scholarly journals RACK1 Interacts with E1A and Rescues E1A-induced Yeast Growth Inhibition and Mammalian Cell Apoptosis

2001 ◽  
Vol 276 (29) ◽  
pp. 27026-27033 ◽  
Author(s):  
Nianli Sang ◽  
Anna Severino ◽  
Patrizia Russo ◽  
Alfonso Baldi ◽  
Antonio Giordano ◽  
...  
Keyword(s):  
Growth Inhibition ◽  
Mammalian Cell ◽  
Cell Apoptosis ◽  
Yeast Growth ◽  
Yeast Growth Inhibition

Parallel Synthesis and Yeast Growth Inhibition Screening of Succinamic Acid Libraries

2007 ◽  
Vol 9 (4) ◽  
pp. 635-643 ◽  
Author(s):  
Pedro Serrano ◽  
Josefina Casas ◽  
Amadeu Llebaria ◽  
Martine Zucco ◽  
Gilbert Emeric ◽  
...  
Keyword(s):  
Growth Inhibition ◽  
Parallel Synthesis ◽  
Yeast Growth ◽  
Succinamic Acid ◽  
Yeast Growth Inhibition

Xylosylation as an effective means for reducing yeast growth inhibition by 2-phenylethanol

2013 ◽  
Vol 53 (9) ◽  
pp. 792-795 ◽  
Author(s):  
Haojun Zhang ◽  
Régis Fauré ◽  
Jean M. François ◽  
Philippe J. Blanc ◽  
Gustavo M. de Billerbeck
Keyword(s):  
Growth Inhibition ◽  
Effective Means ◽  
Yeast Growth ◽  
Yeast Growth Inhibition

Improved Performance in Mammalian Cell Perfusion Cultures by Growth Inhibition

2018 ◽  
Vol 14 (2) ◽  
pp. 1700722 ◽  
Author(s):  
Moritz K. F Wolf ◽  
Aurélie Closet ◽  
Monika Bzowska ◽  
Jean‐Marc Bielser ◽  
Jonathan Souquet ◽  
...  
Keyword(s):  
Growth Inhibition ◽  
Mammalian Cell ◽  
Perfusion Cultures ◽  
Improved Performance

Involvement of autophagy in recombinant human arginase-induced cell apoptosis and growth inhibition of malignant melanoma cells

2013 ◽  
Vol 98 (6) ◽  
pp. 2485-2494 ◽  
Author(s):  
Ziyu Wang ◽  
Xunlong Shi ◽  
Yubin Li ◽  
Xian Zeng ◽  
Jiajun Fan ◽  
...  
Keyword(s):  
Malignant Melanoma ◽  
Growth Inhibition ◽  
Cell Apoptosis ◽  
Melanoma Cells

scholarly journals Oxymatrine Induces Apoptosis in Human Myeloma Cells By Cell Cycle Arrest and Activation of Caspase-Dependent Apoptosis

Blood ◽  
2014 ◽  
Vol 124 (21) ◽  
pp. 5727-5727
Author(s):  
Wenjun Wu ◽  
Cai Wu ◽  
Fuming Zi ◽  
Yi Li ◽  
Li Yang ◽  
...  
Keyword(s):  
Cell Cycle ◽  
Flow Cytometry ◽  
Growth Inhibition ◽  
Signaling Pathway ◽  
Cell Lines ◽  
Western Blotting ◽  
Cell Apoptosis ◽  
Conflicts Of Interest ◽  
Dependent Manner ◽  
Rt Pcr

Abstract Background : Multiple myeloma (MM) is a B cell malignant hematologic cancer. Despite the introduction of new drugs and improvement of chemotherapy, MM is still an incurable disease. Oxymatrine (OMT), the active ingredients of traditional Chinese herbal medicine sophora, has been reported to have antitumor activity. This study was to estimate the therapeutic efficacy of OMT in MM. Methods: The growth inhibition of myeloma cell lines (RPMI8226, U266, ARP-1) or primary cells by OMT was assessed by MTT assay. Apoptosis of MM cells was examined by annexin V-FITC using flow cytometry analysis. DNA content was analyzed by flow cytometry. RT-PCR and western-blot analysis were used to assess the expression of Bcl-2 family proteins and the IAP family proteins. Western blotting was also used to elucidate the signaling pathway that may mediate OMT-induced apoptosis of MM cells. Results: OMT treatment resulted in cell growth inhibition and apoptosis in primary MM cells and all tested MM cell lines in a dose-dependent manner (P <0.05). To elucidate OMT -induced MM cell apoptosis, MM cell lines were treated with or without OMT for 24h and assessed for caspase activation and signaling pathway by Western blotting. The results showed the cleavage of PARP, caspase-3, and caspase-9, and p-AKT were down-regulated after OMT treatment. The mRNA expression of survivin and HIAP by RT-PCR was down-regulated. OMT treatment at 5mM for 48h resulted in increased G-phase cells and decreased S-phase cells in MM cell lines (P <0.05). Cell cycle repressor P21 protein was up-regulated while CDK4, CDK6 and CyclinD1 expression was down-regulated. Our finding also showed a synergistic anti-MM activity of OMT and dexamethasone or adriamycin at a low does (CI<1). In addition, LC3-II expression was significantly increased both in RPMI8226 and U266 cells after treatment with OMT. However, treatment with different doses of OMT and 5 mM autophagy inhibitor 3-MA, significant increased cell apoptosis (P <0.05). Conclusion: Our findings demonstrate the anti-MM activity of OMT and indicate that OMT alone or together with other MM chemotherapeutics may be a prospective treatment for MM. Disclosures No relevant conflicts of interest to declare.

