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Glandular, menopause-independent DFF40, DFF45, and Bcl-2 overexpression may play an important role in the pathogenesis of endometrial polyps and benign endometrial hyperplasia
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evaluate the relative expression levels of miR-196a2 and three of its selected apoptosis-related targets; ANXA1, DFFA and PDCD4 in a sample of GI cancer patients
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Data show that the caspase-activated DNase (CAD) is activated when caspases cleave its endogenous inhibitor ICAD, resulting in the characteristic DNA laddering of apoptosis.
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Data suggest that DFF45 gene silencing, when applied in combination with doxorubicin, may offer a therapeutic strategy for the treatment of breast cancer.
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ICAD deficiency was associated with severe genomic instability.
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mRNA splicing is actively driven toward the pro-apoptotic isoforms of Bim, Bcl-x, and ICAD in Pnn-depleted MCF-7 cells.
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The DFF45 level in human endometrium corresponds to the respective phase of the menstrual cycle and decreases significantly after menopause.
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study reveals a previously unrecognized function of miR-145 in DFF45 processing, which may underlie crucial aspects of cancer biology
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The heterodimer, DFF40-DFF45, is localized to the chromatin fraction under apoptotic as well as non-apoptotic conditions.
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DFF45 at chromosome 1 reveal rare allelic variants in neuroblastoma tumors
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NMR solution structure of the C-terminal domain of DFF45, which is essential for its chaperone-like activity
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Hypoxia-induced cleavage of caspase-3 and DFF45/ICAD in human failed cardiomyocytes.
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subunit structures and stoichiometries in human cells before and after induction of apoptosis
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Hepatitis C virus core protein increases a steady-state level of ICAD protein, possibly through enhancing its promoter activity
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apoptotic DNA fragmentation factor is required for the maintenance of genetic stability and may play a role in tumor suppression
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plays an important and P53-independent role in maintaining chromosome stability and suppressing tumor development
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demonstrate the cellular mechanisms of neuronal cell degeneration induced via c-Jun-N-terminal kinases and caspase-dependent signaling
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C-terminal region of each subunit, DFF40 (RLKRK) and DFF45 (KRAR), is essential for nuclear accumulation of the DFF complex.
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Interestingly, nuclear DNA fragmentation occurred and consistently DNA fragmentation factor (DFF45)/Inhibitor of caspase-activated DNase (ICAD) was cleaved inside the cell as well as in vitro, suggesting a role of caspase-2 in nuclear DNA fragmentation.
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The highest level of DFF45 endometrial expression was found during the early secretory cycle phase, and significantly lower DFF45 expression was found in the endometrium during the mid-secretory as compared to the early secretory cycle phase.
