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EHF  -  ets homologous factor

Homo sapiens

Synonyms: ESE-3, ESE3, ESE3B, ESEJ, ETS domain-containing transcription factor, ...
 
 
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Disease relevance of EHF

  • EHF maps to 11p12, which is deleted in many prostate, breast, and lung carcinomas and is a hot spot for inherited deletion- or amplification-associated developmental defects [1].
  • Although LH-RH could be a local regulator of growth of prostate cancer, the fall in LH-RH receptors is not fully understood and the inhibitory effects of Cetrorelix and bombesin antagonists on DU-145 tumour growth might be attributed at least in part to a downregulation of EHF receptors [2].
  • Effect of EHF radiation on metabolism of Cyanobacteria spirulina platensis and other photosynthesizing organisms [3].
  • The patient with EHF usually seeks medical care as an emergency for an "acute abdomen". Consequently the X-ray examination becomes an essential part of the clinical study [4].
  • The work described here has been the base for the Global Campaign against Headache disorders: "Lifting the Burden", launched in 2004 jointly by WHO, IHS (International Headache Society), WHA (World Headache Alliance) and EHF (European Headache Federation) [5].
 

Psychiatry related information on EHF

 

High impact information on EHF

  • We propose that ESE-3 might be an important determinant in the control of epithelial differentiation, as a modulator of the nuclear response to mitogen-activated protein kinase signaling cascades [6].
  • ESE-3 mRNA is widely expressed in human tissues with high epithelial content, and immunohistochemical analysis with a newly generated monoclonal antibody revealed that ESE-3 is a nuclear protein expressed exclusively in differentiated epithelial cells and that it is absent in the epithelial carcinomas tested [6].
  • In transient transfections, ESE-3 behaves as a repressor of the Ras- or phorbol ester-induced transcriptional activation of a subset of promoters that contain ETS and AP-1 binding sites [6].
  • Using these approaches, we found the ESE-2 and ESE-3 genes, coding for ETS domain-containing transcription factors [6].
  • ESE-3, like ESE-1 and ESE-2, is exclusively expressed in a subset of epithelial cells with highest expression in glandular epithelium such as prostate, pancreas, salivary gland, and trachea [7].
  • We show that ESE-3 functions as a tumor suppressor in the prostate, negatively affecting growth and survival of PCa cells [8].
  • We identified tumor subgroups (i.e., ERG(high), ESE1 (high), ESE3 (low) and NoETS tumors) on the basis of their ETS expression status and showed distinct transcriptional and biological features. ERG (high) and ESE3 (low) tumors had the most robust gene signatures with both distinct and overlapping features. Integrating genomic data with functional studies in multiple cell lines, we demonstrated that ERG and ESE3 controlled in opposite direction transcription of the Polycomb Group protein EZH2. These findings provide new insights into the role of the ETS transcriptional network in prostate tumorigenesis and uncover previously unrecognized links between aberrant expression of ETS factors, deregulation of epigenetic effectors and silencing of tumor suppressor genes. The link between aberrant ETS activity and epigenetic gene silencing may be relevant for the clinical management of prostate cancer and design of new therapeutic strategies[9].
  • Our data suggest that loss of ESE-3 expression is an important event in the pathogenesis of PCa in addition to the activation of oncogenic ETS factors. Moreover, ESE-3 could regulate the equilibrium between proliferation and differentiation through both activation and repression of selected target genes and control the induction and maintenance of PrEC differentiation [10].
 

Biological context of EHF

  • A potential role in branching morphogenesis is suggested, since ESE-3 transactivates the c-MET promoter via three high affinity binding sites [7].
  • Additionally, ESE-3 binding to DNA sequences in the promoters of several glandular epithelium-specific genes suggests a role for ESE-3 in later stages of glandular epithelium differentiation [7].
  • Family studies of asthma suggest that the genes ESE-2 and ESE-3 contain polymorphisms that contribute to disease susceptibility [11].
  • Analysis of three SNPs at the CAT and EHF gene located within the region of maximum linkage showed that T1667T and C(-262)T markers of the CAT gene are strongly associated with the disease [12].
  • In the process of identifying senescence-associated genes, we found significant suppression of the ets homologous factor (EHF) in cancer cells in a state of DNA damage-induced senescence [13].
 

Anatomical context of EHF

 

Associations of EHF with chemical compounds

  • The use of an impairment sum score, the EHF score, is illustrated using data on impairment at diagnosis and after a 2-year interval from MB patients released from MDT in the Western Region of Nepal. The WHO 1988 'disability' grading scale (0-2, for both eyes, hands and feet--six sites) was used as a measure of impairment [16].
  • Mutation in ESE3 decreased pre-mRNA splicing, while mutation in purine-rich sequences in exon 2 did not [17].
 

Other interactions of EHF

 

Analytical, diagnostic and therapeutic context of EHF

  • Both PxSeph and EHF are stable in physiological conditions and proved to be useful adsorbents for removal of contaminated endotoxin from the hemodialysis systems [19].
  • EHF also removed endotoxins from contaminated water by filtration through EHF modules, and its adsorption nature was demonstrated [19].

