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Gene Review

CEBPZ  -  CCAAT/enhancer binding protein (C/EBP), zeta

Homo sapiens

Synonyms: CBF, CBF2, CCAAT-binding factor, CCAAT-box-binding transcription factor, CCAAT/enhancer-binding protein zeta, ...
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Disease relevance of CEBPZ


Psychiatry related information on CEBPZ

  • After CBS all 15 patients had increased physical activity before angina or completion of treadmill exercise with increased heart rate-blood pressure product (HRBP) (+ 63 +/- 3.2 X 10(2) bpm - mm Hg) in 14 of 15 patients indicating increased CBF; four had positive TECG, and five had EA [5].
  • To assess dynamic changes in brain function throughout the sleep-wake cycle, CBF was measured with H2(15)O and PET in 37 normal male volunteers: (i) while awake prior to sleep onset; (ii) during Stage 3-4 sleep, i.e. slow wave sleep (SWS); (iii) during rapid eye movement (REM) sleep; and (iv) upon waking following recovery sleep [6].
  • The pattern of regional change in CBF was not similar to Alzheimer's disease [7].
  • Thus, PET measurements of CBF and metabolism may be artifactually lowered in normal aging and dementia, which are both associated with significant brain atrophy [8].
  • CBF was measured on separate nights during REM sleep and during EEG-verified wakefulness [9].

High impact information on CEBPZ

  • N-Cad/CTF2 binds the transcription factor CBP and promotes its proteasomal degradation, inhibiting CRE-dependent transactivation [10].
  • Here, we show that a PS1-dependent gamma-secretase protease activity promotes an epsilon-like cleavage of N-cadherin to produce its intracellular domain peptide, N-Cad/CTF2 [10].
  • In DNAase I protection experiments, the CCAAT-binding factor of only the testis extract is able to interact with the sperm H2B promoter [11].
  • Thus, the repression of the hsp70 promoter by p53 may be mediated by direct protein-protein interaction with CBF [12].
  • This E1a transactivation of the hsp70 promoter is mediated by CCAAT binding factor (CBF) [12].

Chemical compound and disease context of CEBPZ


Biological context of CEBPZ

  • These results indicate that the CBF/NF-Y proteins regulate the transcription of COL11A1 by directly binding to the ATTGG sequence in the proximal promoter region [18].
  • The mCBF1 mRNA encodes a protein of 997 amino acids, whereas the mCBF2 protein is predicted to be only 461 amino acids in length; mCBF1 and human CBF (hCBF) share>80% amino acid sequence identity [19].
  • PEBP2/CBF is a heterodimeric transcription factor essential for genetic regulation of hematopoiesis and osteogenesis [20].
  • Chromosomal translocations involving the human CBFB gene, which codes for the non-DNA binding subunit of CBF (CBF beta), are associated with a large percentage of human leukemias [21].
  • In contrast to the control proteins, the DeltaACD mutant did not inhibit CBF DNA binding, AML1-mediated reporter activation, or G(1) to S cell cycle progression, the last being dependent upon activation of CBF-regulated genes [2].

Anatomical context of CEBPZ

  • 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 [22].
  • SV40-LT induced a specific CCAAT box-binding factor (CBF) in CV-1 and COS-7 cells, as judged by gel shift and Southwestern analyses [23].
  • To understand the role of the CCAAT-binding factor, CBF, in transcription, we developed a strategy to purify the heterotrimeric CBF complex from HeLa cell extracts using two successive immunoaffinity chromatography steps [24].
  • Thyroid carcinomas and myeloid leukemias both possess transcription factor gene rearrangements-PPARgamma-related translocations in thyroid carcinoma and RARalpha-related and CBF-related translocations (amongst others) in myeloid leukemia [25].
  • Cellular localization by immunofluorescence staining revealed that p32 is present in the cell throughout the cytosol and nucleus, whereas CBF is present primarily in the nucleus [24].

