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==NMR STRUCTURE OF THE TUMOR SUPPRESSOR BIN1: ALTERNATIVE SPLICING IN MELANOMA AND INTERACTION WITH C-MYC==
==NMR STRUCTURE OF THE TUMOR SUPPRESSOR BIN1: ALTERNATIVE SPLICING IN MELANOMA AND INTERACTION WITH C-MYC==
<StructureSection load='1mv0' size='340' side='right'caption='[[1mv0]], [[NMR_Ensembles_of_Models | 20 NMR models]]' scene=''>
<StructureSection load='1mv0' size='340' side='right'caption='[[1mv0]]' scene=''>
== Structural highlights ==
== Structural highlights ==
<table><tr><td colspan='2'>[[1mv0]] is a 2 chain structure with sequence from [https://en.wikipedia.org/wiki/Human Human]. Full experimental information is available from [http://oca.weizmann.ac.il/oca-bin/ocashort?id=1MV0 OCA]. For a <b>guided tour on the structure components</b> use [https://proteopedia.org/fgij/fg.htm?mol=1MV0 FirstGlance]. <br>
<table><tr><td colspan='2'>[[1mv0]] is a 2 chain structure with sequence from [https://en.wikipedia.org/wiki/Homo_sapiens Homo sapiens]. Full experimental information is available from [http://oca.weizmann.ac.il/oca-bin/ocashort?id=1MV0 OCA]. For a <b>guided tour on the structure components</b> use [https://proteopedia.org/fgij/fg.htm?mol=1MV0 FirstGlance]. <br>
</td></tr><tr id='related'><td class="sblockLbl"><b>[[Related_structure|Related:]]</b></td><td class="sblockDat"><div style='overflow: auto; max-height: 3em;'>[[1muz|1muz]], [[1mv3|1mv3]]</div></td></tr>
</td></tr><tr id='method'><td class="sblockLbl"><b>[[Empirical_models|Method:]]</b></td><td class="sblockDat" id="methodDat">Solution NMR</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=1mv0 FirstGlance], [http://oca.weizmann.ac.il/oca-bin/ocaids?id=1mv0 OCA], [https://pdbe.org/1mv0 PDBe], [https://www.rcsb.org/pdb/explore.do?structureId=1mv0 RCSB], [https://www.ebi.ac.uk/pdbsum/1mv0 PDBsum], [https://prosat.h-its.org/prosat/prosatexe?pdbcode=1mv0 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=1mv0 FirstGlance], [http://oca.weizmann.ac.il/oca-bin/ocaids?id=1mv0 OCA], [https://pdbe.org/1mv0 PDBe], [https://www.rcsb.org/pdb/explore.do?structureId=1mv0 RCSB], [https://www.ebi.ac.uk/pdbsum/1mv0 PDBsum], [https://prosat.h-its.org/prosat/prosatexe?pdbcode=1mv0 ProSAT]</span></td></tr>
</table>
</table>
== Disease ==
== Disease ==
[[https://www.uniprot.org/uniprot/MYC_HUMAN MYC_HUMAN]] Note=Overexpression of MYC is implicated in the etiology of a variety of hematopoietic tumors.  Note=A chromosomal aberration involving MYC may be a cause of a form of B-cell chronic lymphocytic leukemia. Translocation t(8;12)(q24;q22) with BTG1.  Defects in MYC are a cause of Burkitt lymphoma (BL) [MIM:[https://omim.org/entry/113970 113970]]. A form of undifferentiated malignant lymphoma commonly manifested as a large osteolytic lesion in the jaw or as an abdominal mass. Note=Chromosomal aberrations involving MYC are usually found in Burkitt lymphoma. Translocations t(8;14), t(8;22) or t(2;8) which juxtapose MYC to one of the heavy or light chain immunoglobulin gene loci. [[https://www.uniprot.org/uniprot/BIN1_HUMAN BIN1_HUMAN]] Defects in BIN1 are the cause of centronuclear myopathy type 2 (CNM2) [MIM:[https://omim.org/entry/255200 255200]]. A congenital muscle disorder characterized by progressive muscular weakness and wasting involving mainly limb girdle, trunk, and neck muscles. It may also affect distal muscles. Weakness may be present during childhood or adolescence or may not become evident until the third decade of life. Ptosis is a frequent clinical feature. The most prominent histopathologic features include high frequency of centrally located nuclei in muscle fibers not secondary to regeneration, radial arrangement of sarcoplasmic strands around the central nuclei, and predominance and hypotrophy of type 1 fibers.<ref>PMID:17676042</ref> 
[https://www.uniprot.org/uniprot/MYC_HUMAN MYC_HUMAN] Note=Overexpression of MYC is implicated in the etiology of a variety of hematopoietic tumors.  Note=A chromosomal aberration involving MYC may be a cause of a form of B-cell chronic lymphocytic leukemia. Translocation t(8;12)(q24;q22) with BTG1.  Defects in MYC are a cause of Burkitt lymphoma (BL) [MIM:[https://omim.org/entry/113970 113970]. A form of undifferentiated malignant lymphoma commonly manifested as a large osteolytic lesion in the jaw or as an abdominal mass. Note=Chromosomal aberrations involving MYC are usually found in Burkitt lymphoma. Translocations t(8;14), t(8;22) or t(2;8) which juxtapose MYC to one of the heavy or light chain immunoglobulin gene loci.
== Function ==
== Function ==
[[https://www.uniprot.org/uniprot/MYC_HUMAN MYC_HUMAN]] Participates in the regulation of gene transcription. Binds DNA in a non-specific manner, yet also specifically recognizes the core sequence 5'-CAC[GA]TG-3'. Seems to activate the transcription of growth-related genes. [[https://www.uniprot.org/uniprot/BIN1_HUMAN BIN1_HUMAN]] May be involved in regulation of synaptic vesicle endocytosis. May act as a tumor suppressor and inhibits malignant cell transformation.  
[https://www.uniprot.org/uniprot/MYC_HUMAN MYC_HUMAN] Participates in the regulation of gene transcription. Binds DNA in a non-specific manner, yet also specifically recognizes the core sequence 5'-CAC[GA]TG-3'. Seems to activate the transcription of growth-related genes.
== Evolutionary Conservation ==
== Evolutionary Conservation ==
[[Image:Consurf_key_small.gif|200px|right]]
[[Image:Consurf_key_small.gif|200px|right]]
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__TOC__
__TOC__
</StructureSection>
</StructureSection>
[[Category: Human]]
[[Category: Homo sapiens]]
[[Category: Large Structures]]
[[Category: Large Structures]]
[[Category: Arrowsmith, C H]]
[[Category: Arrowsmith CH]]
[[Category: Pineda-Lucena, A]]
[[Category: Pineda-Lucena A]]
[[Category: Endocytosis-exocytosis]]
[[Category: Endocytosis/exocytosis]]
[[Category: Transcription complex]]
[[Category: Tumor suppressor/oncoprotein]]

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