Search

Your search keyword '"7AAD, 7-amino-actinomycin D"' showing total 3 results
Start Over Descriptor "7AAD, 7-amino-actinomycin D" Search Limiters Full Text
3 results on '"7AAD, 7-amino-actinomycin D"'

1. Cholecystokinin Receptor Antagonist Suppresses Melanoma Growth by Inducing Apoptosis of Tumor Cells.

Author

Funakoshi A, Honda T, Ito T, and Tokura Y

Abstract

Melanoma is a malignant skin tumor with high metastatic activity. Although melanoma has been well-studied, its cellular kinetics remain elusive. The cholecystokinin (CCK) receptor is expressed in various types of tumors because CCK promotes the survival and proliferation of tumor cells. Thus, we hypothesized that the growth of melanoma was positively regulated by signals from the CCK receptor and sought to investigate whether CCK receptor antagonists affect the growth of melanoma cells expressing CCK receptor. Immunohistochemically, the CCK receptor A is expressed in the clinical specimens of melanoma. CCK receptor antagonists decreased the viability of melanoma cells by suppressing cell division and promoting apoptosis. CCK receptor antagonists also decreased the mitochondrial membrane potential through enhanced gene expression of the proapoptotic protein, Bcl2 -associated X, and tumor suppressor, p53 , suggesting that the antagonist induced the apoptosis of melanoma cells in a mitochondria-dependent manner. In addition, a caspase 3 inhibitor, Z-DEVD-FMK, partially blocked the antiviability of the antagonist, indicating that caspase 3 is involved in antagonist-induced apoptosis. Notably, tumor growth was attenuated when a CCK receptor antagonist was locally administered to the melanoma-bearing mice. Therefore, our study suggests the therapeutic potential of CCK receptor antagonists in the treatment of skin cancer., (© 2022 The Authors.)

Published
2022
Full Text
View/download PDF

2. Human-Gyrovirus-Apoptin Triggers Mitochondrial Death Pathway—Nur77 is Required for Apoptosis Triggering

Author

Joerg Stetefeld, Joanna Rzeszowska-Wolny, Mayur V. Jain, Artur Cieślar-Pobuda, Wiem Chaabane, Saeid Ghavami, Marek J. Łos, Mohamed El-Gazzah, and Mehrdad Rafat

Subjects
Cytoplasm, Cancer Research, TMRM, Tetramethylrhodamine methyl ester perchlorate0, HGV-Apoptin, Human gyrovirus apoptin, Apoptosis, MOMP, Mitochondrial outer membrane permeabilization, Mitochondrial apoptosis-induced channel, AIF, Nur77, Annan medicinsk grundvetenskap, AIF, Apoptosis inducing factor, Nuclear Receptor Subfamily 4, Group A, Member 1, Gyrovirus, BCL-XL, B-cell lymphoma extra-large, DISC, Death-inducing signal complex, FADD, Other Basic Medicine, Membrane Potential, Mitochondrial, biology, Apoptosis Inducing Factor, Cytochromes c, virus diseases, Receptors, Death Domain, lcsh:Neoplasms. Tumors. Oncology. Including cancer and carcinogens, mitochondrial pathway, Mitochondria, Cell biology, Protein Transport, Proto-Oncogene Proteins c-bcl-2, Caspases, Apoptosis-inducing factor, Signal Transduction, CAV-Apoptin, Chicken anemia virus apoptin, Programmed cell death, cyt c, cytochrome c, caspase, Bcl-xL, Models, Biological, lcsh:RC254-282, Article, Cell Line, Viral Proteins, death receptors, Humans, 7AAD, 7-amino-actinomycin D, FADD, Fas-associated death domain, Death domain, Intrinsic apoptosis, MEF, Mouse embryonic fibroblast, cytc, digestive system diseases, Apoptin, biology.protein, Apoptosome
Abstract

