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Gene Review

DEDD  -  death effector domain containing

Homo sapiens

Synonyms: CASP8IP1, DEDD1, DEDPRO1, DEDPro1, DEFT, ...
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Disease relevance of DEDD

  • With deft management of such challenges by local, national, and international health authorities, poliomyelitis, a disease that threatened children everywhere just 2 generations ago, could soon be relegated to history like smallpox before it [1].
  • The clinical examination included registration of decayed, extracted and filled teeth and surfaces (deft and defs), gingival bleeding points (GBI) and presence of open bite or crossbite [2].
  • We hypothesized that some highly exposed persistently seronegative (HEPS) individuals might have intact theta;-defensin (DEFT) genes and produce functional theta;-defensins that might account for their resistance to HIV-1 infection [3].
  • The etiology of clefting per se--isolated deft palate versus cleft lip with or without deft palate--did not seem to explain the associations between dental arch dimensions and the studied misarticulations [4].
  • Shoulder dystocia is an infrequent and unexpected emergency requiring rapid and deft solution [5].

High impact information on DEDD


Biological context of DEDD


Anatomical context of DEDD

  • In situ hybridization analysis further indicated the expression of DEFT mRNA in meiotic male germ cells [14].
  • Northern blot hybridization experiments have shown that the DEFT messenger RNA (mRNA) is expressed in a variety of human and rat tissues, with particularly abundant expression in the testis [14].
  • DEDAF interacts with FADD, procaspase-8, and procaspase-10 in the cytosol as well as with the DED-containing DNA-binding protein (DEDD) in the nucleus [15].
  • In cell lines MCF-7 and Jurkat, the overexpression of DEDDL could induce apoptosis more potently than that of DEDD [16].
  • For example, among 6-yr-olds a mean number of 11.8 defs and 5.2 deft was observed and 82% of the children were affected by caries in primary teeth [17].

Associations of DEDD with chemical compounds

  • We now demonstrate that many of its 16 lysine residues can serve as alternative acceptors for ubiquitination to maintain the monoubiquitination status of DEDD [18].
  • In cells showing a filamentous staining pattern, DEDD was strongly associated with the CK8/18 cytokeratin filaments as evidenced by double immunofluorescence and its resistance to extraction with Triton X-100 [11].
  • Caspase-10/a (Mch4) and caspase-10/b (FLICE2) are related death effector domain-containing cysteine aspartases presumed to be at or near the apex of apoptotic signaling pathways [19].
  • In a regression analysis for the deft, the use of fluoridated salt (standardized coefficient SC=-0.25) and fluoride gel (SC=-0.37) showed the greatest effect, as did the fluoride gel (SC=-0.26) and gingival bleeding (SC=0.50) for the number of active carious lesions [20].
  • During the last decade, several microbiological rapid methods or principles (DEFT, microcolonies, Limulus lysate, ATP, conductance, microcalorimetry, reduction of trimethylamine oxide (TMAO)) have been suggested for estimating the bacteriological quality of seafoods [21].

Physical interactions of DEDD


Other interactions of DEDD

  • The DED in DEDD therefore represents a novel domain that is structurally similar to other DEDs but functionally different from classical DEDs found in FADD or caspase-8 [22].
  • In the nucleus, DEDAF caused the DEDD protein to relocalize from subnuclear structures to a diffuse distribution in the nucleoplasm [15].
  • When overexpressed, DEDD localizes to nucleoli-like structures, activates caspase-6 and specifically inhibits RNA polymerase I (Pol I) dependent transcription in vivo as shown by blockage of BrUTP incorporation [22].
  • CLARP, a death effector domain-containing protein interacts with caspase-8 and regulates apoptosis [23].
  • DEDD association with cytokeratin filaments correlates with sensitivity to apoptosis [11].

Analytical, diagnostic and therapeutic context of DEDD

  • Using a new anti-DEDD antibody that allows us to stain endogenous DEDD in immunofluorescence microscopy we now detect a significant amount of DEDD in nucleoli of all cells tested [22].
  • Studies with the synthetic autoinhibitory domain peptides of CaM-kinase II indicate that CaM-kinase IV has a similarly located autoinhibitory domain, and this was confirmed since site-directed mutagenesis of this region (HMDT308 to DEDD and FN317 to DD) generated fully active Ca2+/CaM-independent kinases [24].
  • That DEDDL could bind FADD and cFLIP more potently than DEDD in vivo was revealed by cotransfection and immunoprecipitation [16].
  • An unhurried, deft, economical technique allied to efficient use of available resources, surgical instruments and support staff is the hallmark of a 'good' surgeon [25].


