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Dffb  -  DNA fragmentation factor, beta subunit

Mus musculus

Synonyms: 40kDa, 5730477D02Rik, CAD, CPAN, Cad, ...
 
 
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Disease relevance of Dffb

  • A caspase-activated deoxyribonuclease (CAD) and its inhibitor (ICAD) have now been identified in the cytoplasmic fraction of mouse lymphoma cells [1].
  • Role of Apoptotic Nuclease Caspase-Activated DNase in Etoposide-Induced Treatment-Related Acute Myelogenous Leukemia [2].
  • During the characterization of the staurosporine-induced apoptotic process in human neuroblastoma cell lines, we have found three novel splice variants of CAD [3].
  • Thus, GnRH-DFF40 is a promising candidate for the treatment of adenocarcinomas in humans [4].
  • CONCLUSIONS: Because GnRH-DFF40 is a whole human-based chimeric protein when applied to humans, the nonspecific toxicity and immunogenicity seen with bacterial/plant-based chimeric proteins should be avoided [4].
 

High impact information on Dffb

 

Chemical compound and disease context of Dffb

 

Biological context of Dffb

 

Anatomical context of Dffb

 

Associations of Dffb with chemical compounds

 

Physical interactions of Dffb

  • In proliferating cells, CAD is complexed with ICAD (inhibitor of CAD) and its DNase activity is suppressed [13].
 

Regulatory relationships of Dffb

 

Other interactions of Dffb

  • On the basis of structural comparison with other protein complexes containing the ubiquitin superfold, the interaction mode of the CAD domains is proposed [12].
  • This molecular mechanism for the inhibition of CAD DNase by ICAD is similar to that proposed for colicin endonuclease and its inhibitor, immunity protein [13].
  • These findings suggest that CIIA is an endogenous antagonist of both ASK1- and CAD-mediated signaling [20].
  • In one, the DNA fragmentation is carried out by CAD in the dying cells and in the other, by lysosomal DNase II after the dying cells are phagocytosed [21].
  • Caspases were activated, and the death substrates of caspases, lamin B and ICAD (an inhibitor of caspase-activated DNase), were cleaved in this cell death process [22].
 

Analytical, diagnostic and therapeutic context of Dffb

  • Here, we report the three-dimensional structure of the CAD domain of CAD determined by multi-dimensional NMR spectroscopy and the property of CAD domains investigated by a surface plasmon resonance experiment [12].
  • ICAD in extracts of wild type Jurkat cells also existed at approximately 440 and 45 K as measured by gel chromatography; so that fractions of CAD coincided with fractions of approximately 440 K of ICAD [23].
  • Southern blot analysis of colonies that survived normally cytotoxic concentrations of PALA exhibited CAD gene amplification [24].
  • Finally, endogenous NT3 was detectable in CAD cell extracts by a specific ELISA assay [25].
  • Biosynthetic radiolabel incorporation studies in concert with urea-sodium dodecylsulfate-polyacrylamide gel electrophoresis (urea-SDS-PAGE) and western immunoblotting revealed that two major proteins of approximately 26 and 40kDa were produced by the construct [26].