HIV-1 Nef Alleles Show Differential Activation of Hematopoietic Cell Kinase in a Yeast Model System.

Blood ◽  
2004 ◽  
Vol 104 (11) ◽  
pp. 3107-3107
Author(s):  
Ronald P. Trible ◽  
Thomas E. Smithgall
Keyword(s):  
Growth Inhibition ◽  
Mammalian Cells ◽  
Sh2 Domain ◽  
Model System ◽  
Hematopoietic Cell ◽  
Yeast Growth ◽  
High Affinity ◽  
Hematopoietic Cell Kinase ◽  
Aids Progression ◽  
Hiv 1

Abstract Hematopoietic cell kinase (Hck) is a member of the Src family of non-receptor protein-tyrosine kinases that is expressed strongly in macrophages, an important target cell type for human immunodeficiency virus (HIV). The HIV Nef protein, a critical AIDS progression factor, binds Hck with unusually high affinity and induces Hck activation. Nef-mediated Hck activation has been proposed to trigger signaling pathways important for the establishment of HIV infection and subsequent progression to AIDS. Previous studies have utilized sequence alignments and binding assays to predict the functionality of Hck-Nef interactions, but these studies do not directly investigate the ability of Nef alleles to activate Hck. To better address this issue, we have created a model system in Saccharomyces cerevisiae based on previous findings that ectopic expression of c-Src arrests yeast growth in a kinase-dependent fashion. To establish the utility of this system for Hck and Nef, we first created a Hck variant containing a C-terminal sequence modified to encode the high-affinity SH2-domain binding sequence Tyr-Glu-Glu-Ile (HckYEEI). This modified sequence allows for autophosphorylation of the new tail and the subsequent intramolecular binding to the Hck SH2 domain. The resulting HckYEEI molecule models the physiologically down-regulated (inactive) form of Hck in structure and function. Unlike wild-type Hck, HckYEEI showed little kinase activity and failed to induce growth suppression in yeast. Importantly, co-expression with the Nef-SF2 allele activated HckYEEI, resulting in growth arrest. This effect was dependent on the conserved Nef proline-rich motif essential for Hck binding through its SH3 domain. However, Nef-SF2 did not activate FynYEEI, consistent with our previous data that the Fyn tyrosine kinase is not activated by Nef in mammalian cells. We then tested several additional laboratory HIV-1 Nef alleles for their ability to activate HckYEEI. Consensus, Lai, NL4.3, SF2, and YU-2 Nef alleles activated HckYEEI to varying degrees, as reflected by yeast growth inhibition. In contrast, Nef-Eli failed to suppress growth in the presence of HckYEEI, consistent with its inability to bind the Hck SH3 domain in vitro. Growth inhibition paralleled tyrosine phosphorylation of yeast proteins on anti-phosphotyrosine immunoblots. The differential effects of these Nef alleles on Hck activation correlated closely with previous results in mammalian cells. Taken together, these studies validate the use of yeast to reconstitute Nef-Hck interactions in a system amenable to screens of clinical Nef isolates, which may have predictive value in terms of AIDS progression.