Associations of CEBPZ with chemical compounds

  • We then tested whether in this system the glutamine- and serine/threonine-rich domains of CBF-B were needed for trans-activation by CBF [26].
  • These findings suggest that, in cisplatin-resistant cells, the expression of HMG1 gene product is enhanced at the transcriptional level and that this probably occurs through the enhanced expression of the CCAAT binding factor, CTF/NF-1 [27].
  • The fusion protein could bind to ssDNA, whereas CBF in C2 cell nuclear extracts could not [28].
  • Treatment of BE2 cells with genistein, known to inhibit the CBF binding to DNA, significantly reduced protein levels of beta1 sGC by inhibiting transcription [29].
  • With the continuous infusion of epinephrine (4 micrograms/kg/min) in another group of animals, MBF was significantly greater at 20 min of CPR and CBF and cerebral O2 uptake were greater at 35 min of CPR as a result of higher perfusion pressures.(ABSTRACT TRUNCATED AT 250 WORDS)[30]

Physical interactions of CEBPZ


Regulatory relationships of CEBPZ


Other interactions of CEBPZ

  • The transcription factor CCAAT-binding factor CBF/NF-Y regulates the proximal promoter activity in the human alpha 1(XI) collagen gene (COL11A1) [18].
  • The transcription factor CCAAT-binding factor CBF/NF-Y and two repressors regulate the core promoter of the human pro-alpha3(V) collagen gene (COL5A3) [38].
  • Chromosomal assignment and tissue expression of CBF-C/NFY-C, the third subunit of the mammalian CCAAT-binding factor [39].
  • Furthermore, CTF2 transactivates p53-induced p21 promoter activity, but inhibits p73alpha-induced p21 promoter activity [31].
  • Electrophoretic mobility-shift assays showed that extracts from cells transformed by CBF beta-SMMHC no longer formed the normal CBF/DNA complex but instead formed a much larger complex that did not migrate into the gel [40].

Analytical, diagnostic and therapeutic context of CEBPZ

  • In a chromatin immunoprecipitation assay, CBF/NF-Y protein directly bound to this region, in vivo [38].
  • CONCLUSION: MRD quantification by real-time RT-PCR allows the identification of patients with a high risk of relapse among the CBF leukemias [3].
  • No CBF reduction occurred in a control group of 15 patients who underwent carotid endarterectomy or extracranial-intracranial shunt operations [41].
  • The reduction in CBF correlated positively with increasing years (p less than 0.05), duration of extracorporeal circulation (p less than 0.05), and low mean arterial blood pressure during the bypass (p less than 0.02) [41].
  • However, when CPR was prolonged beyond 20 min, aortic pressure fell and CBF and MBF declined to the near-zero levels seen in adult preparations [30].


