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Human DNA Fragmentation Factor, 40kDa, beta Polypeptide (Caspase-Activated DNase) (DFFB) interaction partners

1. Glandular, menopause-independent DFF40, DFF45, and Bcl-2 overexpression may play an important role in the pathogenesis of endometrial polyps and benign endometrial hyperplasia

2. we show that executioner caspase activation of the apoptotic nuclease CAD/DFF40 is essential for TRAIL-induced mutations in surviving cells. As exposure to chemotherapy drugs also activates apoptotic caspases and presumably CAD, we hypothesized that these pathways may also contribute to the mutagenesis induced by conventional chemotherapy drugs, perhaps augmenting the mutations that arise from direct DNA damage

3. Dff40 expression is upregulated in atherosclerotic plaque.

4. the low expression levels of DFF40/CAD and the absence of DNA laddering as common molecular traits in glioblastoma

5. Data suggest DFF40 expression in breast cancer cell line is involved in drug sensitivity/resistance to doxorubicin; apoptotic cell death due to doxorubicin (a topoisomerase II inhibitor) is enhanced by DFF40 overexpression in breast cancer cell line.

6. 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.

7. Combinatorial use of some sulfonamides such as acetazolamide along with increased expression of DFF40 can potently kill tumor cells via apoptosis.

8. DFF40/CAD-independent mechanism driving conformational nuclear changes during caspase-dependent cell death

9. the highest order of chromatin compaction observed in the later steps of caspase-dependent apoptosis relies on DFF40/CAD-mediated DNA damage by generating 3'-OH ends in single-strand rather than double-strand DNA nicks/breaks

10. These results suggest a cooperative activity between CAD and DNAS1L3 to accomplish internucleosomal DNA fragmentation .

11. Human papillomavirus type 16 E6 protein inhibits DNA fragmentation via interaction with DNA fragmentation factor 40

12. During apoptotic rearrangement of interchromatin granule clusters, the nuclear matrix (NuMa rearrangement) and chromatin are closely associated. This process occurs in defined stages and depends on the activity of protein phosphatases, caspases and CAD.

13. the cytosolic levels of DFF40/CAD are determinants in achieving a complete apoptotic phenotype, including oligonucleosomal DNA degradation.

14. Data show that among the 13 SNPs in the 3 genes, only 3 were found to be polymorphic: R196K and K277R in the DFFB gene, and S12L in the EndoG gene, and all 6 SNPs in the FEN-1 gene were entirely monoallelic.

15. These data suggest that DFF 40 mediated apoptosis plays a significant role in mediating sepsis induced cellular dysfunction.

16. The heterodimer, DFF40-DFF45, is localized to the chromatin fraction under apoptotic as well as non-apoptotic conditions.

17. Mutations and aberrantly spliced transcripts for the CAD gene are frequently associated with hepatocellular carcinoma.

18. Hsp70 binds free CAD in TCR-stimulated T cells to stabilize and augment its activity.

19. subunit structures and stoichiometries in human cells before and after induction of apoptosis

20. CAD involves unrestricted accessibility of chromosomal DNA at the initial phase of apoptosis, followed by its nuclear immobilization that may prevent the release of the active nuclease into the extracellular environment.

Mouse (Murine) DNA Fragmentation Factor, 40kDa, beta Polypeptide (Caspase-Activated DNase) (DFFB) interaction partners

1. Dff40 expression is upregulated in atherosclerotic plaque. Dff40 deficiency inhibited high-fat diet-induced atherosclerosis, as evidenced by decreased atherosclerotic plaques, inhibited inflammatory response, and macrophage apoptosis, as well as enhanced stability of plaques.

2. the highest order of chromatin compaction observed in the later steps of caspase-dependent apoptosis relies on DFF40/CAD-mediated DNA damage by generating 3'-OH ends in single-strand rather than double-strand DNA nicks/breaks

3. results show that caspase 3/CAD promotes cell differentiation by directly modifying the DNA/nuclear microenvironment, which enhances the expression of critical regulatory genes

4. Co-transfection of mouse DFF45(-/-) fibroblasts with plasmids encoding human DFF40 and DFF45 reversed the apoptosis resistance normally observed in these cells

5. The thymus of DNase II(-/-)CAD(-/-) embryos contained many foci carrying undigested DNA and the cellularity was severely reduced due to a block in T cell development.

6. In transfected HeLa cells, transiently expressed DFF associates with chromatin, suggesting that DFF could be activated during apoptosis in a DNA-bound state

7. Interactions identified here between mouse liver histone H1 carboxyl-terminal domain and DFF40/CAD target and activate linker DNA cleavage during the terminal stages of apoptosis.

8. The results suggest that CAD protein may be preferentially degraded by the ubiquitin-proteasome system in the absence of its inhibitor (ICAD) to maintain protein quality control.

9. A los of caspase-activated DNASE enhances tumorigenesis induced by a chemical carcinogen in a model of skin carcinogenesis in mice.