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Gene Review

ATF6B  -  activating transcription factor 6 beta

Homo sapiens

Synonyms: ATF6-beta, Activating transcription factor 6 beta, CREB-RP, CREBL1, Creb-rp, ...
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Disease relevance of CREBL1

  • Physical interaction between hepatitis C virus NS4B protein and CREB-RP/ATF6beta [1].
  • G12 and G13 are insufficiently characterized pertussis toxin-insensitive G-proteins [2].
  • CONCLUSIONS: In conclusion, we failed to confirm the susceptible effect of the G13 allele, but provide the first data for a protective effect of allele 3 (IL10.G9) for familial psoriasis [3].

High impact information on CREBL1

  • Surprisingly, given previous reports that enforced expression of ATF6alpha induced a subset of UPR target genes, cells deficient in ATF6alpha, ATF6beta, or both had minimal defects in upregulating UPR target genes by gene profiling analysis, suggesting the presence of compensatory mechanism(s) for ATF6 in the UPR [4].
  • We describe here the basis for this strict requirement by demonstrating that both ATF6alpha and ATF6beta physically interact with NF-Y trimer via direct binding to the NF-YC subunit [5].
  • We recently proposed that ER stress response factor (ERSF) binding to ERSE is a heterologous protein complex consisting of the constitutive component NF-Y (CBF) binding to CCAAT and an inducible component binding to CCACG and identified the basic leucine zipper-type transcription factors ATF6alpha and ATF6beta as inducible components of ERSF [5].
  • Opposing roles for ATF6alpha and ATF6beta in endoplasmic reticulum stress response gene induction [6].
  • AEBSF also inhibited production of the mature form of SREBP-2 that was induced in response to sterol depletion, and appeared to directly prevent cleavage of ATF6alpha and ATF6beta by inhibiting Site-1 protease [7].

Chemical compound and disease context of CREBL1


Biological context of CREBL1

  • Furthermore, the soluble forms of ATF6 and the G13 gene product are unable to bind to several point mutants of the cis-acting ER stress response element in vitro that hardly respond to ER stress in vivo [8].
  • The longest open reading frame obtained for G13 codes for a 703 amino acid protein of approx. 77 kDa in molecular mass [9].
  • G13 contains a bZIP motif, a region rich in basic amino acids adjacent to a coiled-coil leucine zipper domain, common to this class of proteins that is known to be involved in dimerization and DNA binding [9].
  • An N-terminal half of NS4B and a central portion of CREB-RP/ATF6beta containing the basic leucine zipper (bZIP) domain were involved in the interaction [1].
  • The structure is generally consistent with the most recent of two earlier secondary structure predictions, with residues G1-G2-C3-G4 and C6-U7 forming standard Watson Crick base-pairs with self-complementary residues C16-G17-C18-C19 and A12-G13, respectively [10].

Anatomical context of CREBL1

  • Even though it contained at least one potential bipartite nuclear localization signal, the G13 protein was present both in the cytoplasm and the nucleus of the fibroblast cells [9].
  • Antibodies raised against a fragment encoding the C-terminal half of the putative G13 protein recognized a major polypeptide of approx. 86 kDa and a minor polypeptide of approx. 78 kDa on immunoblotting of U937 cell extracts; this has been confirmed by immunoprecipitation experiments [9].

Associations of CREBL1 with chemical compounds


Other interactions of CREBL1


Analytical, diagnostic and therapeutic context of CREBL1


  1. Physical interaction between hepatitis C virus NS4B protein and CREB-RP/ATF6beta. Tong, W.Y., Nagano-Fujii, M., Hidajat, R., Deng, L., Takigawa, Y., Hotta, H. Biochem. Biophys. Res. Commun. (2002) [Pubmed]
  2. Distinct biochemical properties of the native members of the G12 G-protein subfamily. Characterization of G alpha 12 purified from rat brain. Harhammer, R., Nürnberg, B., Harteneck, C., Leopoldt, D., Exner, T., Schultz, G. Biochem. J. (1996) [Pubmed]
  3. Interleukin-10 promoter polymorphism IL10.G and familial early onset psoriasis. Hensen, P., Asadullah, K., Windemuth, C., Rüschendorf, F., Hüffmeier, U., Ständer, M., Schmitt-Egenolf, M., Wienker, T.F., Reis, A., Traupe, H. Br. J. Dermatol. (2003) [Pubmed]
  4. XBP-1 regulates a subset of endoplasmic reticulum resident chaperone genes in the unfolded protein response. Lee, A.H., Iwakoshi, N.N., Glimcher, L.H. Mol. Cell. Biol. (2003) [Pubmed]
  5. Endoplasmic reticulum stress-induced formation of transcription factor complex ERSF including NF-Y (CBF) and activating transcription factors 6alpha and 6beta that activates the mammalian unfolded protein response. Yoshida, H., Okada, T., Haze, K., Yanagi, H., Yura, T., Negishi, M., Mori, K. Mol. Cell. Biol. (2001) [Pubmed]
  6. Opposing roles for ATF6alpha and ATF6beta in endoplasmic reticulum stress response gene induction. Thuerauf, D.J., Morrison, L., Glembotski, C.C. J. Biol. Chem. (2004) [Pubmed]
  7. A serine protease inhibitor prevents endoplasmic reticulum stress-induced cleavage but not transport of the membrane-bound transcription factor ATF6. Okada, T., Haze, K., Nadanaka, S., Yoshida, H., Seidah, N.G., Hirano, Y., Sato, R., Negishi, M., Mori, K. J. Biol. Chem. (2003) [Pubmed]
  8. Identification of the G13 (cAMP-response-element-binding protein-related protein) gene product related to activating transcription factor 6 as a transcriptional activator of the mammalian unfolded protein response. Haze, K., Okada, T., Yoshida, H., Yanagi, H., Yura, T., Negishi, M., Mori, K. Biochem. J. (2001) [Pubmed]
  9. The gene G13 in the class III region of the human MHC encodes a potential DNA-binding protein. Khanna, A., Campbell, R.D. Biochem. J. (1996) [Pubmed]
  10. NMR structure of stem-loop SL2 of the HIV-1 psi RNA packaging signal reveals a novel A-U-A base-triple platform. Amarasinghe, G.K., De Guzman, R.N., Turner, R.B., Summers, M.F. J. Mol. Biol. (2000) [Pubmed]
  11. Rho-dependent, Rho kinase-independent inhibitory regulation of Rac and cell migration by LPA1 receptor in Gi-inactivated CHO cells. Sugimoto, N., Takuwa, N., Yoshioka, K., Takuwa, Y. Exp. Cell Res. (2006) [Pubmed]
  12. Coronavirus 3CLpro proteinase cleavage sites: possible relevance to SARS virus pathology. Kiemer, L., Lund, O., Brunak, S., Blom, N. BMC Bioinformatics (2004) [Pubmed]
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