  1. Can we capitalize on the virtues of vaccines? Insights from the polio eradication initiative. Aylward, R.B., Heymann, D.L. American journal of public health. (2005) [Pubmed]
  2. Dental health and parental attitudes in Finnish immigrant preschoolchildren in the north of Sweden. Ekman, A., Holm, A.K., Schelin, B., Gustafsson, L. Community dentistry and oral epidemiology. (1981) [Pubmed]
  3. theta-Defensin pseudogenes in HIV-1-exposed, persistently seronegative female sex-workers from Thailand. Yang, C., Boone, L., Nguyen, T.X., Rudolph, D., Limpakarnjanarat, K., Mastro, T.D., Tappero, J., Cole, A.M., Lal, R.B. Infect. Genet. Evol. (2005) [Pubmed]
  4. The association between dental arch dimensions and occurrence of Finnish dental consonant misarticulations in cleft lip/palate children. Laitinen, J., Ranta, R., Pulkkinen, J., Haapanen, M.L. Acta Odontol. Scand. (1998) [Pubmed]
  5. Shoulder dystocia. Wagner, R.K., Nielsen, P.E., Gonik, B. Obstet. Gynecol. Clin. North Am. (1999) [Pubmed]
  6. Absence of caspase 8 and high expression of PED protect primitive neural cells from cell death. Ricci-Vitiani, L., Pedini, F., Mollinari, C., Condorelli, G., Bonci, D., Bez, A., Colombo, A., Parati, E., Peschle, C., De Maria, R. J. Exp. Med. (2004) [Pubmed]
  7. Inhibition of fas death signals by FLIPs. Tschopp, J., Irmler, M., Thome, M. Curr. Opin. Immunol. (1998) [Pubmed]
  8. DEDD regulates degradation of intermediate filaments during apoptosis. Lee, J.C., Schickling, O., Stegh, A.H., Oshima, R.G., Dinsdale, D., Cohen, G.M., Peter, M.E. J. Cell Biol. (2002) [Pubmed]
  9. DEDD, a novel death effector domain-containing protein, targeted to the nucleolus. Stegh, A.H., Schickling, O., Ehret, A., Scaffidi, C., Peterhänsel, C., Hofmann, T.G., Grummt, I., Krammer, P.H., Peter, M.E. EMBO J. (1998) [Pubmed]
  10. MRIT, a novel death-effector domain-containing protein, interacts with caspases and BclXL and initiates cell death. Han, D.K., Chaudhary, P.M., Wright, M.E., Friedman, C., Trask, B.J., Riedel, R.T., Baskin, D.G., Schwartz, S.M., Hood, L. Proc. Natl. Acad. Sci. U.S.A. (1997) [Pubmed]
  11. DEDD association with cytokeratin filaments correlates with sensitivity to apoptosis. Schutte, B., Henfling, M., Ramaekers, F.C. Apoptosis (2006) [Pubmed]
  12. Regulation of expression of phospholipase D1 and D2 by PEA-15, a novel protein that interacts with them. Zhang, Y., Redina, O., Altshuller, Y.M., Yamazaki, M., Ramos, J., Chneiweiss, H., Kanaho, Y., Frohman, M.A. J. Biol. Chem. (2000) [Pubmed]
  13. Theta defensins protect cells from infection by herpes simplex virus by inhibiting viral adhesion and entry. Yasin, B., Wang, W., Pang, M., Cheshenko, N., Hong, T., Waring, A.J., Herold, B.C., Wagar, E.A., Lehrer, R.I. J. Virol. (2004) [Pubmed]
  14. DEFT, a novel death effector domain-containing molecule predominantly expressed in testicular germ cells. Leo, C.P., Hsu, S.Y., McGee, E.A., Salanova, M., Hsueh, A.J. Endocrinology (1998) [Pubmed]
  15. The death effector domain-associated factor plays distinct regulatory roles in the nucleus and cytoplasm. Zheng, L., Schickling, O., Peter, M.E., Lenardo, M.J. J. Biol. Chem. (2001) [Pubmed]
  16. Identification and characterization of DEDDL, a human-specific isoform of DEDD. Huang, X., Zhang, M., Tang, H., Ruo, C., Cao, X. Gene Expr. (2006) [Pubmed]
  17. Dental caries among urban schoolchildren in Madagascar. Petersen, P.E., Steengaard, M. Community dentistry and oral epidemiology. (1988) [Pubmed]
  18. Fusing DEDD with ubiquitin changes its intracellular localization and apoptotic potential. Lee, J.C., Wang, G.X., Schickling, O., Peter, M.E. Apoptosis (2005) [Pubmed]
  19. Molecular cloning and characterization of two novel pro-apoptotic isoforms of caspase-10. Ng, P.W., Porter, A.G., Jänicke, R.U. J. Biol. Chem. (1999) [Pubmed]
  20. A new in vivo method for measuring caries activity using quantitative light-induced fluorescence. Meller, C., Heyduck, C., Tranaeus, S., Splieth, C. Caries Res. (2006) [Pubmed]
  21. Evaluation of the bacteriological quality of seafood. Gram, L. Int. J. Food Microbiol. (1992) [Pubmed]
  22. Nuclear localization of DEDD leads to caspase-6 activation through its death effector domain and inhibition of RNA polymerase I dependent transcription. Schickling, O., Stegh, A.H., Byrd, J., Peter, M.E. Cell Death Differ. (2001) [Pubmed]
  23. CLARP, a death effector domain-containing protein interacts with caspase-8 and regulates apoptosis. Inohara, N., Koseki, T., Hu, Y., Chen, S., Núñez, G. Proc. Natl. Acad. Sci. U.S.A. (1997) [Pubmed]
  24. Activation mechanisms for Ca2+/calmodulin-dependent protein kinase IV. Identification of a brain CaM-kinase IV kinase. Tokumitsu, H., Brickey, D.A., Glod, J., Hidaka, H., Sikela, J., Soderling, T.R. J. Biol. Chem. (1994) [Pubmed]
  25. Tools of the trade. Singh, S., Maxwell, D. Best practice & research. Clinical obstetrics & gynaecology. (2006) [Pubmed]
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