World Library  
Flag as Inappropriate
Email this Article

Hmga1

Article Id: WHEBN0014118826
Reproduction Date:

Title: Hmga1  
Author: World Heritage Encyclopedia
Language: English
Subject: CEBPB, Transcription factor, Transcription factors, Cancer, NeuroD
Collection:
Publisher: World Heritage Encyclopedia
Publication
Date:
 

Hmga1

High mobility group AT-hook 1
Available structures
PDB Ortholog search: PDBe, RCSB
Identifiers
Symbols  ; HMG-R; HMGA1A; HMGIY
External IDs GeneCards:
RNA expression pattern
Orthologs
Species Human Mouse
Entrez
Ensembl
UniProt
RefSeq (mRNA)
RefSeq (protein)
Location (UCSC)
PubMed search

High-mobility group protein HMG-I/HMG-Y is a integration of retroviruses into chromosomes, and the metastatic progression of cancer cells.

HMGA1 proteins are quite small (~10-12 kDa) and basic molecules, and consist of three AT-hooks with the RGRP (Arg-Gly-Arg-Pro) core motif, a novel cross-linking domain located between the second and third AT-hook, and a C-terminal acidic tail characteristic for the HMG family comprising HMGA, HMGB and HMGN proteins.

HMGA1-GFP fusion proteins are highly dynamic in vivo (determined using FRAP analysis), but in contrast also show nanomolar affinity to AT-rich DNA in vitro (determined biochemically), which might be explained due to the extensive post-transcriptional modifications in vivo. HMGA1 preferentially binds to the minor groove of AT-rich regions in double-stranded DNA using its AT-hooks. It has little secondary structure in solution but assumes distinct conformations when bound to substrates such as DNA or other proteins. HMGA1 proteins have high amounts of diverse posttranslational modifications and are located mainly in the nucleus, especially in heterochromatin, but also in mitochondria and the cytoplasm.

Recently it has been shown that HMGA1 proteins, HMGA1a and HMGA1b, can cross-link DNA fibers in vitro and can induce chromatin clustering in vivo suggesting a structural role of HMGA1 proteins in heterochromatin organization.[3]

At least seven transcript variants encoding two different isoforms (HMGA1a, HMGA1b) have been found for this gene.[4] The splice variant HMGA1c with only two AT hooks and no acidic tail is in discussion to be a real member of the HMGA family.

Mice lacking their variant of HMGA1, i.e., Hmga1-/- mice, are diabetic, show a cardiac hypertrophy and express low levels of the insulin receptor.[5]

Interactions

HMGA1 has been shown to interact with CEBPB[6] and Sp1 transcription factor.[6]

See also

References

  1. ^ Friedmann M, Holth LT, Zoghbi HY, Reeves R (Nov 1993). "Organization, inducible-expression and chromosome localization of the human HMG-I(Y) nonhistone protein gene". Nucleic Acids Res 21 (18): 4259–67.  
  2. ^ Reeves R, Beckerbauer L (Jun 2001). "HMGI/Y proteins: flexible regulators of transcription and chromatin structure". Biochim Biophys Acta 1519 (1-2): 13–29.  
  3. ^ Vogel, B; Löschberger, A; Sauer, M; Hock, R (Sep 1, 2011). "Cross-linking of DNA through HMGA1 suggests a DNA scaffold.". Nucleic Acids Research 39 (16): 7124–33.  
  4. ^ "Entrez Gene: HMGA1 high mobility group AT-hook 1". 
  5. ^  
  6. ^ a b Foti, Daniela; Iuliano Rodolfo; Chiefari Eusebio; Brunetti Antonio (Apr 2003). "A nucleoprotein complex containing Sp1, C/EBP beta, and HMGI-Y controls human insulin receptor gene transcription". Mol. Cell. Biol. (United States) 23 (8): 2720–32.  

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 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.