References

  1. A caspase-activated DNase that degrades DNA during apoptosis, and its inhibitor ICAD. Enari, M., Sakahira, H., Yokoyama, H., Okawa, K., Iwamatsu, A., Nagata, S. Nature (1998) [Pubmed]
  2. Role of Apoptotic Nuclease Caspase-Activated DNase in Etoposide-Induced Treatment-Related Acute Myelogenous Leukemia. Hars, E.S., Lyu, Y.L., Lin, C.P., Liu, L.F. Cancer Res. (2006) [Pubmed]
  3. Characterization of splice variants of human caspase-activated DNase with CIDE-N structure and function. Bayascas, J.R., Yuste, V.J., Solé, C., Sánchez-López, I., Segura, M.F., Perera, R., Comella, J.X. FEBS Lett. (2004) [Pubmed]
  4. Using apoptosis for targeted cancer therapy by a new gonadotropin releasing hormone-DNA fragmentation factor 40 chimeric protein. Ben-Yehudah, A., Aqeilan, R., Robashkevich, D., Lorberboum-Galski, H. Clin. Cancer Res. (2003) [Pubmed]
  5. Cidea-deficient mice have lean phenotype and are resistant to obesity. Zhou, Z., Yon Toh, S., Chen, Z., Guo, K., Ng, C.P., Ponniah, S., Lin, S.C., Hong, W., Li, P. Nat. Genet. (2003) [Pubmed]
  6. An auxiliary mode of apoptotic DNA fragmentation provided by phagocytes. McIlroy, D., Tanaka, M., Sakahira, H., Fukuyama, H., Suzuki, M., Yamamura, K., Ohsawa, Y., Uchiyama, Y., Nagata, S. Genes Dev. (2000) [Pubmed]
  7. Impaired thymic development in mouse embryos deficient in apoptotic DNA degradation. Kawane, K., Fukuyama, H., Yoshida, H., Nagase, H., Ohsawa, Y., Uchiyama, Y., Okada, K., Iida, T., Nagata, S. Nat. Immunol. (2003) [Pubmed]
  8. Posttranscriptional regulation of the expression of CAD gene during differentiation of F9 teratocarcinoma cells by induction with retinoic acid and dibutyryl cyclic AMP. Rao, G.N., Church, R.L., Davidson, J.N. FEBS Lett. (1988) [Pubmed]
  9. Evaluation of a novel Vi conjugate vaccine in a murine model of salmonellosis. Hale, C., Bowe, F., Pickard, D., Clare, S., Haeuw, J.F., Powers, U., Menager, N., Mastroeni, P., Dougan, G. Vaccine (2006) [Pubmed]
  10. Mechanism of inhibition of ascites tumor growth in mice by curcumin is mediated by NF-kB and caspase activated DNase. Belakavadi, M., Salimath, B.P. Mol. Cell. Biochem. (2005) [Pubmed]
  11. Structure and promoter analysis of murine CAD and ICAD genes. Kawane, K., Fukuyama, H., Adachi, M., Sakahira, H., Copeland, N.G., Gilbert, D.J., Jenkin, N.A., Nagata, S. Cell Death Differ. (1999) [Pubmed]
  12. Structure of the CAD domain of caspase-activated DNase and interaction with the CAD domain of its inhibitor. Uegaki, K., Otomo, T., Sakahira, H., Shimizu, M., Yumoto, N., Kyogoku, Y., Nagata, S., Yamazaki, T. J. Mol. Biol. (2000) [Pubmed]
  13. Enzymatic active site of caspase-activated DNase (CAD) and its inhibition by inhibitor of CAD. Sakahira, H., Takemura, Y., Nagata, S. Arch. Biochem. Biophys. (2001) [Pubmed]
  14. Functional differences of two forms of the inhibitor of caspase-activated DNase, ICAD-L, and ICAD-S. Sakahira, H., Enari, M., Nagata, S. J. Biol. Chem. (1999) [Pubmed]
  15. Specific chaperone-like activity of inhibitor of caspase-activated DNase for caspase-activated DNase. Sakahira, H., Iwamatsu, A., Nagata, S. J. Biol. Chem. (2000) [Pubmed]
  16. Cell apoptosis: requirement of H2AX in DNA ladder formation, but not for the activation of caspase-3. Lu, C., Zhu, F., Cho, Y.Y., Tang, F., Zykova, T., Ma, W.Y., Bode, A.M., Dong, Z. Mol. Cell (2006) [Pubmed]
  17. The regulation of DNAse activities in subcellular compartments of activated thymocytes. Nagata, T., Kishi, H., Liu, Q.L., Matsuda, T., Imanaka, T., Tsukada, K., Kang, D., Muraguchi, A. Immunology (2002) [Pubmed]
  18. CAD-ICAD complex structure derived from saturation transfer experiment and simulated annealing without using pairwise NOE information. Matsuda, T., Nakajima, N., Yamazaki, T., Nakamura, H. J. Mol. Recognit. (2004) [Pubmed]
  19. Involvement of conserved histidine, lysine and tyrosine residues in the mechanism of DNA cleavage by the caspase-3 activated DNase CAD. Korn, C., Scholz, S.R., Gimadutdinow, O., Pingoud, A., Meiss, G. Nucleic Acids Res. (2002) [Pubmed]
  20. Identification of a novel antiapoptotic protein that antagonizes ASK1 and CAD activities. Cho, S.G., Kim, J.W., Lee, Y.H., Hwang, H.S., Kim, M.S., Ryoo, K., Kim, M.J., Noh, K.T., Kim, E.K., Cho, J.H., Yoon, K.W., Cho, E.G., Park, H.S., Chi, S.W., Lee, M.J., Kang, S.S., Ichijo, H., Choi, E.J. J. Cell Biol. (2003) [Pubmed]
  21. Degradation of chromosomal DNA during apoptosis. Nagata, S., Nagase, H., Kawane, K., Mukae, N., Fukuyama, H. Cell Death Differ. (2003) [Pubmed]
  22. Caspase activation during apoptotic cell death induced by expanded polyglutamine in N2a cells. Wang, G.H., Mitsui, K., Kotliarova, S., Yamashita, A., Nagao, Y., Tokuhiro, S., Iwatsubo, T., Kanazawa, I., Nukina, N. Neuroreport (1999) [Pubmed]
  23. Large complex formation of the inhibitor of caspase-activated DNase. Kanouchi, H., Nishizaki, H., Minatogawa, Y., Toné, S. Apoptosis (2005) [Pubmed]
  24. Drug resistance and gene amplification potential regulated by transforming growth factor beta 1 gene expression. Huang, A., Jin, H., Wright, J.A. Cancer Res. (1995) [Pubmed]
  25. Neurotrophin-3 mediates the autocrine survival of the catecholaminergic CAD CNS neuronal cell line. Horton, C.D., Qi, Y., Chikaraishi, D., Wang, J.K. J. Neurochem. (2001) [Pubmed]
  26. Expression of the murine CB2 cannabinoid receptor using a recombinant Semliki Forest virus. Olson, J.M., Kennedy, S.J., Cabral, G.A. Biochem. Pharmacol. (2003) [Pubmed]
 
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