  1. Immunoglobulin motif DNA recognition and heterodimerization of the PEBP2/CBF Runt domain. Nagata, T., Gupta, V., Sorce, D., Kim, W.Y., Sali, A., Chait, B.T., Shigesada, K., Ito, Y., Werner, M.H. Nat. Struct. Biol. (1999) [Pubmed]
  2. Multimerization via its myosin domain facilitates nuclear localization and inhibition of core binding factor (CBF) activities by the CBFbeta-smooth muscle myosin heavy chain myeloid leukemia oncoprotein. Kummalue, T., Lou, J., Friedman, A.D. Mol. Cell. Biol. (2002) [Pubmed]
  3. Prognostic value of minimal residual disease quantification by real-time reverse transcriptase polymerase chain reaction in patients with core binding factor leukemias. Krauter, J., Gorlich, K., Ottmann, O., Lubbert, M., Dohner, H., Heit, W., Kanz, L., Ganser, A., Heil, G. J. Clin. Oncol. (2003) [Pubmed]
  4. The transcriptional activity of the CCAAT-binding factor CBF is mediated by two distinct activation domains, one in the CBF-B subunit and the other in the CBF-C subunit. Coustry, F., Maity, S.N., Sinha, S., de Crombrugghe, B. J. Biol. Chem. (1996) [Pubmed]
  5. Determination of improved myocardial perfusion after aortocoronary bypass surgery by exercise rubidium-81 scintigraphy. Lurie, A.J., Salel, A.F., Berman, D.S., DeNardo, G.L., Hurley, E.J., Mason, D.T. Circulation (1976) [Pubmed]
  6. Regional cerebral blood flow throughout the sleep-wake cycle. An H2(15)O PET study. Braun, A.R., Balkin, T.J., Wesenten, N.J., Carson, R.E., Varga, M., Baldwin, P., Selbie, S., Belenky, G., Herscovitch, P. Brain (1997) [Pubmed]
  7. Scopolamine reduces frontal cortex perfusion. Honer, W.G., Prohovnik, I., Smith, G., Lucas, L.R. J. Cereb. Blood Flow Metab. (1988) [Pubmed]
  8. Correction of positron emission tomography data for cerebral atrophy. Herscovitch, P., Auchus, A.P., Gado, M., Chi, D., Raichle, M.E. J. Cereb. Blood Flow Metab. (1986) [Pubmed]
  9. Human regional cerebral blood flow during rapid-eye-movement sleep. Madsen, P.L., Holm, S., Vorstrup, S., Friberg, L., Lassen, N.A., Wildschiødtz, G. J. Cereb. Blood Flow Metab. (1991) [Pubmed]
  10. A CBP binding transcriptional repressor produced by the PS1/epsilon-cleavage of N-cadherin is inhibited by PS1 FAD mutations. Marambaud, P., Wen, P.H., Dutt, A., Shioi, J., Takashima, A., Siman, R., Robakis, N.K. Cell (2003) [Pubmed]
  11. Mutually exclusive interaction of the CCAAT-binding factor and of a displacement protein with overlapping sequences of a histone gene promoter. Barberis, A., Superti-Furga, G., Busslinger, M. Cell (1987) [Pubmed]
  12. Regulation of the human hsp70 promoter by p53. Agoff, S.N., Hou, J., Linzer, D.I., Wu, B. Science (1993) [Pubmed]
  13. The effect of carbon dioxide on cerebral arteries. Madden, J.A. Pharmacol. Ther. (1993) [Pubmed]
  14. ISI values and interhemispheric differences in patients with ischemic cerebrovascular disease; correlations with clinical and angiographic findings. Mosmans, P.C., Veering, M.M., Jonkman, E.J. Stroke (1986) [Pubmed]
  15. Brain blood flow and metabolism after global ischemia and post-insult thiopental therapy in monkeys. Kofke, W.A., Nemoto, E.M., Hossmann, K.A., Taylor, F., Kessler, P.D., Stezoski, S.W. Stroke (1979) [Pubmed]
  16. Effect of adenosine on human cerebral blood flow as determined by positron emission tomography. Sollevi, A., Ericson, K., Eriksson, L., Lindqvist, C., Lagerkranser, M., Stone-Elander, S. J. Cereb. Blood Flow Metab. (1987) [Pubmed]
  17. Duration threshold of induced hypertension on cerebral blood flow, energy metabolism, and edema after transient forebrain ischemia in gerbils. Hosomi, N., Tsuda, Y., Ichihara, S.I., Kitadai, M., Ohyama, H., Matsuo, H. J. Cereb. Blood Flow Metab. (1996) [Pubmed]
  18. The transcription factor CCAAT-binding factor CBF/NF-Y regulates the proximal promoter activity in the human alpha 1(XI) collagen gene (COL11A1). Matsuo, N., Yu-Hua, W., Sumiyoshi, H., Sakata-Takatani, K., Nagato, H., Sakai, K., Sakurai, M., Yoshioka, H. J. Biol. Chem. (2003) [Pubmed]
  19. Cloning and characterization of mouse CCAAT binding factor. Hoeppner, M.A., Gilbert, D.J., Copeland, N.G., Jenkins, N.A., Linzer, D.I., Wu, B. Nucleic Acids Res. (1996) [Pubmed]
  20. Molecular insights into PEBP2/CBF beta-SMMHC associated acute leukemia revealed from the structure of PEBP2/CBF beta. Goger, M., Gupta, V., Kim, W.Y., Shigesada, K., Ito, Y., Werner, M.H. Nat. Struct. Biol. (1999) [Pubmed]
