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Gene Review

Cebpz  -  CCAAT/enhancer binding protein zeta

Mus musculus

Synonyms: AI848081, CBF, CBF2, CCAAT-binding factor, CCAAT-box-binding transcription factor, ...
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Disease relevance of Cebpz

  • Both MyNF1 alpha and -beta supershift with an antiserum raised by using a peptide derived from the N terminus of polyomavirus enhancer-binding protein 2/core-binding factor (PEBP2/CBF) alpha subunit [1].
  • In addition, these studies identify the first B-cell target of CBF, a protein that has been implicated in the development of childhood pre-B-cell leukemias [2].
  • Mutations in CBF genes are found in leukemias and bone disorders [3].
  • Mutations in CBF genes are found in leukemias, bone disorders, and gastric cancer [4].
  • Selection of reversions and suppressors of a mutation in the CBF binding site of a lymphomagenic retrovirus [5].

High impact information on Cebpz

  • Point mutations in the CCAAT motif that show either no binding or a decreased binding of CBF likewise abolish or reduce activation of transcription by CBF [6].
  • Regulation of T cell receptor delta gene rearrangement by CBF/PEBP2 [7].
  • Treatment of cells with genistein converted NF-Y/CBF into a nonbinding, transcriptionally inactive form [8].
  • Likewise, tissues with large or small average cell sizes contained similar levels of the mRNAs encoding Oct1 or NF-Ya, one of the subunits of the heteromeric CCAAT-binding factor NF-Y, per DNA-equivalent [9].
  • The observed phenotype was indistinguishable from that reported for homozygous disruption of AML1, which encodes a DNA binding subunit of PEBP2/CBF [10].

Chemical compound and disease context of Cebpz


Biological context of Cebpz

  • Cbf beta regulates Runx2 function isoform-dependently in postnatal bone development [12].
  • Deletional analysis carried out in the absence of the c-Myb-binding site at -147 located at -301 a second c-Myb-binding site which also synergized with CBF to activate the enhancer [13].
  • Cbf alpha 2 overexpression does not cause any gross morphological changes to NIH 3T3 cells but does result in increased CBF activity, as indicated by electrophoretic mobility shift assays and transactivation of reporter constructs [14].
  • The AML1 gene (recently renamed Runx1), which encodes the DNA-binding subunit of a transcription factor of the core binding factor (CBF) family, is required for the establishment of definitive hematopoiesis [15].
  • In this study, we sequenced five tryptic peptides from two of the bovine CBF proteins and isolated three cDNA clones from a mouse thymus cDNA library encoding three of the tryptic peptides from the bovine proteins [16].

Anatomical context of Cebpz

  • We previously reported the purification of core-binding factors (CBF) from calf thymus nuclei (S. Wang and N.A. Speck, Mol. Cell. Biol. 12:89-102, 1992) [16].
  • In primary cultures of mouse embryonic fibroblasts, conditional inactivation of CBF results in a block in cell proliferation and inhibition of S phase or DNA synthesis, which is followed by induction of apoptosis [17].
  • Within this region, DNase I footprinting and electrophoretic mobility shift assays delineated one element that contains an inverted CCAAT-binding factor site and a protein-DNA binding site using nuclear extracts from odontoblasts [18].
  • Mutation of the CBF-binding site significantly increases transcriptional activity of the rat renin promoter in Calu-6 and COS-7 cells but not in As4.1 cells, whereas mutation of the Ets-binding site reduces promoter activity of the rat renin gene in all three cell lines [19].
  • Loss of the Sp1 binding sites was associated with loss of transgene expression in osteoblasts, whereas elimination of the CBF/NFY binding site (alone or in combination with the TC-rich boxes) was correlated with a lack of activity in the ventral fascia and head dermis and musculature [20].

Associations of Cebpz with chemical compounds

  • The analysis of cell growth using bromodeoxyuridine labeling showed that expression of the mutant CBF-B decreased the number of cells entering into S phase, and also delayed induction of S phase in the quiescent cells after serum stimulation, thus indicating that the inhibition of CBF binding prolonged the progression of S phase in fibroblasts [21].
  • A truncated CBF that lacked the glutamine-rich domains did not activate transcription from nucleosomal wild-type topo IIalpha promoter but disrupted the nucleosomal structure about as much as did the binding of full-length CBF [22].
  • To understand the in vivo function of CBF, a dominant negative mutant of CBF-B subunit that inhibits DNA binding of wild type CBF was stably expressed in mouse fibroblast cells under control of tetracycline-responsive promoter [21].
  • CBF beta-SMMHC reduced endogenous CBF DNA-binding fivefold in both cell types, increased cell generation time 1.9-fold, on average, in 32D cl3 cells and 1.5-fold in Ba/ F3 cells and decreased tritiated thymidine incorporation into DNA correspondingly [23].
  • To resolve the importance of the heparan sulfate-binding or cell-binding activities of the pFN molecule in these adhesive responses, a cell-binding fragment (120K) (CBF) free of any heparan sulfate-binding activity was prepared from human pFN by chymotrypic digestion and isolated as described by Pierschbacher et al [24].

