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==Crystal structure of a RAS p21 protein activator (RASA1) from Homo sapiens at 2.25 A resolution==
==Crystal structure of a RAS p21 protein activator (RASA1) from Homo sapiens at 2.25 A resolution==
<StructureSection load='4fss' size='340' side='right' caption='[[4fss]], [[Resolution|resolution]] 2.25&Aring;' scene=''>
<StructureSection load='4fss' size='340' side='right'caption='[[4fss]], [[Resolution|resolution]] 2.25&Aring;' scene=''>
== Structural highlights ==
== Structural highlights ==
<table><tr><td colspan='2'>[[4fss]] is a 3 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=4FSS OCA]. For a <b>guided tour on the structure components</b> use [http://oca.weizmann.ac.il/oca-docs/fgij/fg.htm?mol=4FSS FirstGlance]. <br>
<table><tr><td colspan='2'>[[4fss]] is a 3 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=4FSS OCA]. For a <b>guided tour on the structure components</b> use [https://proteopedia.org/fgij/fg.htm?mol=4FSS FirstGlance]. <br>
</td></tr><tr id='ligand'><td class="sblockLbl"><b>[[Ligand|Ligands:]]</b></td><td class="sblockDat"><scene name='pdbligand=CL:CHLORIDE+ION'>CL</scene>, <scene name='pdbligand=GOL:GLYCEROL'>GOL</scene>, <scene name='pdbligand=PO4:PHOSPHATE+ION'>PO4</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]] 2.25&#8491;</td></tr>
<tr id='NonStdRes'><td class="sblockLbl"><b>[[Non-Standard_Residue|NonStd Res:]]</b></td><td class="sblockDat"><scene name='pdbligand=MSE:SELENOMETHIONINE'>MSE</scene></td></tr>
<tr id='ligand'><td class="sblockLbl"><b>[[Ligand|Ligands:]]</b></td><td class="sblockDat" id="ligandDat"><scene name='pdbligand=CL:CHLORIDE+ION'>CL</scene>, <scene name='pdbligand=GOL:GLYCEROL'>GOL</scene>, <scene name='pdbligand=MSE:SELENOMETHIONINE'>MSE</scene>, <scene name='pdbligand=PO4:PHOSPHATE+ION'>PO4</scene></td></tr>
<tr id='gene'><td class="sblockLbl"><b>[[Gene|Gene:]]</b></td><td class="sblockDat">BC033015, RASA, RASA1 ([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'>[https://proteopedia.org/fgij/fg.htm?mol=4fss FirstGlance], [http://oca.weizmann.ac.il/oca-bin/ocaids?id=4fss OCA], [https://pdbe.org/4fss PDBe], [https://www.rcsb.org/pdb/explore.do?structureId=4fss RCSB], [https://www.ebi.ac.uk/pdbsum/4fss PDBsum], [https://prosat.h-its.org/prosat/prosatexe?pdbcode=4fss ProSAT]</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=4fss FirstGlance], [http://oca.weizmann.ac.il/oca-bin/ocaids?id=4fss OCA], [http://pdbe.org/4fss PDBe], [http://www.rcsb.org/pdb/explore.do?structureId=4fss RCSB], [http://www.ebi.ac.uk/pdbsum/4fss PDBsum], [http://prosat.h-its.org/prosat/prosatexe?pdbcode=4fss ProSAT]</span></td></tr>
</table>
</table>
== Disease ==
== Disease ==
[[http://www.uniprot.org/uniprot/RASA1_HUMAN RASA1_HUMAN]] Note=Mutations in the SH2 domain of RASA seem to be oncogenic and cause basal cell carcinomas.  Defects in RASA1 are the cause of capillary malformation-arteriovenous malformation (CMAVM) [MIM:[http://omim.org/entry/608354 608354]]. CMAVM is a disorder characterized by atypical capillary malformations that are multiple, small, round to oval in shape and pinkish red in color. These capillary malformations are associated with either arteriovenous malformation, arteriovenous fistula, or Parkes Weber syndrome.<ref>PMID:14639529</ref>  Defects in RASA1 are a cause of Parkes Weber syndrome (PKWS) [MIM:[http://omim.org/entry/608355 608355]]. PKWS is a disorder characterized by a cutaneous flush with underlying multiple micro-arteriovenous fistulas, in association with soft tissue and skeletal hypertrophy of the affected limb.  
[https://www.uniprot.org/uniprot/RASA1_HUMAN RASA1_HUMAN] Note=Mutations in the SH2 domain of RASA seem to be oncogenic and cause basal cell carcinomas.  Defects in RASA1 are the cause of capillary malformation-arteriovenous malformation (CMAVM) [MIM:[https://omim.org/entry/608354 608354]. CMAVM is a disorder characterized by atypical capillary malformations that are multiple, small, round to oval in shape and pinkish red in color. These capillary malformations are associated with either arteriovenous malformation, arteriovenous fistula, or Parkes Weber syndrome.<ref>PMID:14639529</ref>  Defects in RASA1 are a cause of Parkes Weber syndrome (PKWS) [MIM:[https://omim.org/entry/608355 608355]. PKWS is a disorder characterized by a cutaneous flush with underlying multiple micro-arteriovenous fistulas, in association with soft tissue and skeletal hypertrophy of the affected limb.
== Function ==
== Function ==
[[http://www.uniprot.org/uniprot/RASA1_HUMAN RASA1_HUMAN]] Inhibitory regulator of the Ras-cyclic AMP pathway. Stimulates the GTPase of normal but not oncogenic Ras p21; this stimulation may be further increased in the presence of NCK1.<ref>PMID:8360177</ref> <ref>PMID:11389730</ref>
[https://www.uniprot.org/uniprot/RASA1_HUMAN RASA1_HUMAN] Inhibitory regulator of the Ras-cyclic AMP pathway. Stimulates the GTPase of normal but not oncogenic Ras p21; this stimulation may be further increased in the presence of NCK1.<ref>PMID:8360177</ref> <ref>PMID:11389730</ref>  
 
