|1.||Sobrino, Francisco: 2 articles (03/2011 - 12/2007)|
|2.||Martín-Acebes, Miguel A: 2 articles (03/2011 - 12/2007)|
|3.||Yanagisawa, Takahiro: 1 article (11/2015)|
|4.||Yano, Kanako: 1 article (11/2015)|
|5.||Moriyasu, Yuji: 1 article (11/2015)|
|6.||Mukae, Kyosuke: 1 article (11/2015)|
|7.||Niwa, Yasuo: 1 article (11/2015)|
|8.||Inoue, Yuko: 1 article (11/2015)|
|9.||Seabra, Sergio Henrique: 1 article (10/2014)|
|10.||da Silva, Maria de Fátima Sarro: 1 article (10/2014)|
03/01/2011 - "Infection by these mutants was more sensitive to drugs that raise the endosomal pH (NH(4)Cl and concanamycin A) than was infection by the parental C-S8c1 virus, confirming that the increase in acid resistance is related to a lower pH requirement for productive uncoating. "
07/01/2010 - "nidulans has been shown to be induced by concanamycin A, and transcriptional data from Cryptococcus neoformans demonstrate a strong up-regulation of the expression of a homologous gene during infection. "
12/05/2007 - "The effect of NH(4)Cl and concanamycin A on FMDV entry and infection was consistent with the requirement of acidic compartments for decapsidation and virus replication. "
01/01/2001 - "The addition of concanamycin A at different times after infection indicated that the compound also interferes with the release of infectious particles to the extracellular medium. "
10/01/2014 - "iNOS was degraded after parasite infection of J774-A1 macrophages treated with calpeptin or concanamycin A. "
12/01/2006 - "Bafilomycin A1 and its analog, concanamycin A, were found to up-regulate HIF-1alpha in eight human cancer cell-lines, and this effect is attributed to inhibited degradation of HIF-1alpha protein. "
08/01/2002 - "Tumor cell lysis in all cases appeared to be mainly mediated by perforin and could be blocked by concanamycin A. "
10/01/1993 - "Antimycin and concanamycin A increased tumor-killing activity of macrophages when added during the effector phase. "
08/01/2002 - "In the present study, we found that a specific inhibitor of vacuolar type H+-ATPase (V-ATPase), concanamycin A, induced apoptosis in a human submandibular gland ductal cancer cell line, HSG. "
10/15/2002 - "Treatment with concanamycin A or EGTA abrogated CD8+ NKT cytotoxicity indicating that perforin is a major pathway of tumor cell lysis. "
|3.||Breast Neoplasms (Breast Cancer)
03/01/2012 - "To study the associated proteins, we isolated autophagosomes from human breast cancer cells using two different biochemical methods and three stimulus types: amino acid deprivation or rapamycin or concanamycin A treatment. "
05/18/1998 - "This report presents a quantification of the pH for identified compartments of the MCF-7 human breast tumor cell line and demonstrates that (a) the chemotherapeutic Adriamycin concentrates in acidified organelles of drug-resistant but not drug-sensitive cells; (b) the lysosomes and recycling endosomes are not acidified in drug-sensitive cells; (c) the cytosol of drug-sensitive cells is 0.4 pH units more acidic than the cytosol of resistant cells; and (d) disrupting the acidification of the organelles of resistant cells with monensin, bafilomycin A1, or concanamycin A is sufficient to change the Adriamycin distribution to that found in drug-sensitive cells, rendering the cell vulnerable once again to chemotherapy. "
|4.||Melanoma (Melanoma, Malignant)
06/01/1993 - "Folimycin blocked excretion of the glycoprotein (G protein) of vesicular stomatitis virus into the medium and, instead, G protein was accumulated intracellularly. "
06/30/1994 - "Concanamycin A, a selective inhibitor of the vacuolar proton ATPase, blocks the infection of animal cells by vesicular stomatitis virus, Semliki Forest virus and influenza virus even when the drug is present at the low concentration of 5 nM. Nevertheless the antibiotic prevents neither the attachment, to cells, of Semliki Forest virus nor its subsequent internalization. "
12/01/2003 - "An earlier report suggested that SS33410, structurally related to folimycin and bafilomycin A(1), blocked secretion of the glycoprotein (G protein) of vesicular stomatitis virus (VSV) into the medium and, instead, G protein was accumulated intracellulary. "
06/01/1993 - "Folimycin (concanamycin A), a specific inhibitor of V-ATPase, blocks intracellular translocation of the glycoprotein of vesicular stomatitis virus before arrival to the Golgi apparatus."
|2.||Anti-Bacterial Agents (Antibiotics)
|3.||Proton-Translocating ATPases (ATPase, H+)
|4.||Adenosine Triphosphatases (ATPase)
|6.||Monophenol Monooxygenase (Tyrosinase)
|7.||Proteins (Proteins, Gene)
|9.||Vacuolar Proton-Translocating ATPases (V-Type ATPase)
|1.||Drug Therapy (Chemotherapy)