2l4z

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{{STRUCTURE_2l4z| PDB=2l4z | SCENE= }}
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==NMR structure of fusion of CtIP (641-685) to LMO4-LIM1 (18-82)==
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===NMR structure of fusion of CtIP (641-685) to LMO4-LIM1 (18-82)===
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<StructureSection load='2l4z' size='340' side='right' caption='[[2l4z]], [[NMR_Ensembles_of_Models | 20 NMR models]]' scene=''>
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{{ABSTRACT_PUBMED_23353824}}
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== Structural highlights ==
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<table><tr><td colspan='2'>[[2l4z]] is a 1 chain structure with sequence from [http://en.wikipedia.org/wiki/Homo_sapiens Homo sapiens]. Full experimental information is available from [http://oca.weizmann.ac.il/oca-bin/ocashort?id=2L4Z OCA]. For a <b>guided tour on the structure components</b> use [http://oca.weizmann.ac.il/oca-docs/fgij/fg.htm?mol=2L4Z FirstGlance]. <br>
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</td></tr><tr id='ligand'><td class="sblockLbl"><b>[[Ligand|Ligands:]]</b></td><td class="sblockDat"><scene name='pdbligand=ZN:ZINC+ION'>ZN</scene></td></tr>
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<tr id='related'><td class="sblockLbl"><b>[[Related_structure|Related:]]</b></td><td class="sblockDat">[[1m3v|1m3v]], [[1rut|1rut]]</td></tr>
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<tr id='gene'><td class="sblockLbl"><b>[[Gene|Gene:]]</b></td><td class="sblockDat">CTIP, LMO4, RBBP8 ([http://www.ncbi.nlm.nih.gov/Taxonomy/Browser/wwwtax.cgi?mode=Info&srchmode=5&id=9606 Homo sapiens])</td></tr>
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<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=2l4z FirstGlance], [http://oca.weizmann.ac.il/oca-bin/ocaids?id=2l4z OCA], [http://www.rcsb.org/pdb/explore.do?structureId=2l4z RCSB], [http://www.ebi.ac.uk/pdbsum/2l4z PDBsum]</span></td></tr>
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</table>
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== Disease ==
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[[http://www.uniprot.org/uniprot/COM1_HUMAN COM1_HUMAN]] Seckel syndrome. Defects in RBBP8 are a cause of Seckel syndrome type 2 (SCKL2) [MIM:[http://omim.org/entry/606744 606744]]. SCKL2 is a rare autosomal recessive disorder characterized by proportionate dwarfism of prenatal onset associated with low birth weight, growth retardation, severe microcephaly with a bird-headed like appearance, and mental retardation.<ref>PMID:21998596</ref> Defects in RBBP8 are a cause of Jawad disease (JWDS) [MIM:[http://omim.org/entry/251255 251255]]. JWDS is a syndrome characterized by congenital microcephaly, moderately severe mental retardation, and symmetrical digital anomalies. Digital malformations of variable degree inclued hallux valgus, syndactyly of toes 4 and 5, short fifth fingers, single flexion crease of fifth fingers, polydactyly and synpolydactyly.<ref>PMID:21998596</ref> Note=Genetic variability in RBBP8 is noted as a factor in BRCA1-associated breast cancer risk. Exhibits sensitivity to tamoxifen in certain breast cancer cell lines.
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== Function ==
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[[http://www.uniprot.org/uniprot/COM1_HUMAN COM1_HUMAN]] Endonuclease that cooperates with the MRE11-RAD50-NBN (MRN) complex in processing meiotic and mitotic double-strand breaks (DSBs) by ensuring both resection and intrachromosomal association of the broken ends. Functions downstream of the MRN complex and ATM, promotes ATR activation and its recruitment to DSBs in the S/G2 phase facilitating the generation of ssDNA. Component of the BRCA1-RBBP8 complex that regulates CHEK1 activation and controls cell cycle G2/M checkpoints on DNA damage. Promotes microhomology-mediated alternative end joining (A-NHEJ) during class-switch recombination and plays an essential role in chromosomal translocations.<ref>PMID:10764811</ref> <ref>PMID:10910365</ref> <ref>PMID:15485915</ref> <ref>PMID:16818604</ref> <ref>PMID:16581787</ref> <ref>PMID:17965729</ref> <ref>PMID:19202191</ref> <ref>PMID:19759395</ref> <ref>PMID:20064462</ref> <ref>PMID:20829486</ref>
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<div style="background-color:#fffaf0;">
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== Publication Abstract from PubMed ==
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LIM-only protein 4 (LMO4) is strongly linked to the progression of breast cancer. Although the mechanisms underlying this phenomenon are not well understood, a role is emerging for LMO4 in regulation of the cell cycle. We determined the solution structure of LMO4 in complex with CtIP (C-terminal binding protein interacting protein)/RBBP8, a tumour suppressor protein that is involved in cell cycle progression, DNA repair and transcriptional regulation. Our data reveal that CtIP and the essential LMO cofactor LDB1 (LIM-domain binding protein 1) bind to the same face on LMO4 and cannot simultaneously bind to LMO4. We hypothesise that overexpression of LMO4 may disrupt some of the normal tumour suppressor activities of CtIP, thereby contributing to breast cancer progression.
