8ycm
From Proteopedia
(Difference between revisions)
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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=8ycm FirstGlance], [http://oca.weizmann.ac.il/oca-bin/ocaids?id=8ycm OCA], [https://pdbe.org/8ycm PDBe], [https://www.rcsb.org/pdb/explore.do?structureId=8ycm RCSB], [https://www.ebi.ac.uk/pdbsum/8ycm PDBsum], [https://prosat.h-its.org/prosat/prosatexe?pdbcode=8ycm 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=8ycm FirstGlance], [http://oca.weizmann.ac.il/oca-bin/ocaids?id=8ycm OCA], [https://pdbe.org/8ycm PDBe], [https://www.rcsb.org/pdb/explore.do?structureId=8ycm RCSB], [https://www.ebi.ac.uk/pdbsum/8ycm PDBsum], [https://prosat.h-its.org/prosat/prosatexe?pdbcode=8ycm ProSAT]</span></td></tr> | ||
</table> | </table> | ||
| - | == Disease == | ||
| - | [https://www.uniprot.org/uniprot/STK19_HUMAN STK19_HUMAN] Gain-of-function variants in STK19 are involved in NRAS-driven melanomagenesis (PubMed:30712867). Melanoma are malignant neoplasm of melanocytes, arising de novo or from a pre-existing benign nevus, which occurs most often in the skin but may also involve other sites (PubMed:30712867). Conditional knockin mice overexpressing Asn-89 variant exhibit hyperpigmentation of the skin, ears, and tail, and the melanin content in skin was significantly increased after tamoxifen induction (PubMed:30712867). Moreover, knockin mice overexpressing Asn-89 variant promote NRAS 'Arg-61'-driven melanomagenesis (PubMed:30712867).<ref>PMID:30712867</ref> | ||
== Function == | == Function == | ||
| - | [https://www.uniprot.org/uniprot/STK19_HUMAN STK19_HUMAN] | + | [https://www.uniprot.org/uniprot/STK19_HUMAN STK19_HUMAN] Inactive serine/threonine-protein kinase (Probable) (PubMed:32531245, PubMed:32531246). May control NRAS activity via an associated kinase (Probable) (PubMed:32531246).<ref>PMID:32531245</ref> <ref>PMID:32531246</ref> Inactive serine/threonine-protein kinase.<ref>PMID:32531245</ref> |
| + | <div style="background-color:#fffaf0;"> | ||
| + | == Publication Abstract from PubMed == | ||
| + | Serine/threonine protein kinase 19 (STK19) has been reported to phosphorylate and activate oncogenic NRAS to promote melanomagenesis. However, concerns have been raised about whether STK19 is a kinase. STK19 has also been identified as a putative factor involved in the transcription-coupled nucleotide excision repair (TC-NER) pathway. In this study, we determined the 1.32 A crystal structure of human STK19. The structure reveals that STK19 is a winged helix (WH) protein consisting of three tandem WH domains. STK19 binds more strongly to double-stranded DNA and RNA (dsDNA/dsRNA) than to ssDNA. A positively charged patch centered on helix WH3-H1 contributes to dsDNA binding, which is unusual because the WH domain typically uses helix H3 as the recognition helix. Importantly, mutations of the conserved residues in the basic patch, K186N, R200W, and R215W, are found in cancer patients, and these mutations compromise STK19 DNA binding. Other mutations have been predicted to produce a similar effect, including two mutations that disrupt the nuclear localization signal (NLS) motif. These mutations may indirectly impact the DNA binding capacity of STK19 by interfering with its nuclear localization. | ||
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| + | Mutations found in cancer patients compromise DNA binding of the winged helix protein STK19.,Li J, Ma X, Wang X, Hu X, Fang S, Jin G, Liu K, Dong Z Sci Rep. 2024 Jun 18;14(1):14098. doi: 10.1038/s41598-024-64840-9. PMID:38890355<ref>PMID:38890355</ref> | ||
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| + | From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine.<br> | ||
| + | </div> | ||
| + | <div class="pdbe-citations 8ycm" style="background-color:#fffaf0;"></div> | ||
== References == | == References == | ||
<references/> | <references/> | ||
Current revision
Monomeric Human STK19
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Categories: Homo sapiens | Large Structures | Dong Z | Li J | Ma X
