Gene interactions and pathways from curated databases and text-mining

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ANXA5 — CASP5

Text-mined interactions from Literome

Pozarowski et al., Cytometry A 2003 : These included : collapse of the mitochondrial transmembrane potential ; activation of caspase-3 ( detected immunocytochemically ) ; binding of annexin V ; chromatin condensation ; the presence of DNA strand breaks ; and loss of plasma membrane capability to exclude propidium iodide ( PI )
Chelbi-alix et al., Oncogene 2003 (Leukemia, Promyelocytic, Acute) : IFNgamma boosted As2O3 induced apoptosis in APL cells as tested by TUNEL, Annexin V staining and activation of caspase 3
Brest et al., Infect Immun 2004 : Infection of PMNs by Afa/Dr DAEC strains induced PMN apoptosis characterized by morphological nuclear changes, DNA fragmentation, caspase activation , and a high level of annexin V expression
Starenki et al., Clin Cancer Res 2004 (Carcinoma...) : In the in vitro experiments, the induction of apoptosis by DHMEQ in various human thyroid carcinoma cell types was determined by flow cytometry analysis of annexin-V binding and the caspase activation by Western blotting
Minervini et al., Toxicology 2005 : Cytotoxicity appeared to be due to early apoptosis in MOLT-4 cells, as indicated by increased Annexin V binding and activation of caspase-3 , and to direct cell membrane damage in IM-9 cells
Voisin et al., Endocrinology 2006 : On addition of either orexin ( 10 ( -6 ) m ) for 48 h, apoptosis was demonstrated by DNA fragmentation, chromatin condensation, annexin-V binding, and activation of caspase-3 and caspase-9
Wang et al., J Cell Sci 2007 (Prostatic Neoplasms) : The TNFalpha induced cell death was dependent on cell density, and it was associated with increased annexin V staining, an increased proportion of sub-G1 cells, and activation of caspase 8
Schaecher et al., J Virol 2007 (Severe Acute Respiratory Syndrome) : Deletion of gene 7 had no effect on SARS-CoV replication in transformed cell lines, nor did it alter the induction of early apoptosis markers such as annexin V binding and activation of caspase 3
Oikawa et al., J Biol Chem 2008 : Knockdown of CIBZ by small interfering RNA in C2C12 cells induced apoptosis, as determined by an increase of annexin V/propidium iodide labeling, activation of caspase-3 , and cleavage of poly ( ADP-ribose ) polymerase
Risek et al., Mol Endocrinol 2008 (Prostatic Neoplasms) : Cell death occurred via apoptosis as demonstrated by annexin V immunostaining, nuclear condensation, and caspase inhibition
Liu et al., Am J Physiol Heart Circ Physiol 2008 : Cell death was measured by terminal deoxynucleotidyl transferase dUTP mediated nick-end labeling, annexin V-fluorescein isothiocyanate, activation of caspase-9 and -3, and cleavage of poly ( ADP-ribose ) polymerase ( PARP )
Li et al., Yao Xue Xue Bao 2008 (Breast Neoplasms) : However, the cleavages of PARP, caspase-6 and -7 in MCF-7/DOX cells delayed after exposure to NAM for 24 h and obviously increased at 48 h with appearance of chromatin condensation and Annexin V positive cells
Hossain et al., J Cell Biochem 2009 : We also found that a reducing agent dithiothreitol ( DTT ) and an anti-oxidant N-acetyl cysteine (NAC) inhibited BMTS mediated caspase-9 and -3 activation, ROS production and induction of Annexin V/propidium iodide double positive cells, suggesting the involvement of ROS in the apoptosis process
Phromnoi et al., Anticancer Res 2010 (Neoplasms) : Furthermore, DH-PMF inhibited AKT and glycogen synthase kinase 3 beta ( GSK3ß ) activation, reduced cell survival proteins, and induced apoptosis, as indicated by annexin V staining, TUNEL assay, and activation of caspase-8 , -9 and -3
Przygodzka et al., Exp Cell Res 2011 : It does not cause ( c ) membrane asymmetry of cells as indicated by lack of Annexin V binding as well as ( d ) activation of caspase 3 and cleavage of PARP
Boltzen et al., J Mol Cell Cardiol 2012 (MAP Kinase Signaling System) : Apoptosis was assessed by annexin-V assay, propidium iodide assay, as well as activation of caspase-3 and -9
Makpol et al., Oxidative medicine and cellular longevity 2012 : Both SIPS and senescent HDFs shared similar apoptotic changes such as increased Annexin V-FITC positive cells, increased cytochrome c release and increased activation of caspase-9 and caspase-3 ( P < 0.05 )
You et al., Mol Biol Rep 2013 : Dose dependent inhibition of cell growth was observed in HeLa cells with an IC50 of approximately 15 µM at 72 h. SBHA also induced apoptosis in HeLa cells, as evidenced by sub-G1 cells, annexin V-FITC staining cells, activations of caspase 3 and 8, and the loss of mitochondrial membrane potential ( d?m )
Towhid et al., Cell Physiol Biochem 2013 : Results : A 30 minutes exposure to vancomycin ( =1 µg/ ml ) decreased cell volume, triggered annexin V-binding , increased [ Ca ], activated caspase 3, stimulated ceramide formation, triggered release of thromboxane B, and upregulated surface expression of CD62P ( P-selectin ) as well as activated integrin aß
Monma et al., Mol Cancer Ther 2013 (Disease Models, Animal...) : When applied alone, PFT-µ increased Annexin V ( + ) cells in both caspase dependent and -independent manners
Wang et al., Vet Microbiol 2013 (Enterobacteriaceae Infections...) : Apoptosis was observed in EPC cells upon infection, characterized by the occurrence of apoptotic bodies, DNA ladder, increased Annexin V binding and the activation of caspase-3 , whereas E. tarda infected FG-9307 cells were negative for all of those features
Kim et al., Int J Oncol 2013 (MAP Kinase Signaling System...) : Magnolol induced the generation of reactive oxygen species ( ROS ) by mitochondria, a process that was associated with the induction of apoptosis as determined by positive Annexin V staining and the activation of cleaved caspase-3