Physical interactions of Cebpz


Other interactions of Cebpz


Analytical, diagnostic and therapeutic context of Cebpz


  1. PEBP2/CBF, the murine homolog of the human myeloid AML1 and PEBP2 beta/CBF beta proto-oncoproteins, regulates the murine myeloperoxidase and neutrophil elastase genes in immature myeloid cells. Nuchprayoon, I., Meyers, S., Scott, L.M., Suzow, J., Hiebert, S., Friedman, A.D. Mol. Cell. Biol. (1994) [Pubmed]
  2. ETS-core binding factor: a common composite motif in antigen receptor gene enhancers. Erman, B., Cortes, M., Nikolajczyk, B.S., Speck, N.A., Sen, R. Mol. Cell. Biol. (1998) [Pubmed]
  3. Energetic and functional contribution of residues in the core binding factor beta (CBFbeta ) subunit to heterodimerization with CBFalpha. Tang, Y.Y., Shi, J., Zhang, L., Davis, A., Bravo, J., Warren, A.J., Speck, N.A., Bushweller, J.H. J. Biol. Chem. (2000) [Pubmed]
  4. Energetic contribution of residues in the Runx1 Runt domain to DNA binding. Li, Z., Yan, J., Matheny, C.J., Corpora, T., Bravo, J., Warren, A.J., Bushweller, J.H., Speck, N.A. J. Biol. Chem. (2003) [Pubmed]
  5. Selection of reversions and suppressors of a mutation in the CBF binding site of a lymphomagenic retrovirus. Martiney, M.J., Rulli, K., Beaty, R., Levy, L.S., Lenz, J. J. Virol. (1999) [Pubmed]
  6. Selective activation of transcription by a novel CCAAT binding factor. Maity, S.N., Golumbek, P.T., Karsenty, G., de Crombrugghe, B. Science (1988) [Pubmed]
  7. Regulation of T cell receptor delta gene rearrangement by CBF/PEBP2. Lauzurica, P., Zhong, X.P., Krangel, M.S., Roberts, J.L. J. Exp. Med. (1997) [Pubmed]
  8. Mechanism for the suppression of the mammalian stress response by genistein, an anticancer phytoestrogen from soy. Zhou, Y., Lee, A.S. J. Natl. Cancer Inst. (1998) [Pubmed]
  9. Cell size regulation, a mechanism that controls cellular RNA accumulation: consequences on regulation of the ubiquitous transcription factors Oct1 and NF-Y and the liver-enriched transcription factor DBP. Schmidt, E.E., Schibler, U. J. Cell Biol. (1995) [Pubmed]
  10. Hematopoiesis in the fetal liver is impaired by targeted mutagenesis of a gene encoding a non-DNA binding subunit of the transcription factor, polyomavirus enhancer binding protein 2/core binding factor. Niki, M., Okada, H., Takano, H., Kuno, J., Tani, K., Hibino, H., Asano, S., Ito, Y., Satake, M., Noda, T. Proc. Natl. Acad. Sci. U.S.A. (1997) [Pubmed]
  11. A reproducible model of middle cerebral artery occlusion in mice: hemodynamic, biochemical, and magnetic resonance imaging. Hata, R., Mies, G., Wiessner, C., Fritze, K., Hesselbarth, D., Brinker, G., Hossmann, K.A. J. Cereb. Blood Flow Metab. (1998) [Pubmed]
  12. Cbf beta regulates Runx2 function isoform-dependently in postnatal bone development. Kanatani, N., Fujita, T., Fukuyama, R., Liu, W., Yoshida, C.A., Moriishi, T., Yamana, K., Miyazaki, T., Toyosawa, S., Komori, T. Dev. Biol. (2006) [Pubmed]
  13. Core binding factor cannot synergistically activate the myeloperoxidase proximal enhancer in immature myeloid cells without c-Myb. Britos-Bray, M., Friedman, A.D. Mol. Cell. Biol. (1997) [Pubmed]
  14. Overexpression of core-binding factor alpha (CBF alpha) reverses cellular transformation by the CBF beta-smooth muscle myosin heavy chain chimeric oncoprotein. Hajra, A., Liu, P.P., Speck, N.A., Collins, F.S. Mol. Cell. Biol. (1995) [Pubmed]
  15. Haploinsufficiency of Runx1 results in the acceleration of mesodermal development and hemangioblast specification upon in vitro differentiation of ES cells. Lacaud, G., Kouskoff, V., Trumble, A., Schwantz, S., Keller, G. Blood (2004) [Pubmed]
  16. Cloning and characterization of subunits of the T-cell receptor and murine leukemia virus enhancer core-binding factor. Wang, S., Wang, Q., Crute, B.E., Melnikova, I.N., Keller, S.R., Speck, N.A. Mol. Cell. Biol. (1993) [Pubmed]
