2a41: Difference between revisions
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<tr id='related'><td class="sblockLbl"><b>[[Related_structure|Related:]]</b></td><td class="sblockDat">[[2a3z|2a3z]], [[2a40|2a40]], [[2a42|2a42]]</td></tr> | <tr id='related'><td class="sblockLbl"><b>[[Related_structure|Related:]]</b></td><td class="sblockDat">[[2a3z|2a3z]], [[2a40|2a40]], [[2a42|2a42]]</td></tr> | ||
<tr id='activity'><td class="sblockLbl"><b>Activity:</b></td><td class="sblockDat"><span class='plainlinks'>[http://en.wikipedia.org/wiki/Deoxyribonuclease_I Deoxyribonuclease I], with EC number [http://www.brenda-enzymes.info/php/result_flat.php4?ecno=3.1.21.1 3.1.21.1] </span></td></tr> | <tr id='activity'><td class="sblockLbl"><b>Activity:</b></td><td class="sblockDat"><span class='plainlinks'>[http://en.wikipedia.org/wiki/Deoxyribonuclease_I Deoxyribonuclease I], with EC number [http://www.brenda-enzymes.info/php/result_flat.php4?ecno=3.1.21.1 3.1.21.1] </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=2a41 FirstGlance], [http://oca.weizmann.ac.il/oca-bin/ocaids?id=2a41 OCA], [http://www.rcsb.org/pdb/explore.do?structureId=2a41 RCSB], [http://www.ebi.ac.uk/pdbsum/2a41 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=2a41 FirstGlance], [http://oca.weizmann.ac.il/oca-bin/ocaids?id=2a41 OCA], [http://pdbe.org/2a41 PDBe], [http://www.rcsb.org/pdb/explore.do?structureId=2a41 RCSB], [http://www.ebi.ac.uk/pdbsum/2a41 PDBsum]</span></td></tr> | ||
</table> | </table> | ||
== Disease == | |||
[[http://www.uniprot.org/uniprot/WIPF1_HUMAN WIPF1_HUMAN]] Defects in WIPF1 are the cause of Wiskott-Aldrich syndrome type 2 (WAS2) [MIM:[http://omim.org/entry/614493 614493]]. WAS2 is an immunodeficiency disorder characterized by eczema, thrombocytopenia, recurrent infections, defective T-cell proliferation, and impaired natural killer cell function.<ref>PMID:22231303</ref> | |||
== Function == | == Function == | ||
[[http://www.uniprot.org/uniprot/ACTS_RABIT ACTS_RABIT]] Actins are highly conserved proteins that are involved in various types of cell motility and are ubiquitously expressed in all eukaryotic cells. [[http://www.uniprot.org/uniprot/DNAS1_BOVIN DNAS1_BOVIN]] Among other functions, seems to be involved in cell death by apoptosis. Binds specifically to G-actin and blocks actin polymerization (By similarity). | [[http://www.uniprot.org/uniprot/ACTS_RABIT ACTS_RABIT]] Actins are highly conserved proteins that are involved in various types of cell motility and are ubiquitously expressed in all eukaryotic cells. [[http://www.uniprot.org/uniprot/WIPF1_HUMAN WIPF1_HUMAN]] May have direct activity on the actin cytoskeleton. Induces actin polymerization and redistribution. Contributes with NCK1 and GRB2 in the recruitment and activation of WASL. May participate in regulating the subcellular localization of WASL, resulting in the disassembly of stress fibers in favor of filopodia formation (By similarity). Plays an important role in the intracellular motility of vaccinia virus by functioning as an adapter for recruiting WASL to vaccinia virus.<ref>PMID:9405671</ref> <ref>PMID:10878810</ref> [[http://www.uniprot.org/uniprot/DNAS1_BOVIN DNAS1_BOVIN]] Among other functions, seems to be involved in cell death by apoptosis. Binds specifically to G-actin and blocks actin polymerization (By similarity). | ||
== Evolutionary Conservation == | == Evolutionary Conservation == | ||
[[Image:Consurf_key_small.gif|200px|right]] | [[Image:Consurf_key_small.gif|200px|right]] | ||
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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 2a41" style="background-color:#fffaf0;"></div> | |||
==See Also== | ==See Also== | ||