2mjv

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'''Unreleased structure'''
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{{STRUCTURE_2mjv| PDB=2mjv | SCENE= }}
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===Solution structures of second bromodomain of Brd4 with di-acetylated Twist peptide===
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{{ABSTRACT_PUBMED_24525235}}
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The entry 2mjv is ON HOLD
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==Disease==
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[[http://www.uniprot.org/uniprot/TWST1_HUMAN TWST1_HUMAN]] Isolated scaphocephaly;Isolated brachycephaly;Saethre-Chotzen syndrome. The disease is caused by mutations affecting the gene represented in this entry. The disease is caused by mutations affecting the gene represented in this entry. The disease is caused by mutations affecting the gene represented in this entry. [[http://www.uniprot.org/uniprot/BRD4_HUMAN BRD4_HUMAN]] Note=A chromosomal aberration involving BRD4 is found in a rare, aggressive, and lethal carcinoma arising in midline organs of young people. Translocation t(15;19)(q14;p13) with NUT which produces a BRD4-NUT fusion protein.<ref>PMID:12543779</ref> <ref>PMID:11733348</ref>
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Authors: Zeng, L., Zhou, M.
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==Function==
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[[http://www.uniprot.org/uniprot/TWST1_HUMAN TWST1_HUMAN]] Acts as a transcriptional regulator. Inhibits myogenesis by sequestrating E proteins, inhibiting trans-activation by MEF2, and inhibiting DNA-binding by MYOD1 through physical interaction. This interaction probably involves the basic domains of both proteins. Also represses expression of proinflammatory cytokines such as TNFA and IL1B. Regulates cranial suture patterning and fusion. Activates transcription as a heterodimer with E proteins. Regulates gene expression differentially, depending on dimer composition. Homodimers induce expression of FGFR2 and POSTN while heterodimers repress FGFR2 and POSTN expression and induce THBS1 expression. Heterodimerization is also required for osteoblast differentiation.<ref>PMID:12553906</ref> [[http://www.uniprot.org/uniprot/BRD4_HUMAN BRD4_HUMAN]] Plays a role in a process governing chromosomal dynamics during mitosis (By similarity).
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Description: Solution structures of second bromodomain of Brd4 with di-acetylated Twist peptide
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==About this Structure==
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[[2mjv]] is a 2 chain structure. Full experimental information is available from [http://oca.weizmann.ac.il/oca-bin/ocashort?id=2MJV OCA].
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==Reference==
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<ref group="xtra">PMID:024525235</ref><references group="xtra"/><references/>
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[[Category: Zeng, L.]]
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[[Category: Zhou, M.]]
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[[Category: Transcription]]
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[[Category: Tumorigenesis]]

Revision as of 08:42, 19 March 2014

Template:STRUCTURE 2mjv

Contents

Solution structures of second bromodomain of Brd4 with di-acetylated Twist peptide

Template:ABSTRACT PUBMED 24525235

Disease

[TWST1_HUMAN] Isolated scaphocephaly;Isolated brachycephaly;Saethre-Chotzen syndrome. The disease is caused by mutations affecting the gene represented in this entry. The disease is caused by mutations affecting the gene represented in this entry. The disease is caused by mutations affecting the gene represented in this entry. [BRD4_HUMAN] Note=A chromosomal aberration involving BRD4 is found in a rare, aggressive, and lethal carcinoma arising in midline organs of young people. Translocation t(15;19)(q14;p13) with NUT which produces a BRD4-NUT fusion protein.[1] [2]

Function

[TWST1_HUMAN] Acts as a transcriptional regulator. Inhibits myogenesis by sequestrating E proteins, inhibiting trans-activation by MEF2, and inhibiting DNA-binding by MYOD1 through physical interaction. This interaction probably involves the basic domains of both proteins. Also represses expression of proinflammatory cytokines such as TNFA and IL1B. Regulates cranial suture patterning and fusion. Activates transcription as a heterodimer with E proteins. Regulates gene expression differentially, depending on dimer composition. Homodimers induce expression of FGFR2 and POSTN while heterodimers repress FGFR2 and POSTN expression and induce THBS1 expression. Heterodimerization is also required for osteoblast differentiation.[3] [BRD4_HUMAN] Plays a role in a process governing chromosomal dynamics during mitosis (By similarity).

About this Structure

2mjv is a 2 chain structure. Full experimental information is available from OCA.

Reference

  • Shi J, Wang Y, Zeng L, Wu Y, Deng J, Zhang Q, Lin Y, Li J, Kang T, Tao M, Rusinova E, Zhang G, Wang C, Zhu H, Yao J, Zeng YX, Evers BM, Zhou MM, Zhou BP. Disrupting the Interaction of BRD4 with Diacetylated Twist Suppresses Tumorigenesis in Basal-like Breast Cancer. Cancer Cell. 2014 Feb 10;25(2):210-25. doi: 10.1016/j.ccr.2014.01.028. PMID:24525235 doi:http://dx.doi.org/10.1016/j.ccr.2014.01.028
  1. ↑ French CA, Miyoshi I, Kubonishi I, Grier HE, Perez-Atayde AR, Fletcher JA. BRD4-NUT fusion oncogene: a novel mechanism in aggressive carcinoma. Cancer Res. 2003 Jan 15;63(2):304-7. PMID:12543779
  2. ↑ French CA, Miyoshi I, Aster JC, Kubonishi I, Kroll TG, Dal Cin P, Vargas SO, Perez-Atayde AR, Fletcher JA. BRD4 bromodomain gene rearrangement in aggressive carcinoma with translocation t(15;19). Am J Pathol. 2001 Dec;159(6):1987-92. PMID:11733348 doi:10.1016/S0002-9440(10)63049-0
  3. ↑ Sosic D, Richardson JA, Yu K, Ornitz DM, Olson EN. Twist regulates cytokine gene expression through a negative feedback loop that represses NF-kappaB activity. Cell. 2003 Jan 24;112(2):169-80. PMID:12553906

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