==See Also==
*[[Ras GTPase activating protein|Ras GTPase activating protein]]
== References ==
== References ==
<references/>
<references/>
__TOC__
__TOC__
</StructureSection>
</StructureSection>
[[Category: Human]]
[[Category: Homo sapiens]]
[[Category: Structural genomic]]
[[Category: Large Structures]]
[[Category: TCELL, Partnership for T-Cell Biology]]
[[Category: Gtpase activating protein]]
[[Category: Jcsg]]
[[Category: Partnership for t-cell biology]]
[[Category: PSI, Protein structure initiative]]
[[Category: Psi-biology]]
[[Category: Ras signaling pathway]]
[[Category: Sh3 domain]]
[[Category: Signaling protein]]
[[Category: Tcell]]

Latest revision as of 05:54, 21 November 2024

Crystal structure of a RAS p21 protein activator (RASA1) from Homo sapiens at 2.25 A resolutionCrystal structure of a RAS p21 protein activator (RASA1) from Homo sapiens at 2.25 A resolution

Structural highlights

4fss is a 3 chain structure with sequence from Homo sapiens. Full crystallographic information is available from OCA. For a guided tour on the structure components use FirstGlance.
Method:X-ray diffraction, Resolution 2.25Å
Ligands:, , ,
Resources:FirstGlance, OCA, PDBe, RCSB, PDBsum, ProSAT

Disease

RASA1_HUMAN Note=Mutations in the SH2 domain of RASA seem to be oncogenic and cause basal cell carcinomas. Defects in RASA1 are the cause of capillary malformation-arteriovenous malformation (CMAVM) [MIM:608354. CMAVM is a disorder characterized by atypical capillary malformations that are multiple, small, round to oval in shape and pinkish red in color. These capillary malformations are associated with either arteriovenous malformation, arteriovenous fistula, or Parkes Weber syndrome.[1] Defects in RASA1 are a cause of Parkes Weber syndrome (PKWS) [MIM:608355. PKWS is a disorder characterized by a cutaneous flush with underlying multiple micro-arteriovenous fistulas, in association with soft tissue and skeletal hypertrophy of the affected limb.

Function

RASA1_HUMAN Inhibitory regulator of the Ras-cyclic AMP pathway. Stimulates the GTPase of normal but not oncogenic Ras p21; this stimulation may be further increased in the presence of NCK1.[2] [3]

See Also

References

  1. ↑ Eerola I, Boon LM, Mulliken JB, Burrows PE, Dompmartin A, Watanabe S, Vanwijck R, Vikkula M. Capillary malformation-arteriovenous malformation, a new clinical and genetic disorder caused by RASA1 mutations. Am J Hum Genet. 2003 Dec;73(6):1240-9. Epub 2003 Nov 24. PMID:14639529 doi:S0002-9297(07)63977-9
  2. ↑ Zhang Y, Zhang G, Mollat P, Carles C, Riva M, Frobert Y, Malassine A, Rostene W, Thang DC, Beltchev B, et al.. Purification, characterization, and cellular localization of the 100-kDa human placental GTPase-activating protein. J Biol Chem. 1993 Sep 5;268(25):18875-81. PMID:8360177
  3. ↑ Giglione C, Gonfloni S, Parmeggiani A. Differential actions of p60c-Src and Lck kinases on the Ras regulators p120-GAP and GDP/GTP exchange factor CDC25Mm. Eur J Biochem. 2001 Jun;268(11):3275-83. PMID:11389730

4fss, resolution 2.25Å

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