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==Disease==
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Structural Basis of the Interaction of the Breast Cancer Oncogene LMO4 with the Tumour Suppressor CtIP/RBBP8.,Stokes PH, Liew CW, Kwan AH, Foo P, Barker HE, Djamirze A, O'Reilly V, Visvader JE, Mackay JP, Matthews JM J Mol Biol. 2013 Apr 12;425(7):1101-10. doi: 10.1016/j.jmb.2013.01.017. Epub 2013, Jan 23. PMID:23353824<ref>PMID:23353824</ref>
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[[http://www.uniprot.org/uniprot/COM1_HUMAN COM1_HUMAN]] Seckel syndrome. Defects in RBBP8 are a cause of Seckel syndrome type 2 (SCKL2) [MIM:[http://omim.org/entry/606744 606744]]. SCKL2 is a rare autosomal recessive disorder characterized by proportionate dwarfism of prenatal onset associated with low birth weight, growth retardation, severe microcephaly with a bird-headed like appearance, and mental retardation.<ref>PMID:21998596</ref> Defects in RBBP8 are a cause of Jawad disease (JWDS) [MIM:[http://omim.org/entry/251255 251255]]. JWDS is a syndrome characterized by congenital microcephaly, moderately severe mental retardation, and symmetrical digital anomalies. Digital malformations of variable degree inclued hallux valgus, syndactyly of toes 4 and 5, short fifth fingers, single flexion crease of fifth fingers, polydactyly and synpolydactyly.<ref>PMID:21998596</ref> Note=Genetic variability in RBBP8 is noted as a factor in BRCA1-associated breast cancer risk. Exhibits sensitivity to tamoxifen in certain breast cancer cell lines.
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==Function==
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From MEDLINE&reg;/PubMed&reg;, a database of the U.S. National Library of Medicine.<br>
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[[http://www.uniprot.org/uniprot/COM1_HUMAN COM1_HUMAN]] Endonuclease that cooperates with the MRE11-RAD50-NBN (MRN) complex in processing meiotic and mitotic double-strand breaks (DSBs) by ensuring both resection and intrachromosomal association of the broken ends. Functions downstream of the MRN complex and ATM, promotes ATR activation and its recruitment to DSBs in the S/G2 phase facilitating the generation of ssDNA. Component of the BRCA1-RBBP8 complex that regulates CHEK1 activation and controls cell cycle G2/M checkpoints on DNA damage. Promotes microhomology-mediated alternative end joining (A-NHEJ) during class-switch recombination and plays an essential role in chromosomal translocations.<ref>PMID:10764811</ref><ref>PMID:10910365</ref><ref>PMID:15485915</ref><ref>PMID:16818604</ref><ref>PMID:16581787</ref><ref>PMID:17965729</ref><ref>PMID:19202191</ref><ref>PMID:19759395</ref><ref>PMID:20064462</ref><ref>PMID:20829486</ref>
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</div>
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== References ==
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==About this Structure==
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<references/>
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[[2l4z]] is a 1 chain structure with sequence from [http://en.wikipedia.org/wiki/Homo_sapiens Homo sapiens]. Full experimental information is available from [http://oca.weizmann.ac.il/oca-bin/ocashort?id=2L4Z OCA].
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__TOC__
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</StructureSection>
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==Reference==
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<references group="xtra"/><references/>
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[[Category: Homo sapiens]]
[[Category: Homo sapiens]]
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[[Category: Kwan, A H.]]
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[[Category: Kwan, A H]]
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[[Category: Liew, C.]]
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[[Category: Liew, C]]
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[[Category: Matthews, J M.]]
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[[Category: Matthews, J M]]
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[[Category: Stokes, P H.]]
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[[Category: Stokes, P H]]
[[Category: Hydrolase]]
[[Category: Hydrolase]]
[[Category: Lim domain]]
[[Category: Lim domain]]

Revision as of 12:11, 18 December 2014

NMR structure of fusion of CtIP (641-685) to LMO4-LIM1 (18-82)

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