [MIM:[https://omim.org/entry/109800 109800]]. A malignancy originating in tissues of the urinary bladder. It often presents with multiple tumors appearing at different times and at different sites in the bladder. Most bladder cancers are transitional cell carcinomas. They begin in cells that normally make up the inner lining of the bladder. Other types of bladder cancer include squamous cell carcinoma (cancer that begins in thin, flat cells) and adenocarcinoma (cancer that begins in cells that make and release mucus and other fluids). Bladder cancer is a complex disorder with both genetic and environmental influences. Note=Defects in HRAS are the cause of oral squamous cell carcinoma (OSCC).<ref>PMID:1459726</ref> Defects in HRAS are the cause of Schimmelpenning-Feuerstein-Mims syndrome (SFM) [MIM:[https://omim.org/entry/163200 163200]]. A disease characterized by sebaceous nevi, often on the face, associated with variable ipsilateral abnormalities of the central nervous system, ocular anomalies, and skeletal defects. Many oral manifestations have been reported, not only including hypoplastic and malformed teeth, and mucosal papillomatosis, but also ankyloglossia, hemihyperplastic tongue, intraoral nevus, giant cell granuloma, ameloblastoma, bone cysts, follicular cysts, oligodontia, and odontodysplasia. Sebaceous nevi follow the lines of Blaschko and these can continue as linear intraoral lesions, as in mucosal papillomatosis.<ref>PMID:22683711</ref>
		+	== Function ==
		+	[[https://www.uniprot.org/uniprot/RASH_HUMAN RASH_HUMAN]] Ras proteins bind GDP/GTP and possess intrinsic GTPase activity.<ref>PMID:14500341</ref> <ref>PMID:9020151</ref> <ref>PMID:12740440</ref>
		+	<div style="background-color:#fffaf0;">
		+	== Publication Abstract from PubMed ==
		+	A unifying feature of the RAS superfamily is a conserved GTPase cycle by which these proteins transition between active and inactive states. We demonstrate that autophosphorylation of some GTPases is an intrinsic regulatory mechanism that reduces nucleotide hydrolysis and enhances nucleotide exchange, altering the on/off switch that forms the basis for their signaling functions. Using X-ray crystallography, nuclear magnetic resonance spectroscopy, binding assays, and molecular dynamics on autophosphorylated mutants of H-RAS and K-RAS, we show that phosphoryl transfer from GTP requires dynamic movement of the switch II region and that autophosphorylation promotes nucleotide exchange by opening the active site and extracting the stabilizing Mg(2+). Finally, we demonstrate that autophosphorylated K-RAS exhibits altered effector interactions, including a reduced affinity for RAF proteins in mammalian cells. Thus, autophosphorylation leads to altered active site dynamics and effector interaction properties, creating a pool of GTPases that are functionally distinct from their non-phosphorylated counterparts.
		+
		+	Regulation of GTPase function by autophosphorylation.,Johnson CW, Seo HS, Terrell EM, Yang MH, KleinJan F, Gebregiworgis T, Gasmi-Seabrook GMC, Geffken EA, Lakhani J, Song K, Bashyal P, Popow O, Paulo JA, Liu A, Mattos C, Marshall CB, Ikura M, Morrison DK, Dhe-Paganon S, Haigis KM Mol Cell. 2022 Mar 3;82(5):950-968.e14. doi: 10.1016/j.molcel.2022.02.011. Epub, 2022 Feb 23. PMID:35202574<ref>PMID:35202574</ref>
		+
		+	From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine.<br>
		+	</div>
		+	<div class="pdbe-citations 7jif" style="background-color:#fffaf0;"></div>
		+	== References ==
		+	<references/>
	__TOC__		__TOC__
	</StructureSection>		</StructureSection>
	[[Category: Large Structures]]		[[Category: Large Structures]]
-	[[Category: Haigis KM]]	+	[[Category: Haigis, K M]]
-	[[Category: Johnson CW]]	+	[[Category: Johnson, C W]]
		+	[[Category: Mutant cancer gtpase]]
		+	[[Category: Oncoprotein]]

OCA at 06:16, 2 March 2022

OCA — Wed, 02 Mar 2022 06:16:52 GMT

←Older revision		Revision as of 06:16, 2 March 2022
Line 1:		Line 1:
-	'''Unreleased structure'''

