|Safety Information according to GHS|
|Storage and Shipping Information|
|Storage Conditions||1 year at -20°C from date of shipment|
|Material Size||25 assays|
|Acid DNases and their interest among apoptotic endonucleases|
Counis, Marie-France and Torriglia, Alicia
Biochimie, 88:1851-8 (2006) 2006
|Semi-artificial Fluorescent Molecular Machine for DNA Damage Detection|
Didenko VV, Minchew CL, Shuman S, Baskin DS.
Didenko, Vladimir V, et al 2004
|Molecular cloning and characterization of human caspase-activated DNase|
Mukae, N, et al
Proc Natl Acad Sci USA, 95:9123-8 (1998) 1998
|Cytometry in cell necrobiology: analysis of apoptosis and accidental cell death (necrosis)|
Darzynkiewicz, Z, et al
Cytometry, 27:1-20 (1997) 1997
|Ultrastructural detection of DNA strand breaks in apoptotic neural cells by in situ end-labelling techniques.|
Migheli, A, et al.
J. Pathol., 176: 27-35 (1995) 1995
Recently developed techniques based on 'in situ end-labelling' (ISEL) of DNA strand breaks may help to identify apoptotic cells in tissue sections. We have applied ISEL techniques at the electron microscopic (EM) level, in order to verify if ultrastructural features of apoptosis are indeed associated with evidence of DNA fragmentation, and whether cells committed to, but which have not yet entered the stage of cell death are also labelled. Terminal transferase and DNA polymerase assays were applied to thin sections of Araldite and LR Gold-embedded medulloblastomas and embryonic mouse dorsal root ganglia. Digoxigenin-labelled nucleotides were used; incorporation was demonstrated by immunogold staining. Apoptotic cells in various stages of the death process were easily labelled in both tissues. In addition, DNA fragmentation was demonstrated in cells with initial chromatin condensation, but otherwise indistinguishable from adjacent unstained cells. Our results show that EM-ISEL techniques effectively demonstrate the occurrence of DNA strand breaks in apoptotic and possibly 'pre-apoptotic' cells in neural tissues. Since the labelling is easily obtained on tissue that is routinely processed for electron microscopy, this technique may allow retrospective studies on archival material.
|Anatomical methods in cell death|
Kerr, J F, et al
Methods Cell Biol, 46:1-27 (1995) 1995
|Programmed cell death during mammary gland involution.|
Strange, R, et al.
Methods Cell Biol., 46: 355-68 (1995) 1995
Understanding the cascade of gene expression and subsequent protein interactions that result both in the death of secretory mammary epithelium and the remodeling and renewal of the mammary gland for another cycle of lactation poses significant challenges (see Chapters 7 and 8, this volume). The complexity of mammary gland involution warrants caution in sorting through the various potential regulators and executors of apoptotic cell death in the mammary gland. As demonstrated by the number of remodeling enzymes expressed during involution, the relationship between mammary epithelium and its related mesenchyme is important for maintenance of differentiated function (Barcellos-Hoff et al., 1989; Streuli et al., 1991). Components of the extracellular matrix may play the role of survival factors, or may provide a source of factors, as a reserve of matrix-bound growth factors, necessary for survival of the secretory epithelium. Perturbation of this interaction alters mammary-specific differentiation gene expression, for example, production of milk proteins (Parry et al., 1987; Strange et al., 1991; Talhouk et al., 1992). Thus, alteration of the interaction between epithelium and its associated mesenchyme, which is an integral part of mammary involution, may also play a role in epithelial cell death. However, the epithelial-mesenchymal interactions that are the determining features in either mediating or modulating this cell death are just beginning to be defined. Stimuli that alter differentiated function may also induce apoptotic cell death of the epithelium but may have no physiological correlate. They may, however, have significant application in prevention or control of breast neoplasia.
|Microwave irradiation of paraffin-embedded tissue sensitizes the TUNEL method for in situ detection of apoptotic cells|
Sträter, J, et al
Histochem Cell Biol, 103:157-60 (1995) 1995
|BCR-ABL maintains resistance of chronic myelogenous leukemia cells to apoptotic cell death|
McGahon, A, et al
Blood, 83:1179-87 (1994) 1994
|Identification of programmed cell death in situ via specific labeling of nuclear DNA fragmentation.|
Gavrieli, Y, et al.
J. Cell Biol., 119: 493-501 (1992) 1992
Programmed cell death (PCD) plays a key role in developmental biology and in maintenance of the steady state in continuously renewing tissues. Currently, its existence is inferred mainly from gel electrophoresis of a pooled DNA extract as PCD was shown to be associated with DNA fragmentation. Based on this observation, we describe here the development of a method for the in situ visualization of PCD at the single-cell level, while preserving tissue architecture. Conventional histological sections, pretreated with protease, were nick end labeled with biotinylated poly dU, introduced by terminal deoxy-transferase, and then stained using avidin-conjugated peroxidase. The reaction is specific, only nuclei located at positions where PCD is expected are stained. The initial screening includes: small and large intestine, epidermis, lymphoid tissues, ovary, and other organs. A detailed analysis revealed that the process is initiated at the nuclear periphery, it is relatively short (1-3 h from initiation to cell elimination) and that PCD appears in tissues in clusters. The extent of tissue-PCD revealed by this method is considerably greater than apoptosis detected by nuclear morphology, and thus opens the way for a variety of studies.
|Hallmarks of Aging|
|A Comparative Analysis of Human Embryonic Stem Cells Cultured in a Variety of Media Conditions|
|New in Apoptosis Imaging: Dual Detection of Self-Execution and Waste-Management|
|ApopTag® ISOL Dual Fluorescence Apoptosis Detection Kit (DNase Types I & II)|