The human gyrovirus derived protein Apoptin (HGV-Apoptin) a homologue of the chicken anemia virus Apoptin (CAV-Apoptin), a protein with high cancer cells selective toxicity, triggers apoptosis selectively in cancer cells. In this paper, we show that HGV-Apoptin acts independently from the death receptor pathway as it induces apoptosis in similar rates in Jurkat cells deficient in either FADD (fas-associated death domain) function or caspase-8 (key players of the extrinsic pathway) and their parental clones. HGV-Apoptin induces apoptosis via the activation of the mitochondrial intrinsic pathway. It induces both mitochondrial inner and outer membrane permebilization, characterized by the loss of the mitochondrial potential and the release into cytoplasm of the pro-apoptotic molecules including apoptosis inducing factor and cytochrome c. HGV-Apoptin acts via the apoptosome, as lack of expression of apoptotic protease-activating factor 1 in murine embryonic fibroblast strongly protected the cells from HGV-Apoptin–induced apoptosis. Moreover, QVD-oph a broad-spectrum caspase inhibitor delayed HGV-Apoptin–induced death. On the other hand, overexpression of the anti-apoptotic BCL-XL confers resistance to HGV-Apoptin–induced cell death. In contrast, cells that lack the expression of the pro-apoptotic BAX and BAK are protected from HGV-Apoptin induced apoptosis. Furthermore, HGV-Apoptin acts independently from p53 signal but triggers the cytoplasmic translocation of Nur77. Taking together these data indicate that HGV-Apoptin acts through the mitochondrial pathway, in a caspase-dependent manner but independently from the death receptor pathway.

Published
2014
Full Text
View/download PDF

3. MIG (CXCL9) is a more sensitive measure than IFN-gamma of vaccine induced T-cell responses in volunteers receiving investigated malaria vaccines

Author

Tamara Berthoud, Stephen Todryk, Susanna Dunachie, Helen A. Fletcher, and Adrian V. S. Hill

Subjects
Male, Cellular immunity, ESAT6, six-kDa early secreted antigenic target, T-Lymphocytes, STAT, signal transducers and activators of transcription, MVA, modified vaccinia virus Ankara, APC, antigen presenting cell, Chemokine CXCL9, ELISA, enzyme linked immunoSorbant assay, FP9, fowlpox strain FP9, BME, β-mercaptoethanol, Immunology and Allergy, M, MVA, Interferon gamma, Flow cytometry, Malaria, Falciparum, PPD, purified protein derivative, IFN-γ, RLT, RNA lysis buffer, Vaccines, Synthetic, HPRT, hypoxanthine phosphoribosyl transferase, medicine.diagnostic_test, Malaria vaccine, Reverse Transcriptase Polymerase Chain Reaction, ELISPOT, MIG, Middle Aged, MIG, monokine induced by gamma, TRAP, thrombospondin related adhesive protein, Monokine, P, PEV3A, ELISPOT, enzyme linked immuno SPOT, PBMC, peripheral blood mononuclear cells, CXCL9, F, FP9, Female, medicine.drug, Research Paper, Adult, CSP, circumsporozoite protein, Adolescent, SEB, staphylococcal enterotoxin B, Immunology, Plasmodium falciparum, Biology, JAK, janus kinase, Interferon-gamma, Young Adult, RT-PCR, reverse transcription polymerase chain reaction, stomatognathic system, RPMI, Roswell Park Memorial Institute media, Malaria Vaccines, medicine, Animals, Humans, RNA, Messenger, AMA1, apical membrane antigen 1, 7AAD, 7-amino-actinomycin D, Aged, CFP10, culture filtrate protein 10, DOC, day of challenge, Brefeldin A, IFN-γ, interferon gamma, CXCL9, CXC chemokine ligand 9, CMV, cytomegalovirus, EBV, Epstein Barr Virus, Virology, Malaria, stomatognathic diseases, PHA, phytohaemagglutinin, Vaccine, Ex vivo, ICS, intracellular staining, ME, multi-epitope string
Abstract

For many years the IFN-gamma ex vivo ELISPOT has been a major assay for assessing human T-cell responses generated by malaria vaccines. The ELISPOT assay is a sensitive assay, but an imperfect correlate of protection against malaria. Monokine induced by gamma (MIG), or CXCL9, is a chemokine induced by IFN-gamma and has the potential to provide amplification of the IFN-gamma signal. MIG secretion could provide a measure of bio-active IFN-gamma and a functional IFN-gamma signalling pathway. We report that detecting MIG by flow cytometry and by RT-PCR can be more sensitive than the detection of IFN-gamma using these methods. We also find that there is little inter-individual variability in MIG secretion when detected by flow cytometry and that the MIG assay may be used to estimate the amount of bio-active IFN-gamma present. Measurement of MIG alongside IFN-gamma may provide a fuller picture of Th1 type responses post-vaccination.

Published
2009

Catalog

Books, media, physical & digital resources
See catalog results