3o1e

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[[Image:3o1e.png|left|200px]]
 
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{{STRUCTURE_3o1e| PDB=3o1e | SCENE= }}
{{STRUCTURE_3o1e| PDB=3o1e | SCENE= }}
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===Structure-function of Gemini derivatives with two different side chains at C-20, Gemini-0072 and Gemini-0097.===
===Structure-function of Gemini derivatives with two different side chains at C-20, Gemini-0072 and Gemini-0097.===
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{{ABSTRACT_PUBMED_22180837}}
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==Disease==
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[[http://www.uniprot.org/uniprot/NCOA2_HUMAN NCOA2_HUMAN]] Note=Chromosomal aberrations involving NCOA2 may be a cause of acute myeloid leukemias. Inversion inv(8)(p11;q13) generates the KAT6A-NCOA2 oncogene, which consists of the N-terminal part of KAT6A and the C-terminal part of NCOA2/TIF2. KAT6A-NCOA2 binds to CREBBP and disrupts its function in transcription activation.
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==Function==
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[[http://www.uniprot.org/uniprot/VDRA_DANRE VDRA_DANRE]] Nuclear hormone receptor. Transcription factor that mediates the action of vitamin D3 by controlling the expression of hormone sensitive genes. Regulates transcription of hormone sensitive genes via its association with the WINAC complex, a chromatin-remodeling complex. Plays a central role in calcium homeostasis.<ref>PMID:17218092</ref> [[http://www.uniprot.org/uniprot/NCOA2_HUMAN NCOA2_HUMAN]] Transcriptional coactivator for steroid receptors and nuclear receptors. Coactivator of the steroid binding domain (AF-2) but not of the modulating N-terminal domain (AF-1). Required with NCOA1 to control energy balance between white and brown adipose tissues.<ref>PMID:9430642</ref>
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(as it appears on PubMed at http://www.pubmed.gov), where 22180837 is the PubMed ID number.
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{{ABSTRACT_PUBMED_22180837}}
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==About this Structure==
==About this Structure==
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==Reference==
==Reference==
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<ref group="xtra">PMID:022180837</ref><references group="xtra"/>
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<ref group="xtra">PMID:022180837</ref><references group="xtra"/><references/>
[[Category: Danio rerio]]
[[Category: Danio rerio]]
[[Category: Huet, T.]]
[[Category: Huet, T.]]

Revision as of 22:03, 24 March 2013

Template:STRUCTURE 3o1e

Contents

Structure-function of Gemini derivatives with two different side chains at C-20, Gemini-0072 and Gemini-0097.

Template:ABSTRACT PUBMED 22180837

Disease

[NCOA2_HUMAN] Note=Chromosomal aberrations involving NCOA2 may be a cause of acute myeloid leukemias. Inversion inv(8)(p11;q13) generates the KAT6A-NCOA2 oncogene, which consists of the N-terminal part of KAT6A and the C-terminal part of NCOA2/TIF2. KAT6A-NCOA2 binds to CREBBP and disrupts its function in transcription activation.

Function

[VDRA_DANRE] Nuclear hormone receptor. Transcription factor that mediates the action of vitamin D3 by controlling the expression of hormone sensitive genes. Regulates transcription of hormone sensitive genes via its association with the WINAC complex, a chromatin-remodeling complex. Plays a central role in calcium homeostasis.[1] [NCOA2_HUMAN] Transcriptional coactivator for steroid receptors and nuclear receptors. Coactivator of the steroid binding domain (AF-2) but not of the modulating N-terminal domain (AF-1). Required with NCOA1 to control energy balance between white and brown adipose tissues.[2]

About this Structure

3o1e is a 2 chain structure with sequence from Danio rerio. Full crystallographic information is available from OCA.

Reference

  • Huet T, Maehr H, Lee HJ, Uskokovic MR, Suh N, Moras D, Rochel N. Structure-function study of gemini derivatives with two different side chains at C-20, Gemini-0072 and Gemini-0097. Medchemcomm. 2011;2(5):424-429. PMID:22180837 doi:10.1039/C1MD00059D
  1. ↑ Ciesielski F, Rochel N, Moras D. Adaptability of the Vitamin D nuclear receptor to the synthetic ligand Gemini: remodelling the LBP with one side chain rotation. J Steroid Biochem Mol Biol. 2007 Mar;103(3-5):235-42. Epub 2007 Jan 10. PMID:17218092 doi:http://dx.doi.org/10.1016/j.jsbmb.2006.12.003
  2. ↑ Voegel JJ, Heine MJ, Tini M, Vivat V, Chambon P, Gronemeyer H. The coactivator TIF2 contains three nuclear receptor-binding motifs and mediates transactivation through CBP binding-dependent and -independent pathways. EMBO J. 1998 Jan 15;17(2):507-19. PMID:9430642 doi:10.1093/emboj/17.2.507

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