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MeSH Review

In Situ Nick-End Labeling

 
 
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Disease relevance of In Situ Nick-End Labeling

  • These data suggesting that anti-IL-12 leads to reversal of colitis by elimination of the Th1 T cells were substantiated by studies showing that anti-IL-12 treatment led to increased numbers of apoptotic cells in the lamina propria and spleen by both TUNEL staining of tissues and dispersed spleen cell populations [1].
  • In tissue sections of CD437-treated MeWo tumors from these animals, apoptotic melanoma cells and c-fos overexpressing cells were colocalized by TdT-mediated deoxyuridine triphosphate-digoxigenin nick end labeling (TUNEL) staining and in situ hybridization [2].
  • In the HT22 hippocampal cell line, we find that toxicity within individual cells induced by polyQ-expanded htt, as revealed by a TUNEL assay, is associated with the localization of the mutant htt within either nuclear or perinuclear aggregates [3].
  • Apoptosis after global ischemia was observed by DNA electrophoresis and terminal deoxynucleotidyl transferase-mediated uridine 5'-triphosphate-biotin nick end labeling (TUNEL) staining [4].
  • Tumour growth fraction and apoptosis in salivary gland acinic cell carcinomas. Prognostic implications of Ki-67 and bcl-2 expression and of in situ end labelling (TUNEL) [5].
 

Psychiatry related information on In Situ Nick-End Labeling

 

High impact information on In Situ Nick-End Labeling

  • Reduction of cps-6 activity caused by a genetic mutation or RNA-mediated interference (RNAi) affects normal DNA degradation, as revealed by increased staining in a TUNEL assay, and results in delayed appearance of cell corpses during development in C. elegans [8].
  • In situ TUNEL staining of tumour sections revealed that DAP kinase expression from the transgene raised the incidence of apoptosis in vivo [9].
  • Genomic DNA replicated in extracts immunodepleted of X-Mre11 complex accumulates DSBs as demonstrated by TUNEL assay and reactivity to phosphorylated histone H2AX antibodies [10].
  • A combination of TUNEL and immunostaining for death-inducing tumor necrosis factor (TNF) family molecules indicated that the apoptotic cells were frequently found in conjugation with TNF-related apoptosis-inducing ligand (TRAIL)-expressing CD3+CD4+ human T cells [11].
  • After fixation, embedding, and sectioning, the growth fraction was quantified by measuring expression of the proliferation marker Ki-67/myb, differentiation was assessed by expression of mucin, and apoptosis was evaluated by the TUNEL assay [12].
 

Chemical compound and disease context of In Situ Nick-End Labeling

 

Biological context of In Situ Nick-End Labeling

 

Anatomical context of In Situ Nick-End Labeling

 

Associations of In Situ Nick-End Labeling with chemical compounds

 

Gene context of In Situ Nick-End Labeling

  • Direct evidence for apoptosis was obtained by double staining for terminal deoxynucleotide transferase nick end labeling (TUNEL) and PS-2 expression and by following green fluorescent protein-tagged PS-2 over time [33].
  • Hair cell nuclei showed both apoptotic- and necrotic-like appearances but markers for classic apoptotic pathways (cytochrome c, caspase-9, caspase-3, JNK, TUNEL) were absent [34].
  • Interestingly, TUNEL staining and PCNA staining showed neither enhanced apoptosis nor reduced cell proliferation in the mutant myocardium [35].
  • In the subventricular zone (SVZ) and the granular cell layer (GCL) of the dentate gyrus, harboring neural and other progenitor cells, nitrosylation and p53 peaked 2-12 h after IR, followed by markers for active caspase-3, apoptosis-inducing factor and TUNEL (6-24 h) [36].
  • In patients with a prominent classic vascular pattern, there was no difference of MIB1 labeling index whereas microvessel density and apoptotic index (TUNEL) were significantly higher as compared to all other patients (p<0.05) [37].
 

