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Gene Review

Elk3  -  ELK3, member of ETS oncogene family

Mus musculus

Synonyms: D430049E23Rik, ETS domain-containing protein Elk-3, ETS-related protein ERP, ETS-related protein NET, Erp, ...
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Disease relevance of Elk3

  • In a mouse model of endotoxemia, the expression of Elk-3 in kidney, lung, and heart was significantly down-regulated after systemic administration of LPS, and this down-regulation also preceded NOS2 induction [1].
  • Mycobacterium marinum Erp is a virulence determinant required for cell wall integrity and intracellular survival [2].
  • B. burgdorferi Erp (OspE-F related lipoprotein) family members are encoded on members of the 32 kb circular plasmid-like prophage family (cp32s) [3].

High impact information on Elk3

  • The transcription factor Net is activated by phosphorylation induced by Ras, an indirect regulator of angiogenesis [4].
  • However, Net differs from Elk1 and SAP1 in a number of ways [5].
  • The study of Net should help in understanding the interplay between Net and other members of the Elk subfamily and their contribution to signal transduction through Ras to the nucleus [5].
  • We show that Net inhibits transcription under basal conditions, in which SAP-1a is inactive and ELK-1 stimulates [6].
  • The ternary complex factor Net regulates cell migration through inhibition of PAI-1 expression [7].

Biological context of Elk3


Anatomical context of Elk3

  • Moreover, TGF-beta 1 significantly increased endogenous Elk-3 mRNA levels that had been down-regulated by LPS in macrophages [1].
  • When nuclear extracts of COS-7 cells expressing various Ets family repressors were incubated with DNA probes, binding of Net to the probes was observed [8].
  • The major CQE1-binding proteins in HeLa cell nuclear extract was recognized by anti-Elk-1 or anti-Sap-1a antibodies in electrophoretic mobility shift assay, and recombinant Elk-1, Sap-1a, or Net specifically recognized CQE1 [11].
  • Elk-3 and Caspase-7 were not expressed in vitro in cultured cell lines, suggesting that their expression was induced by the tumor microenvironment [12].
  • Many Erp proteins serve as receptors for the complement inhibitory factor H molecules of numerous vertebrate hosts, providing one mechanism by which the bacteria potentially evade the innate immune system [3].

Regulatory relationships of Elk3

  • The present study demonstrates that of several ternary complex factor subfamily members, only Elk-3 represses HO-1 promoter activity in macrophages [10].
  • Furthermore, Elk-3 can suppress the activity of Ets-2 as the transcriptional activator on the EndoA enhancer [13].

Other interactions of Elk3


Analytical, diagnostic and therapeutic context of Elk3

  • We studied Net expression during mouse development (E7.5-E18.5) by in situ hybridization [14].
  • Molecular cloning of Elk-3, a new member of the Ets family expressed during mouse embryogenesis and analysis of its transcriptional repression activity [13].
  • Indirect immunofluorescence analyses (IFA) have demonstrated that Erp expression is temporally regulated throughout the mammal-tick infectious cycle, indicating that Erp proteins perform an important role (or even roles) during mammalian infection [3].


  1. Elk-3 is a transcriptional repressor of nitric-oxide synthase 2. Chen, Y.H., Layne, M.D., Chung, S.W., Ejima, K., Baron, R.M., Yet, S.F., Perrella, M.A. J. Biol. Chem. (2003) [Pubmed]
  2. Mycobacterium marinum Erp is a virulence determinant required for cell wall integrity and intracellular survival. Cosma, C.L., Klein, K., Kim, R., Beery, D., Ramakrishnan, L. Infect. Immun. (2006) [Pubmed]
  3. Borrelia burgdorferi erp genes are expressed at different levels within tissues of chronically infected mammalian hosts. Miller, J.C., Stevenson, B. Int. J. Med. Microbiol. (2006) [Pubmed]
  4. The transcription factor Net regulates the angiogenic switch. Zheng, H., Wasylyk, C., Ayadi, A., Abecassis, J., Schalken, J.A., Rogatsch, H., Wernert, N., Maira, S.M., Multon, M.C., Wasylyk, B. Genes Dev. (2003) [Pubmed]
  5. Net, a new ets transcription factor that is activated by Ras. Giovane, A., Pintzas, A., Maira, S.M., Sobieszczuk, P., Wasylyk, B. Genes Dev. (1994) [Pubmed]
  6. Net (ERP/SAP2) one of the Ras-inducible TCFs, has a novel inhibitory domain with resemblance to the helix-loop-helix motif. Maira, S.M., Wurtz, J.M., Wasylyk, B. EMBO J. (1996) [Pubmed]
  7. The ternary complex factor Net regulates cell migration through inhibition of PAI-1 expression. Buchwalter, G., Gross, C., Wasylyk, B. Mol. Cell. Biol. (2005) [Pubmed]
  8. Sp1 is a co-activator with Ets-1, and Net is an important repressor of the transcription of CTP:phosphocholine cytidylyltransferase alpha. Sugimoto, H., Okamura, K., Sugimoto, S., Satou, M., Hattori, T., Vance, D.E., Izumi, T. J. Biol. Chem. (2005) [Pubmed]
  9. Gene expression analysis of Tek/Tie2 signaling. Chen, S.H., Babichev, Y., Rodrigues, N., Voskas, D., Ling, L., Nguyen, V.P., Dumont, D.J. Physiol. Genomics (2005) [Pubmed]
  10. Endotoxin-induced down-regulation of Elk-3 facilitates heme oxygenase-1 induction in macrophages. Chung, S.W., Chen, Y.H., Yet, S.F., Layne, M.D., Perrella, M.A. J. Immunol. (2006) [Pubmed]
  11. Transcriptional regulation of the cytosolic chaperonin theta subunit gene, Cctq, by Ets domain transcription factors Elk-1, Sap-1a, and Net in the absence of serum response factor. Yamazaki, Y., Kubota, H., Nozaki, M., Nagata, K. J. Biol. Chem. (2003) [Pubmed]
  12. Capsaicin-induced inactivation of sensory neurons promotes a more aggressive gene expression phenotype in breast cancer cells. Erin, N., Zhao, W., Bylander, J., Chase, G., Clawson, G. Breast Cancer Res. Treat. (2006) [Pubmed]
  13. Molecular cloning of Elk-3, a new member of the Ets family expressed during mouse embryogenesis and analysis of its transcriptional repression activity. Nozaki, M., Onishi, Y., Kanno, N., Ono, Y., Fujimura, Y. DNA Cell Biol. (1996) [Pubmed]
  14. Net, an Ets ternary complex transcription factor, is expressed in sites of vasculogenesis, angiogenesis, and chondrogenesis during mouse development. Ayadi, A., Suelves, M., Dollé, P., Wasylyk, B. Mech. Dev. (2001) [Pubmed]
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