References

  1. Human chromosomal localization, tissue/tumor expression, and regulatory function of the ets family gene EHF. Kleinbaum, L.A., Duggan, C., Ferreira, E., Coffey, G.P., Butticè, G., Burton, F.H. Biochem. Biophys. Res. Commun. (1999) [Pubmed]
  2. Inhibition of growth of androgen-independent DU-145 prostate cancer in vivo by luteinising hormone-releasing hormone antagonist Cetrorelix and bombesin antagonists RC-3940-II and RC-3950-II. Jungwirth, A., Pinski, J., Galvan, G., Halmos, G., Szepeshazi, K., Cai, R.Z., Groot, K., Vadillo-Buenfil, M., Schally, A.V. Eur. J. Cancer (1997) [Pubmed]
  3. Effect of EHF radiation on metabolism of Cyanobacteria spirulina platensis and other photosynthesizing organisms. Tambiev, A.K., Kirikova, N.N. Critical reviews in biomedical engineering. (2000) [Pubmed]
  4. Radiologic manifestations of epidemic haemorrhagic fever with renal syndrome. Bahk, Y.W., Kim, C.Y. The British journal of radiology. (1978) [Pubmed]
  5. The global burden of migraine: measuring disability in headache disorders with WHO's Classification of Functioning, Disability and Health (ICF). Leonardi, M., Steiner, T.J., Scher, A.T., Lipton, R.B. The journal of headache and pain : official journal of the Italian Society for the Study of Headaches. (2005) [Pubmed]
  6. The epithelium-specific ETS protein EHF/ESE-3 is a context-dependent transcriptional repressor downstream of MAPK signaling cascades. Tugores, A., Le, J., Sorokina, I., Snijders, A.J., Duyao, M., Reddy, P.S., Carlee, L., Ronshaugen, M., Mushegian, A., Watanaskul, T., Chu, S., Buckler, A., Emtage, S., McCormick, M.K. J. Biol. Chem. (2001) [Pubmed]
  7. ESE-3, a novel member of an epithelium-specific ets transcription factor subfamily, demonstrates different target gene specificity from ESE-1. Kas, K., Finger, E., Grall, F., Gu, X., Akbarali, Y., Boltax, J., Weiss, A., Oettgen, P., Kapeller, R., Libermann, T.A. J. Biol. Chem. (2000) [Pubmed]
  8. Reduced expression and tumor suppressor function of the ETS transcription factor ESE-3 in prostate cancer. Cangemi, R., Mensah, A., Albertini, V., Jain, A., Mello-Grand, M., Chiorino, G., Catapano, C.V., Carbone, G.M. Oncogene. (2008) [Pubmed]
  9. ETS transcription factors control transcription of EZH2 and epigenetic silencing of the tumor suppressor gene Nkx3.1 in prostate cancer. Kunderfranco, P., Mello-Grand, M., Cangemi, R., Pellini, S., Mensah, A., Albertini, V., Malek, A., Chiorino, G., Catapano, C.V., Carbone, G.M. PLoS. One. (2010) [Pubmed]
  10. ESE3/EHF controls epithelial cell differentiation and its loss leads to prostate tumors with mesenchymal and stem-like features. Albino, D., Longoni, N., Curti, L., Mello-Grand, M., Pinton, S., Civenni, G., Thalmann, G., D'Ambrosio, G., Sarti, M., Sessa, F., Chiorino, G., Catapano, C.V., Carbone, G.M. Cancer. Res. (2012) [Pubmed]
  11. Constitutive and cytokine-induced expression of the ETS transcription factor ESE-3 in the lung. Silverman, E.S., Baron, R.M., Palmer, L.J., Le, L., Hallock, A., Subramaniam, V., Riese, R.J., McKenna, M.D., Gu, X., Libermann, T.A., Tugores, A., Haley, K.J., Shore, S., Drazen, J.M., Weiss, S.T. Am. J. Respir. Cell Mol. Biol. (2002) [Pubmed]
  12. A new type 1 diabetes susceptibility locus containing the catalase gene (chromosome 11p13) in a Russian population. Chistiakov, D.A., Savost'anov, K.V., Turakulov, R.I., Titovich, E.V., Zilberman, L.I., Kuraeva, T.L., Dedov, I.I., Nosikov, V.V. Diabetes Metab. Res. Rev. (2004) [Pubmed]
  13. Influence of small interfering RNA corresponding to ets homologous factor on senescence-associated modulation of prostate carcinogenesis. Park, C., Lee, I., Kang, W.K. Mol. Cancer Ther. (2006) [Pubmed]
  14. Identification of 9 genes differentially expressed in head and neck squamous cell carcinoma. Gonzalez, H.E., Gujrati, M., Frederick, M., Henderson, Y., Arumugam, J., Spring, P.W., Mitsudo, K., Kim, H.W., Clayman, G.L. Arch. Otolaryngol. Head Neck Surg. (2003) [Pubmed]
  15. Usefulness of a triple fluorochrome combination Merocyanine 540/Yo-Pro 1/Hoechst 33342 in assessing membrane stability of viable frozen-thawed spermatozoa from Estonian Holstein AI bulls. Hallap, T., Nagy, S., Jaakma, U., Johannisson, A., Rodriguez-Martinez, H. Theriogenology (2006) [Pubmed]
  16. Grading impairment in leprosy. van Brakel, W.H., Reed, N.K., Reed, D.S. Leprosy review. (1999) [Pubmed]
  17. Analysis of exonic splicing enhancers in the mouse gonadotropin-releasing hormone (GnRH) gene. Han, J., Seong, J.Y., Kim, K., Wuttke, W., Jarry, H. Mol. Cell. Endocrinol. (2001) [Pubmed]
  18. ESE-3 transcription factor is involved in the expression of death receptor (DR)-5 through putative Ets sites. Lim, J.H., Cho, J.Y., Park, Y.B., Park, J.W., Kwon, T.K. Biochem. Biophys. Res. Commun. (2006) [Pubmed]
  19. Novel endotoxin adsorbing materials, polymyxin-sepharose and polyporous polyethylene membrane for removal of endotoxin from dialysis systems. Umeda, M., Niwa, M., Yamagami, S., Kishimot, T., Maekawa, M., Sawada, Y. Biomaterials, artificial cells, and artificial organs. (1990) [Pubmed]
 
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