  21. Altered affinity of CBF beta-SMMHC for Runx1 explains its role in leukemogenesis. Lukasik, S.M., Zhang, L., Corpora, T., Tomanicek, S., Li, Y., Kundu, M., Hartman, K., Liu, P.P., Laue, T.M., Biltonen, R.L., Speck, N.A., Bushweller, J.H. Nat. Struct. Biol. (2002) [Pubmed]
  22. 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]
  23. SV40 large T antigen transactivates the human cdc2 promoter by inducing a CCAAT box binding factor. Chen, H., Campisi, J., Padmanabhan, R. J. Biol. Chem. (1996) [Pubmed]
  24. Human p32, interacts with B subunit of the CCAAT-binding factor, CBF/NF-Y, and inhibits CBF-mediated transcription activation in vitro. Chattopadhyay, C., Hawke, D., Kobayashi, R., Maity, S.N. Nucleic Acids Res. (2004) [Pubmed]
  25. Molecular events in follicular thyroid tumors. Kroll, T.G. Cancer Treat. Res. (2004) [Pubmed]
  26. Studies on transcription activation by the multimeric CCAAT-binding factor CBF. Coustry, F., Maity, S.N., de Crombrugghe, B. J. Biol. Chem. (1995) [Pubmed]
  27. Transcriptional activation of the human HMG1 gene in cisplatin-resistant human cancer cells. Nagatani, G., Nomoto, M., Takano, H., Ise, T., Kato, K., Imamura, T., Izumi, H., Makishima, K., Kohno, K. Cancer Res. (2001) [Pubmed]
  28. A protein binding to CArG box motifs and to single-stranded DNA functions as a transcriptional repressor. Kamada, S., Miwa, T. Gene (1992) [Pubmed]
  29. CCAAT-binding factor regulates expression of the beta1 subunit of soluble guanylyl cyclase gene in the BE2 human neuroblastoma cell line. Sharina, I.G., Martin, E., Thomas, A., Uray, K.L., Murad, F. Proc. Natl. Acad. Sci. U.S.A. (2003) [Pubmed]
  30. Effect of epinephrine on cerebral and myocardial perfusion in an infant animal preparation of cardiopulmonary resuscitation. Schleien, C.L., Dean, J.M., Koehler, R.C., Michael, J.R., Chantarojanasiri, T., Traystman, R., Rogers, M.C. Circulation (1986) [Pubmed]
  31. Physical interaction of tumour suppressor p53/p73 with CCAAT-binding transcription factor 2 (CTF2) and differential regulation of human high-mobility group 1 (HMG1) gene expression. Uramoto, H., Izumi, H., Nagatani, G., Ohmori, H., Nagasue, N., Ise, T., Yoshida, T., Yasumoto, K., Kohno, K. Biochem. J. (2003) [Pubmed]
  32. Three classes of mutations in the A subunit of the CCAAT-binding factor CBF delineate functional domains involved in the three-step assembly of the CBF-DNA complex. Sinha, S., Kim, I.S., Sohn, K.Y., de Crombrugghe, B., Maity, S.N. Mol. Cell. Biol. (1996) [Pubmed]
  33. HSP-CBF is an NF-Y-dependent coactivator of the heat shock promoters CCAAT boxes. Imbriano, C., Bolognese, F., Gurtner, A., Piaggio, G., Mantovani, R. J. Biol. Chem. (2001) [Pubmed]
  34. Methylation in hMLH1 promoter interferes with its binding to transcription factor CBF and inhibits gene expression. Deng, G., Chen, A., Pong, E., Kim, Y.S. Oncogene (2001) [Pubmed]
  35. Transcription repression of a CCAAT-binding transcription factor CBF/HSP70 by p53. Chae, H.D., Yun, J., Shi, D.Y. Exp. Mol. Med. (2005) [Pubmed]
  36. The core binding factor (CBF) alpha interaction domain and the smooth muscle myosin heavy chain (SMMHC) segment of CBFbeta-SMMHC are both required to slow cell proliferation. Cao, W., Adya, N., Britos-Bray, M., Liu, P.P., Friedman, A.D. J. Biol. Chem. (1998) [Pubmed]
  37. Regulation of the human SOX9 promoter by Sp1 and CREB. Piera-Velazquez, S., Hawkins, D.F., Whitecavage, M.K., Colter, D.C., Stokes, D.G., Jimenez, S.A. Exp. Cell Res. (2007) [Pubmed]
  38. The transcription factor CCAAT-binding factor CBF/NF-Y and two repressors regulate the core promoter of the human pro-alpha3(V) collagen gene (COL5A3). Nagato, H., Matsuo, N., Sumiyoshi, H., Sakata-Takatani, K., Nasu, M., Yoshioka, H. J. Biol. Chem. (2004) [Pubmed]
  39. Chromosomal assignment and tissue expression of CBF-C/NFY-C, the third subunit of the mammalian CCAAT-binding factor. Sinha, S., Maity, S.N., Seldin, M.F., de Crombrugghe, B. Genomics (1996) [Pubmed]
  40. The leukemic core binding factor beta-smooth muscle myosin heavy chain (CBF beta-SMMHC) chimeric protein requires both CBF beta and myosin heavy chain domains for transformation of NIH 3T3 cells. Hajra, A., Liu, P.P., Wang, Q., Kelley, C.A., Stacy, T., Adelstein, R.S., Speck, N.A., Collins, F.S. Proc. Natl. Acad. Sci. U.S.A. (1995) [Pubmed]
  41. Evidence suggestive of diffuse brain damage following cardiac operations. Henriksen, L. Lancet (1984) [Pubmed]
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