1awi: Difference between revisions

From Proteopedia
Jump to navigation Jump to search
← Older edit
No edit summary
No edit summary
 
(10 intermediate revisions by the same user not shown)
Line 1: Line 1:
{{Seed}}
[[Image:1awi.png|left|200px]]


<!--
==HUMAN PLATELET PROFILIN COMPLEXED WITH THE L-PRO10 PEPTIDE==
The line below this paragraph, containing "STRUCTURE_1awi", creates the "Structure Box" on the page.
<StructureSection load='1awi' size='340' side='right'caption='[[1awi]], [[Resolution|resolution]] 2.20&Aring;' scene=''>
You may change the PDB parameter (which sets the PDB file loaded into the applet)
== Structural highlights ==
or the SCENE parameter (which sets the initial scene displayed when the page is loaded),
<table><tr><td colspan='2'>[[1awi]] 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=1AWI OCA]. For a <b>guided tour on the structure components</b> use [https://proteopedia.org/fgij/fg.htm?mol=1AWI FirstGlance]. <br>
or leave the SCENE parameter empty for the default display.
</td></tr><tr id='method'><td class="sblockLbl"><b>[[Empirical_models|Method:]]</b></td><td class="sblockDat" id="methodDat">X-ray diffraction, [[Resolution|Resolution]] 2.2&#8491;</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=1awi FirstGlance], [http://oca.weizmann.ac.il/oca-bin/ocaids?id=1awi OCA], [https://pdbe.org/1awi PDBe], [https://www.rcsb.org/pdb/explore.do?structureId=1awi RCSB], [https://www.ebi.ac.uk/pdbsum/1awi PDBsum], [https://prosat.h-its.org/prosat/prosatexe?pdbcode=1awi ProSAT]</span></td></tr>
{{STRUCTURE_1awi| PDB=1awi |  SCENE= }}
</table>
== Disease ==
[https://www.uniprot.org/uniprot/PROF1_HUMAN PROF1_HUMAN] Defects in PFN1 are the cause of amyotrophic lateral sclerosis 18 (ALS18) [MIM:[https://omim.org/entry/614808 614808]. A neurodegenerative disorder affecting upper motor neurons in the brain and lower motor neurons in the brain stem and spinal cord, resulting in fatal paralysis. Sensory abnormalities are absent. The pathologic hallmarks of the disease include pallor of the corticospinal tract due to loss of motor neurons, presence of ubiquitin-positive inclusions within surviving motor neurons, and deposition of pathologic aggregates. The etiology of amyotrophic lateral sclerosis is likely to be multifactorial, involving both genetic and environmental factors. The disease is inherited in 5-10% of the cases.<ref>PMID:22801503</ref>
== Function ==
[https://www.uniprot.org/uniprot/PROF1_HUMAN PROF1_HUMAN] Binds to actin and affects the structure of the cytoskeleton. At high concentrations, profilin prevents the polymerization of actin, whereas it enhances it at low concentrations. By binding to PIP2, it inhibits the formation of IP3 and DG. Inhibits androgen receptor (AR) and HTT aggregation and binding of G-actin is essential for its inhibition of AR.<ref>PMID:18573880</ref>
== 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/aw/1awi_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/main_output.php?pdb_ID=1awi ConSurf].
<div style="clear:both"></div>


===HUMAN PLATELET PROFILIN COMPLEXED WITH THE L-PRO10 PEPTIDE===
==See Also==
 
*[[Profilin 3D Structures|Profilin 3D Structures]]
 
== References ==
<!--
<references/>
The line below this paragraph, {{ABSTRACT_PUBMED_9360613}}, adds the Publication Abstract to the page
__TOC__
(as it appears on PubMed at http://www.pubmed.gov), where 9360613 is the PubMed ID number.
</StructureSection>
-->
{{ABSTRACT_PUBMED_9360613}}
 
==About this Structure==
1AWI is a [[Single protein]] structure of 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=1AWI OCA].
 
