World Library  
Flag as Inappropriate
Email this Article

Apoptosis-antagonizing transcription factor

Article Id: WHEBN0014773744
Reproduction Date:

Title: Apoptosis-antagonizing transcription factor  
Author: World Heritage Encyclopedia
Language: English
Subject: Retinoblastoma protein, NeuroD, EMX homeogene, NOBOX, Winged-helix transcription factors
Collection:
Publisher: World Heritage Encyclopedia
Publication
Date:
 

Apoptosis-antagonizing transcription factor

Apoptosis antagonizing transcription factor
Identifiers
Symbols  ; BFR2; CHE-1; CHE1; DED
External IDs GeneCards:
Orthologs
Species Human Mouse
Entrez
Ensembl
UniProt
RefSeq (mRNA)
RefSeq (protein)
Location (UCSC)
PubMed search

Protein AATF is a protein that in humans is encoded by the AATF gene.[1][2][3] The protein encoded by this gene was identified on the basis of its interaction with MAP3K12/DLK, a protein kinase known to be involved in the induction of cell apoptosis. This gene product contains a leucine zipper, which is a characteristic motif of transcription factors, and was shown to exhibit strong transactivation activity when fused to Gal4 DNA binding domain. Overexpression of this gene interfered with MAP3K12 induced apoptosis.[3]

Interactions

Apoptosis-antagonizing transcription factor has been shown to interact with Sp1 transcription factor,[4] POLR2J,[2] PAWR[5] and Retinoblastoma protein.[2][6]

References

  1. ^ Lindfors K, Halttunen T, Huotari P, Nupponen N, Vihinen M, Visakorpi T, Maki M, Kainulainen H (Oct 2000). "Identification of novel transcription factor-like gene from human intestinal cells". Biochem Biophys Res Commun 276 (2): 660–6.  
  2. ^ a b c Fanciulli M, Bruno T, Di Padova M, De Angelis R, Iezzi S, Iacobini C, Floridi A, Passananti C (Jun 2000). "Identification of a novel partner of RNA polymerase II subunit 11, Che-1, which interacts with and affects the growth suppression function of Rb". FASEB J 14 (7): 904–12.  
  3. ^ a b "Entrez Gene: AATF apoptosis antagonizing transcription factor". 
  4. ^ Di Padova, Monica; Bruno Tiziana, De Nicola Francesca, Iezzi Simona, D'Angelo Carmen, Gallo Rita, Nicosia Daniela, Corbi Nicoletta, Biroccio Annamaria, Floridi Aristide, Passananti Claudio, Fanciulli Maurizio (Sep 2003). "Che-1 arrests human colon carcinoma cell proliferation by displacing HDAC1 from the p21WAF1/CIP1 promoter". J. Biol. Chem. (United States) 278 (38): 36496–504.  
  5. ^ Guo, Qing; Xie Jun (Feb 2004). "AATF inhibits aberrant production of amyloid beta peptide 1-42 by interacting directly with Par-4". J. Biol. Chem. (United States) 279 (6): 4596–603.  
  6. ^ Bruno, Tiziana; De Angelis Roberta, De Nicola Francesca, Barbato Christian, Di Padova Monica, Corbi Nicoletta, Libri Valentina, Benassi Barbara, Mattei Elisabetta, Chersi Alberto, Soddu Silvia, Floridi Aristide, Passananti Claudio, Fanciulli Maurizio (Nov 2002). "Che-1 affects cell growth by interfering with the recruitment of HDAC1 by Rb". Cancer Cell (United States) 2 (5): 387–99.  

Further reading

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 Project Gutenberg 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.