The world's first wiki where authorship really matters (Nature Genetics, 2008). Due credit and reputation for authors. Imagine a global collaborative knowledge base for original thoughts. Search thousands of articles and collaborate with scientists around the globe.

wikigene or wiki gene protein drug chemical gene disease author authorship tracking collaborative publishing evolutionary knowledge reputation system wiki2.0 global collaboration genes proteins drugs chemicals diseases compound
Hoffmann, R. A wiki for the life sciences where authorship matters. Nature Genetics (2008)



Gene Review

CrebA  -  Cyclic-AMP response element binding protein A

Drosophila melanogaster

Synonyms: BBF-2, BBF2_DROME, BOX B Binding Factor-2, Bbbf2, BcDNA:SD05937, ...
Welcome! If you are familiar with the subject of this article, you can contribute to this open access knowledge base by deleting incorrect information, restructuring or completely rewriting any text. Read more.

Disease relevance of CrebA


High impact information on CrebA

  • In the prevailing view, patterned synaptic activity causes kinase-mediated activation of the transcription factor cyclic AMP response-element-binding protein, CREB [3].
  • Observations from genetic epistasis and RNA quantification experiments indicate that AP-1 acts upstream of CREB, regulates levels of CREB messenger RNA, and functions at the top of the hierarchy of transcription factors known to regulate long-term plasticity [3].
  • Thus, BBF-2 and the DNA sequence to which it binds may be important components of a tissue-specific regulatory mechanism conserved between Drosophila and man [4].
  • A number of observations suggest that BBF-2 is involved in fat body-specific expression: Mutations that disrupt BBF-2 binding to two different Adh fat body enhancers in vitro decrease the activity of these enhancers in transgenic flies [4].
  • A mutation in the Drosophila homolog of CREB, dCREB2, enhances lethality due to polyglutamine peptides (polyQ), and an additional copy of dCREB2 partially rescues this lethality [1].

Biological context of CrebA

  • This high level expression requires two early salivary gland transcription factors; CrebA is required throughout embryogenesis and Fkh is required only during late embryonic stages [5].
  • We show that zygotic mutations in several individual secretory pathway genes result in larval cuticle phenotypes nearly identical to those of CrebA mutants [5].
  • The DNA-binding domain is more closely related to mammalian CREB than to the AP-1 factors in both sequence homology and specificity of cAMP-responsive element binding [6].
  • Based on results from epistasis tests with known dorsal/ventral patterning genes, we propose that dCREB-A encodes a transcription factor that functions near the end of both the DPP- and SPI-signaling cascades to translate the corresponding extracellular signals into changes in gene expression [7].
  • Evidence was presented indicating that PGE(1) stimulation was mediated through the binding of cAMP-regulatory element binding protein (CREB) to a prostaglandin-responsive element (PGRE) as well as Sp1 binding to an adjacent Sp1 site [8].

Anatomical context of CrebA


Associations of CrebA with chemical compounds

  • The protective effects of CREB and heat-shock protein 70 against polyQ are additive, suggesting that targeting multiple pathways may be effective for treatment of polyglutamine diseases [1].
  • Sequence analysis demonstrates that this protein is a member of the leucine zipper family of transcription factors. dCREB-A is unusual in that it contains six hydrophobic residue iterations in the zipper domain rather than the four or five commonly found in this group of proteins [6].

Analytical, diagnostic and therapeutic context of CrebA

  • In this report, we describe the isolation and initial characterization of a Drosophila protein, dCREB-A, that can bind the somatostatin cyclic AMP (cAMP)-responsive element and is capable of activating transcription in cell culture [6].


  1. cAMP-response element-binding protein and heat-shock protein 70 additively suppress polyglutamine-mediated toxicity in Drosophila. Iijima-Ando, K., Wu, P., Drier, E.A., Iijima, K., Yin, J.C. Proc. Natl. Acad. Sci. U.S.A. (2005) [Pubmed]
  2. Phenotypes of Drosophila brain neurons in primary culture reveal a role for fascin in neurite shape and trajectory. Kraft, R., Escobar, M.M., Narro, M.L., Kurtis, J.L., Efrat, A., Barnard, K., Restifo, L.L. J. Neurosci. (2006) [Pubmed]
  3. AP-1 functions upstream of CREB to control synaptic plasticity in Drosophila. Sanyal, S., Sandstrom, D.J., Hoeffer, C.A., Ramaswami, M. Nature (2002) [Pubmed]
  4. A Drosophila CREB/ATF transcriptional activator binds to both fat body- and liver-specific regulatory elements. Abel, T., Bhatt, R., Maniatis, T. Genes Dev. (1992) [Pubmed]
  5. CrebA regulates secretory activity in the Drosophila salivary gland and epidermis. Abrams, E.W., Andrew, D.J. Development (2005) [Pubmed]
  6. A cyclic AMP-responsive element-binding transcriptional activator in Drosophila melanogaster, dCREB-A, is a member of the leucine zipper family. Smolik, S.M., Rose, R.E., Goodman, R.H. Mol. Cell. Biol. (1992) [Pubmed]
  7. The Drosophila dCREB-A gene is required for dorsal/ventral patterning of the larval cuticle. Andrew, D.J., Baig, A., Bhanot, P., Smolik, S.M., Henderson, K.D. Development (1997) [Pubmed]
  8. Regulation of the Na-K-ATPase beta(1)-subunit promoter by multiple prostaglandin-responsive elements. Matlhagela, K., Taub, M. Am. J. Physiol. Renal Physiol. (2006) [Pubmed]
  9. The CRE-binding protein dCREB-A is required for Drosophila embryonic development. Rose, R.E., Gallaher, N.M., Andrew, D.J., Goodman, R.H., Smolik, S.M. Genetics (1997) [Pubmed]
WikiGenes - Universities