World Library  
Flag as Inappropriate
Email this Article

Bach2

Article Id: WHEBN0014875443
Reproduction Date:

Title: Bach2  
Author: World Heritage Encyclopedia
Language: English
Subject: BZIP domain, NeuroD, EMX homeogene, NOBOX, Nur (biology)
Collection: Transcription Factors
Publisher: World Heritage Encyclopedia
Publication
Date:
 

Bach2

BTB and CNC homology 1, basic leucine zipper transcription factor 2

Crystal structure of the human Bach2 BTB/POZ domain dimer. PDB entry [1]
Available structures
PDB Ortholog search: PDBe, RCSB
Identifiers
Symbols  ; BTBD25
External IDs GeneCards:
RNA expression pattern
Orthologs
Species Human Mouse
Entrez
Ensembl
UniProt
RefSeq (mRNA)
RefSeq (protein)
Location (UCSC)
PubMed search

Transcription regulator protein BACH2 is a protein that in humans is encoded by the BACH2 gene.[2][3][4] It contains a BTB/POZ domain at its N-terminus which forms a disulphide-linked dimer [5] and a bZip_Maf domain at the C-terminus.


References

  1. ^ Rosbrook, G. O.; Stead, M. A.; Carr, S. B.; Wright, S. C. (2011). "The structure of the Bach2 POZ-domain dimer reveals an intersubunit disulfide bond". Acta Crystallographica Section D Biological Crystallography 68 (Pt 1): 26–34.  
  2. ^ Sasaki S, Ito E, Toki T, Maekawa T, Kanezaki R, Umenai T, Muto A, Nagai H, Kinoshita T, Yamamoto M, Inazawa J, Taketo MM, Nakahata T, Igarashi K, Yokoyama M (Sep 2000). "Cloning and expression of human B cell-specific transcription factor BACH2 mapped to chromosome 6q15". Oncogene 19 (33): 3739–49.  
  3. ^ Kamio T, Toki T, Kanezaki R, Sasaki S, Tandai S, Terui K, Ikebe D, Igarashi K, Ito E (Oct 2003). "B-cell-specific transcription factor BACH2 modifies the cytotoxic effects of anticancer drugs". Blood 102 (9): 3317–22.  
  4. ^ "Entrez Gene: BACH2 BTB and CNC homology 1, basic leucine zipper transcription factor 2". 
  5. ^ Rosbrook, G. O.; Stead, M. A.; Carr, S. B.; Wright, S. C. (2011). "The structure of the Bach2 POZ-domain dimer reveals an intersubunit disulfide bond". Acta Crystallographica Section D Biological Crystallography 68 (Pt 1): 26–34.  

Further reading

  • Oyake T, Itoh K, Motohashi H, et al. (1996). "Bach proteins belong to a novel family of BTB-basic leucine zipper transcription factors that interact with MafK and regulate transcription through the NF-E2 site.". Mol. Cell. Biol. 16 (11): 6083–95.  
  • Kobayashi A, Yamagiwa H, Hoshino H, et al. (2000). "A combinatorial code for gene expression generated by transcription factor Bach2 and MAZR (MAZ-related factor) through the BTB/POZ domain.". Mol. Cell. Biol. 20 (5): 1733–46.  
  • Hoshino H, Kobayashi A, Yoshida M, et al. (2000). "Oxidative stress abolishes leptomycin B-sensitive nuclear export of transcription repressor Bach2 that counteracts activation of Maf recognition element.". J. Biol. Chem. 275 (20): 15370–6.  
  • Vieira SA, Deininger MW, Sorour A, et al. (2002). "Transcription factor BACH2 is transcriptionally regulated by the BCR/ABL oncogene.". Genes Chromosomes Cancer 32 (4): 353–63.  
  • Muto A, Tashiro S, Tsuchiya H, et al. (2002). "Activation of Maf/AP-1 repressor Bach2 by oxidative stress promotes apoptosis and its interaction with promyelocytic leukemia nuclear bodies.". J. Biol. Chem. 277 (23): 20724–33.  
  • Mungall AJ, Palmer SA, Sims SK, et al. (2003). "The DNA sequence and analysis of human chromosome 6.". Nature 425 (6960): 805–11.  
  • Takakuwa T, Luo WJ, Ham MF, et al. (2004). "Integration of Epstein-Barr virus into chromosome 6q15 of Burkitt lymphoma cell line (Raji) induces loss of BACH2 expression.". Am. J. Pathol. 164 (3): 967–74.  
  • Tashiro S, Muto A, Tanimoto K, et al. (2004). "Repression of PML nuclear body-associated transcription by oxidative stress-activated Bach2.". Mol. Cell. Biol. 24 (8): 3473–84.  
  • Motamed-Khorasani A, Jurisica I, Letarte M, et al. (2007). "Differentially androgen-modulated genes in ovarian epithelial cells from BRCA mutation carriers and control patients predict ovarian cancer survival and disease progression.". Oncogene 26 (2): 198–214.  
  • Yoshida C, Yoshida F, Sears DE, et al. (2007). "Bcr-Abl signaling through the PI-3/S6 kinase pathway inhibits nuclear translocation of the transcription factor Bach2, which represses the antiapoptotic factor heme oxygenase-1.". Blood 109 (3): 1211–9.  
  • Ono A, Kono K, Ikebe D, et al. (2007). "Nuclear positioning of the BACH2 gene in BCR-ABL positive leukemic cells.". Genes Chromosomes Cancer 46 (1): 67–74.  
  • Ikeda T, Shibata J, Yoshimura K, et al. (2007). "Recurrent  
  • Hoshino H, Nishino TG, Tashiro S, et al. (2007). "Co-repressor SMRT and class II histone deacetylases promote Bach2 nuclear retention and formation of nuclear foci that are responsible for local transcriptional repression.". J. Biochem. 141 (5): 719–27.  

External links


This article incorporates text from the United States National Library of Medicine, which is in the public domain.

This article was sourced from Creative Commons Attribution-ShareAlike License; additional terms may apply. World Heritage Encyclopedia content is assembled from numerous content providers, Open Access Publishing, and in compliance with The Fair Access to Science and Technology Research Act (FASTR), Wikimedia Foundation, Inc., Public Library of Science, The Encyclopedia of Life, Open Book Publishers (OBP), PubMed, U.S. National Library of Medicine, National Center for Biotechnology Information, U.S. National Library of Medicine, National Institutes of Health (NIH), U.S. Department of Health & Human Services, and USA.gov, which sources content from all federal, state, local, tribal, and territorial government publication portals (.gov, .mil, .edu). Funding for USA.gov and content contributors is made possible from the U.S. Congress, E-Government Act of 2002.
 
Crowd sourced content that is contributed to World Heritage Encyclopedia is peer reviewed and edited by our editorial staff to ensure quality scholarly research articles.
 
By using this site, you agree to the Terms of Use and Privacy Policy. World Heritage Encyclopedia™ is a registered trademark of the World Public Library Association, a non-profit organization.
 



Copyright © World Library Foundation. All rights reserved. eBooks from Hawaii eBook Library are sponsored by the World Library Foundation,
a 501c(4) Member's Support Non-Profit Organization, and is NOT affiliated with any governmental agency or department.