7ztl

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Current revision (14:18, 6 November 2024) (edit) (undo)
 
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<tr id='resources'><td class="sblockLbl"><b>Resources:</b></td><td class="sblockDat"><span class='plainlinks'>[https://proteopedia.org/fgij/fg.htm?mol=7ztl FirstGlance], [http://oca.weizmann.ac.il/oca-bin/ocaids?id=7ztl OCA], [https://pdbe.org/7ztl PDBe], [https://www.rcsb.org/pdb/explore.do?structureId=7ztl RCSB], [https://www.ebi.ac.uk/pdbsum/7ztl PDBsum], [https://prosat.h-its.org/prosat/prosatexe?pdbcode=7ztl 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=7ztl FirstGlance], [http://oca.weizmann.ac.il/oca-bin/ocaids?id=7ztl OCA], [https://pdbe.org/7ztl PDBe], [https://www.rcsb.org/pdb/explore.do?structureId=7ztl RCSB], [https://www.ebi.ac.uk/pdbsum/7ztl PDBsum], [https://prosat.h-its.org/prosat/prosatexe?pdbcode=7ztl ProSAT]</span></td></tr>
</table>
</table>
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== Disease ==
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[https://www.uniprot.org/uniprot/MYCN_HUMAN MYCN_HUMAN] Unilateral retinoblastoma;Neuroblastoma;Feingold syndrome type 1. Amplification of the N-MYC gene is associated with a variety of human tumors, most frequently neuroblastoma, where the level of amplification appears to increase as the tumor progresses.<ref>PMID:2834684</ref> The disease is caused by mutations affecting the gene represented in this entry.
== Function ==
== Function ==
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[https://www.uniprot.org/uniprot/AURKA_HUMAN AURKA_HUMAN] Mitotic serine/threonine kinases that contributes to the regulation of cell cycle progression. Associates with the centrosome and the spindle microtubules during mitosis and plays a critical role in various mitotic events including the establishment of mitotic spindle, centrosome duplication, centrosome separation as well as maturation, chromosomal alignment, spindle assembly checkpoint, and cytokinesis. Required for initial activation of CDK1 at centrosomes. Phosphorylates numerous target proteins, including ARHGEF2, BORA, BRCA1, CDC25B, DLGP5, HDAC6, KIF2A, LATS2, NDEL1, PARD3, PPP1R2, PLK1, RASSF1, TACC3, p53/TP53 and TPX2. Regulates KIF2A tubulin depolymerase activity. Required for normal axon formation. Plays a role in microtubule remodeling during neurite extension. Important for microtubule formation and/or stabilization. Also acts as a key regulatory component of the p53/TP53 pathway, and particularly the checkpoint-response pathways critical for oncogenic transformation of cells, by phosphorylating and stabilizing p53/TP53. Phosphorylates its own inhibitors, the protein phosphatase type 1 (PP1) isoforms, to inhibit their activity. Necessary for proper cilia disassembly prior to mitosis.<ref>PMID:9606188</ref> <ref>PMID:11039908</ref> <ref>PMID:11551964</ref> <ref>PMID:12390251</ref> <ref>PMID:13678582</ref> <ref>PMID:14523000</ref> <ref>PMID:15147269</ref> <ref>PMID:14990569</ref> <ref>PMID:15128871</ref> <ref>PMID:14702041</ref> <ref>PMID:15987997</ref> <ref>PMID:18056443</ref> <ref>PMID:17604723</ref> <ref>PMID:17360485</ref> <ref>PMID:18615013</ref> <ref>PMID:19812038</ref> <ref>PMID:19351716</ref> <ref>PMID:19668197</ref> <ref>PMID:19357306</ref> <ref>PMID:20643351</ref> <ref>PMID:17125279</ref>
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[https://www.uniprot.org/uniprot/MYCN_HUMAN MYCN_HUMAN] Positively regulates the transcription of NCYM in neuroblastoma cells (PubMed:24391509).<ref>PMID:24391509</ref>
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<div style="background-color:#fffaf0;">
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== Publication Abstract from PubMed ==
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Formation of the Aurora-A-MYCN complex increases levels of the oncogenic transcription factor MYCN in neuroblastoma cells by abrogating its degradation through the ubiquitin proteasome system. While some small-molecule inhibitors of Aurora-A were shown to destabilize MYCN, clinical trials have not been satisfactory to date. MYCN itself is considered to be ;undruggable' due to its large intrinsically disordered regions. Targeting the Aurora-A-MYCN complex rather than Aurora-A or MYCN alone will open new possibilities for drug development and screening campaigns. To overcome the challenges that a ternary system composed of Aurora-A, MYCN and a small molecule entails, a covalently cross-linked construct of the Aurora-A-MYCN complex was designed, expressed and characterized, thus enabling screening and design campaigns to identify selective binders.
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Crystal structure of a covalently linked Aurora-A-MYCN complex.,Diebold M, Schonemann L, Eilers M, Sotriffer C, Schindelin H Acta Crystallogr D Struct Biol. 2023 Jan 1;79(Pt 1):1-9. doi: , 10.1107/S2059798322011433. Epub 2023 Jan 1. PMID:36601802<ref>PMID:36601802</ref>
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From MEDLINE&reg;/PubMed&reg;, a database of the U.S. National Library of Medicine.<br>
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</div>
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<div class="pdbe-citations 7ztl" style="background-color:#fffaf0;"></div>
==See Also==
==See Also==

Current revision

Crystal structure of a covalently linked Aurora-A N-Myc complex

PDB ID 7ztl

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Proteopedia Page Contributors and Editors (what is this?)

OCA

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