Analytical, diagnostic and therapeutic context of In Situ Nick-End Labeling

References

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  2. Treatment of melanoma cells with the synthetic retinoid CD437 induces apoptosis via activation of AP-1 in vitro, and causes growth inhibition in xenografts in vivo. Schadendorf, D., Kern, M.A., Artuc, M., Pahl, H.L., Rosenbach, T., Fichtner, I., Nürnberg, W., Stüting, S., von Stebut, E., Worm, M., Makki, A., Jurgovsky, K., Kolde, G., Henz, B.M. J. Cell Biol. (1996) [Pubmed]
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  12. Effects of retinoids on cancerous phenotype and apoptosis in organotypic cultures of ovarian carcinoma. Guruswamy, S., Lightfoot, S., Gold, M.A., Hassan, R., Berlin, K.D., Ivey, R.T., Benbrook, D.M. J. Natl. Cancer Inst. (2001) [Pubmed]
  13. Leukotriene B4 receptor antagonist LY293111 inhibits proliferation and induces apoptosis in human pancreatic cancer cells. Tong, W.G., Ding, X.Z., Hennig, R., Witt, R.C., Standop, J., Pour, P.M., Adrian, T.E. Clin. Cancer Res. (2002) [Pubmed]
  14. N-(4-hydroxyphenyl) retinamide is cytotoxic to melanoma cells in vitro through induction of programmed cell death. Montaldo, P.G., Pagnan, G., Pastorino, F., Chiesa, V., Raffaghello, L., Kirchmeier, M., Allen, T.M., Ponzoni, M. Int. J. Cancer (1999) [Pubmed]
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  18. Flavopiridol, a novel cyclin-dependent kinase inhibitor, suppresses the growth of head and neck squamous cell carcinomas by inducing apoptosis. Patel, V., Senderowicz, A.M., Pinto, D., Igishi, T., Raffeld, M., Quintanilla-Martinez, L., Ensley, J.F., Sausville, E.A., Gutkind, J.S. J. Clin. Invest. (1998) [Pubmed]
  19. Death of smooth muscle cells and expression of mediators of apoptosis by T lymphocytes in human abdominal aortic aneurysms. Henderson, E.L., Geng, Y.J., Sukhova, G.K., Whittemore, A.D., Knox, J., Libby, P. Circulation (1999) [Pubmed]
  20. Tenascin-C is induced with progressive pulmonary vascular disease in rats and is functionally related to increased smooth muscle cell proliferation. Jones, P.L., Rabinovitch, M. Circ. Res. (1996) [Pubmed]
  21. Cripto-1 induces apoptosis in HC-11 mouse mammary epithelial cells. De Santis, M.L., Martinez-Lacaci, I., Bianco, C., Seno, M., Wallace-Jones, B., Kim, N., Ebert, A., Wechselberger, C., Salomon, D.S. Cell Death Differ. (2000) [Pubmed]
  22. Combination treatment with 17-N-allylamino-17-demethoxy geldanamycin and acute irradiation produces supra-additive growth suppression in human prostate carcinoma spheroids. Enmon, R., Yang, W.H., Ballangrud, A.M., Solit, D.B., Heller, G., Rosen, N., Scher, H.I., Sgouros, G. Cancer Res. (2003) [Pubmed]
  23. Fas enhances fibrogenesis in the bile duct ligated mouse: a link between apoptosis and fibrosis. Canbay, A., Higuchi, H., Bronk, S.F., Taniai, M., Sebo, T.J., Gores, G.J. Gastroenterology (2002) [Pubmed]
  24. Effect of ovariectomy on the proliferative capacity of intrahepatic rat cholangiocytes. Alvaro, D., Alpini, G., Onori, P., Franchitto, A., Glaser, S., Le Sage, G., Gigliozzi, A., Vetuschi, A., Morini, S., Attili, A.F., Gaudio, E. Gastroenterology (2002) [Pubmed]
  25. Decreased nuclear beta-catenin, tau hyperphosphorylation and neurodegeneration in GSK-3beta conditional transgenic mice. Lucas, J.J., Hernández, F., Gómez-Ramos, P., Morán, M.A., Hen, R., Avila, J. EMBO J. (2001) [Pubmed]
  26. Retinoid-related orphan receptor gamma (RORgamma) is essential for lymphoid organogenesis and controls apoptosis during thymopoiesis. Kurebayashi, S., Ueda, E., Sakaue, M., Patel, D.D., Medvedev, A., Zhang, F., Jetten, A.M. Proc. Natl. Acad. Sci. U.S.A. (2000) [Pubmed]
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  28. A local action of neurotrophin-3 prevents the death of proliferating sensory neuron precursor cells. ElShamy, W.M., Ernfors, P. Neuron (1996) [Pubmed]
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  32. Role of Rho-associated kinase in neointima formation after vascular injury. Shibata, R., Kai, H., Seki, Y., Kato, S., Morimatsu, M., Kaibuchi, K., Imaizumi, T. Circulation (2001) [Pubmed]
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  36. Irradiation-induced progenitor cell death in the developing brain is resistant to erythropoietin treatment and caspase inhibition. Fukuda, H., Fukuda, A., Zhu, C., Korhonen, L., Swanpalmer, J., Hertzman, S., Leist, M., Lannering, B., Lindholm, D., Björk-Eriksson, T., Marky, I., Blomgren, K. Cell Death Differ. (2004) [Pubmed]
  37. Vascular patterns in glioblastoma influence clinical outcome and associate with variable expression of angiogenic proteins: evidence for distinct angiogenic subtypes. Birner, P., Piribauer, M., Fischer, I., Gatterbauer, B., Marosi, C., Ambros, P.F., Ambros, I.M., Bredel, M., Oberhuber, G., Rössler, K., Budka, H., Harris, A.L., Hainfellner, J.A. Brain Pathol. (2003) [Pubmed]
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