  17. The B subunit of the CCAAT box binding transcription factor complex (CBF/NF-Y) is essential for early mouse development and cell proliferation. Bhattacharya, A., Deng, J.M., Zhang, Z., Behringer, R., de Crombrugghe, B., Maity, S.N. Cancer Res. (2003) [Pubmed]
  18. Regulation of the Cell Type-specific dentin sialophosphoprotein gene expression in mouse odontoblasts by a novel transcription repressor and an activator CCAAT-binding factor. Chen, S., Unterbrink, A., Kadapakkam, S., Dong, J., Gu, T.T., Dickson, J., Chuang, H.H., MacDougall, M. J. Biol. Chem. (2004) [Pubmed]
  19. Activation of the rat renin promoter by HOXD10.PBX1b.PREP1, Ets-1, and the intracellular domain of notch. Pan, L., Glenn, S.T., Jones, C.A., Gross, K.W. J. Biol. Chem. (2005) [Pubmed]
  20. Cooperativity between far upstream enhancer and proximal promoter elements of the human {alpha}2(I) collagen (COL1A2) gene instructs tissue specificity in transgenic mice. Tanaka, S., Antoniv, T.T., Liu, K., Wang, L., Wells, D.J., Ramirez, F., Bou-Gharios, G. J. Biol. Chem. (2004) [Pubmed]
  21. Stable expression of a dominant negative mutant of CCAAT binding factor/NF-Y in mouse fibroblast cells resulting in retardation of cell growth and inhibition of transcription of various cellular genes. Hu, Q., Maity, S.N. J. Biol. Chem. (2000) [Pubmed]
  22. CBF/NF-Y functions both in nucleosomal disruption and transcription activation of the chromatin-assembled topoisomerase IIalpha promoter. Transcription activation by CBF/NF-Y in chromatin is dependent on the promoter structure. Coustry, F., Hu, Q., de Crombrugghe, B., Maity, S.N. J. Biol. Chem. (2001) [Pubmed]
  23. CBF beta-SMMHC, expressed in M4Eo AML, reduced CBF DNA-binding and inhibited the G1 to S cell cycle transition at the restriction point in myeloid and lymphoid cells. Cao, W., Britos-Bray, M., Claxton, D.F., Kelley, C.A., Speck, N.A., Liu, P.P., Friedman, A.D. Oncogene (1997) [Pubmed]
  24. Substratum contacts and cytoskeletal reorganization of BALB/c 3T3 cells on a cell-binding fragment and heparin-binding fragments of plasma fibronectin. Izzard, C.S., Radinsky, R., Culp, L.A. Exp. Cell Res. (1986) [Pubmed]
  25. Transcriptional activation of the small GTPase gene rhoB by genotoxic stress is regulated via a CCAAT element. Fritz, G., Kaina, B. Nucleic Acids Res. (2001) [Pubmed]
  26. The regulation of catalase gene expression in mouse muscle cells is dependent on the CCAAT-binding factor NF-Y. Luo, D., Rando, T.A. Biochem. Biophys. Res. Commun. (2003) [Pubmed]
  27. Differential binding of a CCAAT DNA binding factor to the promoters of the mouse alpha 2(I) and alpha 1(III) collagen genes. Hatamochi, A., Paterson, B., de Crombrugghe, B. J. Biol. Chem. (1986) [Pubmed]
  28. Ubiquitous factors that interact simultaneously with two distinct cis-elements on the rat aldolase B gene promoter. Yabuki, T., Ejiri, S., Tsutsumi, K. Biochim. Biophys. Acta (1993) [Pubmed]
  29. AML1/RUNX1 increases during G1 to S cell cycle progression independent of cytokine-dependent phosphorylation and induces cyclin D3 gene expression. Bernardin-Fried, F., Kummalue, T., Leijen, S., Collector, M.I., Ravid, K., Friedman, A.D. J. Biol. Chem. (2004) [Pubmed]
  30. Enlarged infarcts in endothelial nitric oxide synthase knockout mice are attenuated by nitro-L-arginine. Huang, Z., Huang, P.L., Ma, J., Meng, W., Ayata, C., Fishman, M.C., Moskowitz, M.A. J. Cereb. Blood Flow Metab. (1996) [Pubmed]
  31. Attenuation of transient focal cerebral ischemic injury in transgenic mice expressing a mutant ICE inhibitory protein. Hara, H., Fink, K., Endres, M., Friedlander, R.M., Gagliardini, V., Yuan, J., Moskowitz, M.A. J. Cereb. Blood Flow Metab. (1997) [Pubmed]
  32. Regulation of the human Sox9 promoter by the CCAAT-binding factor. Colter, D.C., Piera-Velazquez, S., Hawkins, D.F., Whitecavage, M.K., Jimenez, S.A., Stokes, D.G. Matrix Biol. (2005) [Pubmed]
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