==Reference==
Structure of the profilin-poly-L-proline complex involved in morphogenesis and cytoskeletal regulation., Mahoney NM, Janmey PA, Almo SC, Nat Struct Biol. 1997 Nov;4(11):953-60. PMID:[http://www.ncbi.nlm.nih.gov/pubmed/9360613 9360613]
[[Category: Homo sapiens]]
[[Category: Homo sapiens]]
[[Category: Single protein]]
[[Category: Large Structures]]
[[Category: Almo, S C.]]
[[Category: Almo SC]]
[[Category: Mahoney, N M.]]
[[Category: Mahoney NM]]
[[Category: Actin cytoskeleton]]
[[Category: Poly-l-proline]]
[[Category: Profilin]]
 
''Page seeded by [http://oca.weizmann.ac.il/oca OCA ] on Mon Jun 30 17:45:06 2008''

Latest revision as of 09:33, 7 February 2024

HUMAN PLATELET PROFILIN COMPLEXED WITH THE L-PRO10 PEPTIDEHUMAN PLATELET PROFILIN COMPLEXED WITH THE L-PRO10 PEPTIDE

Structural highlights

1awi 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 2.2Å
Resources:FirstGlance, OCA, PDBe, RCSB, PDBsum, ProSAT

Disease

PROF1_HUMAN Defects in PFN1 are the cause of amyotrophic lateral sclerosis 18 (ALS18) [MIM:614808. A neurodegenerative disorder affecting upper motor neurons in the brain and lower motor neurons in the brain stem and spinal cord, resulting in fatal paralysis. Sensory abnormalities are absent. The pathologic hallmarks of the disease include pallor of the corticospinal tract due to loss of motor neurons, presence of ubiquitin-positive inclusions within surviving motor neurons, and deposition of pathologic aggregates. The etiology of amyotrophic lateral sclerosis is likely to be multifactorial, involving both genetic and environmental factors. The disease is inherited in 5-10% of the cases.[1]

Function

PROF1_HUMAN Binds to actin and affects the structure of the cytoskeleton. At high concentrations, profilin prevents the polymerization of actin, whereas it enhances it at low concentrations. By binding to PIP2, it inhibits the formation of IP3 and DG. Inhibits androgen receptor (AR) and HTT aggregation and binding of G-actin is essential for its inhibition of AR.[2]

Evolutionary Conservation

Check, as determined by ConSurfDB. You may read the explanation of the method and the full data available from ConSurf.

See Also

References

  1. ↑ Wu CH, Fallini C, Ticozzi N, Keagle PJ, Sapp PC, Piotrowska K, Lowe P, Koppers M, McKenna-Yasek D, Baron DM, Kost JE, Gonzalez-Perez P, Fox AD, Adams J, Taroni F, Tiloca C, Leclerc AL, Chafe SC, Mangroo D, Moore MJ, Zitzewitz JA, Xu ZS, van den Berg LH, Glass JD, Siciliano G, Cirulli ET, Goldstein DB, Salachas F, Meininger V, Rossoll W, Ratti A, Gellera C, Bosco DA, Bassell GJ, Silani V, Drory VE, Brown RH Jr, Landers JE. Mutations in the profilin 1 gene cause familial amyotrophic lateral sclerosis. Nature. 2012 Aug 23;488(7412):499-503. doi: 10.1038/nature11280. PMID:22801503 doi:10.1038/nature11280
  2. ↑ Shao J, Welch WJ, Diprospero NA, Diamond MI. Phosphorylation of profilin by ROCK1 regulates polyglutamine aggregation. Mol Cell Biol. 2008 Sep;28(17):5196-208. doi: 10.1128/MCB.00079-08. Epub 2008 Jun, 23. PMID:18573880 doi:10.1128/MCB.00079-08

1awi, resolution 2.20Å

Drag the structure with the mouse to rotate

Proteopedia Page Contributors and Editors (what is this?)Proteopedia Page Contributors and Editors (what is this?)

OCA
Retrieved from "https://proteopedia.openfox.io/wiki/index.php?title=1awi&oldid=4040408"