Effect of 5-fluoro-2′-deoxycytidine (FdCyd) on p16INK4a, p14ARF, p15INK4b, and DNA methyltransferase 1, 3a, and 3b Genes Expression, Apoptosis Induction, and Cell Growth Inhibition in Pancreatic Cancer AsPC-1 and Hepatocellular Carcinoma LCL-PI 11 Cell Li

2020 ◽  
Author(s):  
Masumeh Sanaei ◽  
Fraidoon Kavoosi
Keyword(s):  
Cell Growth ◽  
Growth Inhibition ◽  
Cell Apoptosis ◽  
Dna Methyltransferase ◽  
Dna Methyltransferase 1 ◽  
Dependent Manner ◽  
Apoptosis Induction ◽  
Cell Growth Inhibition ◽  
Genes Expression ◽  
Methyltransferase 1

Background: Aberrant DNA methylation of the promoter region is one of the most epigenetic changes in numerous cancers. DNA methyltransferase inhibitors (DNMTIs) can revert DNA hypermethylation in tumor suppressor genes (TSGs). The present study was designed to investigate the effect of 5-fluoro-2′-deoxycytidine (FdCyd) on p16INK4a, p14ARF, p15INK4b, and DNA methyltransferase 1, 3a, and 3b genes expression, apoptosis induction, cell growth inhibition in pancreatic cancer AsPC-1 and hepatocellular carcinoma LCL-PI 11 cell lines. Materials and Methods: The cells were treated with FdCyd at different periods. Then, the MTT assay, cell apoptosis assay, and qRT-PCR were done to determine cell viability, cell apoptosis, and the relative gene expression level respectively. Results: The FdCyd decreased DNA methyltransferase 1, 3a, and 3b and increased p16INK4a, p14ARF, and p15INK4b genes expression significantly (P<0.001). Besides, LCL-PI 11 cell was more sensitive to FdCyd in comparison to AsPC-1 cell. FdCyd induced significant cell growth inhibition with a dose- and time-dependent manner (P<0.001). The IC50 value of FdCyd was obtained with approximately 1μM. Further, FdCyd induced cell apoptosis significantly as a time-dependent manner. The number of apoptotic cells was significantly increased in all groups. The percentage of apoptotic cells after 24 and 48 h were 13.86 and 29.6 % in AsPC-1 and 21.04 and 41.52 % in LCL-PI 11 cell line respectively (P<0.001). Conclusion: The FdCyd can reactivate the p16INK4a, p14ARF, and p15INK4b through inhibition of DNA methyltransferase 1, 3a, and 3b gene expression.

scholarly journals Nitrogen source-dependent inhibition of yeast growth by glycine and its N-methylated derivatives

2019 ◽  
Vol 113 (3) ◽  
pp. 437-445
Author(s):  
Tomas Linder
Keyword(s):  
Growth Inhibition ◽  
Nitrogen Source ◽  
Minimal Medium ◽  
Kluyveromyces Lactis ◽  
Nitrogen Sources ◽  
Growth Efficiency ◽  
Sole Source ◽  
Yeast Growth ◽  
Glycine Species ◽  
Dependent Inhibition

Abstract The effect of nitrogen source on the inhibitory properties of glycine and its N-methylated derivatives N-methylglycine (sarcosine), N,N-dimethylglycine, N,N,N-trimethylglycine (glycine betaine) on yeast growth was investigated. On solid minimal medium, all four glycine species completely or partially inhibited growth of Kluyveromyces lactis, Komagataella pastoris, Ogataea arabinofermentans, Spathaspora passalidarum and Yamadazyma tenuis at concentrations 5–10 mM when 10 mM NH4Cl was the sole source of nitrogen. If NH4Cl was substituted by sodium L-glutamate as the sole source of nitrogen, obvious growth inhibition by glycine and its N-methylated derivatives was generally not observed in any of these species. No obvious growth inhibition by any of the glycine species at a concentration of 10 mM was observed in Cyberlindnera jadinii, Lipomyces starkeyi, Lodderomyces elongisporus, Scheffersomyces stipitis or Yarrowia lipolytica on solid minimal medium irrespective of whether the nitrogen source was NH4Cl or sodium L-glutamate. Growth inhibition assays of K. pastoris in liquid minimal medium supplemented with increasing concentrations of N,N-dimethylglycine demonstrated inhibitory effects for nine tested nitrogen sources. In most cases, N,N-dimethylglycine supplementation caused a decrease in growth efficiency that appeared to be proportional to the concentration of N,N-dimethylglycine. The biological relevance of these results is discussed.

Effective Antitumor Candidates Based upon Ferrocenylseleno-Dopamine Derivatives: Growth Inhibition by Induction Cell Apoptosis and Antivascular Effects

2016 ◽  
Vol 35 (11) ◽  
pp. 1866-1875 ◽  
Author(s):  
Hai-Yan Zhou ◽  
Meng Li ◽  
Jian Qu ◽  
Su Jing ◽  
Heng Xu ◽  
...  
Keyword(s):  
Growth Inhibition ◽  
Cell Apoptosis
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