-	~~The entry~~ 7jif ~~is ON HOLD~~	+	==HRAS A59T GppNHp==
-		+	<StructureSection load='7jif' size='340' side='right'caption='[[7jif]]' scene=''>
-	~~Authors~~: ~~Johnson~~, C.W., ~~Haigis~~, K.M.	+	== Structural highlights ==
-		+	<table><tr><td colspan='2'>Full crystallographic information is available from [http://oca.weizmann.ac.il/oca-bin/ocashort?id=7JIF OCA]. For a <b>guided tour on the structure components</b> use [https://proteopedia.org/fgij/fg.htm?mol=7JIF FirstGlance]. <br>
-	~~Description: HRAS A59T GppNHp~~	+	</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=7jif FirstGlance], [http://oca.weizmann.ac.il/oca-bin/ocaids?id=7jif OCA], [https://pdbe.org/7jif PDBe], [https://www.rcsb.org/pdb/explore.do?structureId=7jif RCSB], [https://www.ebi.ac.uk/pdbsum/7jif PDBsum], [https://prosat.h-its.org/prosat/prosatexe?pdbcode=7jif ProSAT]</span></td></tr>
-	[[Category: ~~Unreleased~~ Structures]]	+	</table>
-	[[Category: Haigis~~, K.M~~]]	+	__TOC__
-	[[Category: Johnson~~, C.W~~]]	+	</StructureSection>
		+	[[Category: Large Structures]]
		+	[[Category: Haigis KM]]
		+	[[Category: Johnson CW]]

OCA at 08:26, 12 January 2022

OCA — Wed, 12 Jan 2022 08:26:09 GMT

←Older revision		Revision as of 08:26, 12 January 2022
Line 1:		Line 1:
	'''Unreleased structure'''		'''Unreleased structure'''

-	The entry 7jif is ON HOLD ~~until Jan 23 2023~~	+	The entry 7jif is ON HOLD

	Authors: Johnson, C.W., Haigis, K.M.		Authors: Johnson, C.W., Haigis, K.M.

OCA at 13:34, 17 June 2021

OCA — Thu, 17 Jun 2021 13:34:45 GMT

←Older revision		Revision as of 13:34, 17 June 2021
Line 1:		Line 1:
	'''Unreleased structure'''		'''Unreleased structure'''

-	The entry 7jif is ON HOLD until ~~Jul~~ 23 ~~2022~~	+	The entry 7jif is ON HOLD until Jan 23 2023

	Authors: Johnson, C.W., Haigis, K.M.		Authors: Johnson, C.W., Haigis, K.M.

OCA at 05:18, 2 September 2020

OCA — Wed, 02 Sep 2020 05:18:47 GMT

←Older revision		Revision as of 05:18, 2 September 2020
Line 1:		Line 1:
	'''Unreleased structure'''		'''Unreleased structure'''

-	The entry 7jif is ON HOLD	+	The entry 7jif is ON HOLD until Jul 23 2022

	Authors: Johnson, C.W., Haigis, K.M.		Authors: Johnson, C.W., Haigis, K.M.

OCA: Protected "7jif" [edit=sysop:move=sysop]

OCA — Wed, 29 Jul 2020 09:52:05 GMT

Protected "7jif" [edit=sysop:move=sysop]

←Older revision

Revision as of 09:52, 29 July 2020

OCA: New page: '''Unreleased structure''' The entry 7jif is ON HOLD Authors: Johnson, C.W., Haigis, K.M. Description: HRAS A59T GppNHp Category: Unreleased Structures Category: Haigis, K.M [[...

OCA — Wed, 29 Jul 2020 09:52:03 GMT

New page: '''Unreleased structure''' The entry 7jif is ON HOLD Authors: Johnson, C.W., Haigis, K.M. Description: HRAS A59T GppNHp Category: Unreleased Structures Category: Haigis, K.M [[...

New page

'''Unreleased structure'''

The entry 7jif is ON HOLD

Authors: Johnson, C.W., Haigis, K.M.

Description: HRAS A59T GppNHp
[[Category: Unreleased Structures]]
[[Category: Haigis, K.M]]
[[Category: Johnson, C.W]]