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  • Articles  (6)
  • Springer  (6)
  • American Physical Society (APS)
  • Medicine  (6)
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  • Articles  (6)
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  • 1
    Electronic Resource
    Electronic Resource
    Structure and analysis of the mouse Na+/H+ exchanger (NHE1) gene: Homology and conservation of splice sites (1996)
    Springer
    Molecular and cellular biochemistry 165 (1996), S. 155-159 
    Details
    ISSN: 1573-4919
    Keywords: sodium-hydrogen exchange ; mouse ; gene sequence
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology , Chemistry and Pharmacology , Medicine
    Notes: Abstract The Na+/H+ exchanger is a widely distributed integral membrane protein that is responsible for pH regulation in mammalian tissues. We have cloned and analyzed the NHE1 isoform of the mouse genomic Na+/H+exchanger. A clone from a mouse genomic library contained the NHE1 promoter region and the 5′-untranslated region. It also contained the first 121 amino acids of the coding region of the Na+/H+ exchanger. A splice site occurred after amino acid 121, at the same region as in the human NHE1 gene. The deduced amino terminal coding sequence was 76 and 88% identical to the human and rat NHE1 sequences respectively. The 5′-untranslated region was highly homologous to that of other species and two minicistrons contained in the human Na+/H+ exchanger were present in the mouse sequence. The results show that the deduced protein sequence of the mouse NHE1 gene has a high level of homology with other species and that the splice site of the first intron is conserved. These results suggest that the first large intron may play an important role in the NHE1 gene expression.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00229478
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  • 2
    Electronic Resource
    Electronic Resource
    Increased cyclin B1/CDC 2 kinase activity and phosphorylation of Bcl-2 associated with paclitaxel-induced apoptosis in human nasopharyngeal carcinoma cells (1996)
    Springer
    Apoptosis 1 (1996), S. 141-146 
    Details
    ISSN: 1573-675X
    Keywords: Apoptosis ; Bax ; Bcl-2 ; CDC 2 ; cyclin B1 ; paclitaxel
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology , Medicine
    Notes: Abstract Paclitaxel is a potential cancer chemotherapeutic agent for ovary, breast, and head and neck cancers; its effects on nasopharyngeal carcinoma (NPC) have not been reported previously. This study investigated the cytotoxic mechanism of paclitaxel in two NPC cell lines, NPC-TW01 and NPC-TW04. NPC cells treated with pacli-taxel showed convoluted nuclei, condensed chromatin and decreased cellular and nuclear volume, and also exhibited genomic DNA degradation into multiple oligonucleosomal fragments, suggesting that pacli-taxel induced apoptosis in these cells. The effects of paclitaxel on apoptosis-related proteins including Bcl-2, Bax and CDC 2 were also detected. Although the levels of Bcl-2 and Bax were not changed in NPC cells following treatment with 5 nM-1 μM of paclitaxel, phosphorylation of Bcl-2 was significantly observed in the cells treated with 1 μM of paclitaxel for 12 hours. In addition, cyclin B1-associated CDC 2 kinase was highly activated in the NPC cells exposed to paclitaxel even at low (5 nM) concentration, and this result is associated with the finding that low concentration of paclitaxel is able to induce apoptosis in NPC cells.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF01321020
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  • 3
    Electronic Resource
    Electronic Resource
    GL331-induced disruption of cyclin B1/CDC 2 complex and inhibition of CDC 2 kinase activity (1996)
    Springer
    Apoptosis 1 (1996), S. 213-217 
    Details
    ISSN: 1573-675X
    Keywords: CDC 2 ; cell cycle ; cyclin B1 ; etoposide (VP-16) ; GL331
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology , Medicine
    Notes: Abstract GL331, a new homologue of etoposide (VP-16), was developed to cope with the multiple drug resistance occurring in certain malignant tumours. We previously indicated that GL331, like VP-16 and other major cancer chemotherapeutic agents, induced apoptosis in a variety of human cancer cell lines including nasopharyngeal carcinoma (NPC) NPC-TW01 and NPC-TW04 cells. In this study, we further explored the effect of GL331 on the cell cycle progression of NPC cells. Flow cytometric analysis of DNA content was first used to demonstrate the ability of GL331 to induce cell growth arrest at S-G2 phase in most NPC cells. Besides acting as a topoisomerase II inhibitor, GL331 inhibited cellular cyclin B1-associated CDC 2 kinase activity 6 h after treatment, accounting partly at least for its induction of the cell cycle arrest. As with cyclin A, D1, E, CDK 2 and PCNA, the levels of cyclin B1 and CDC 2 proteins were not changed after GL331 treatment; however, the ability to form complex between cyclin B1 and CDC 2 was obviously affected in GL331-treated NPC cells, which associates with the inhibition of cyclin B1/CDC 2 kinase activity elicited by GL331. These data could provide more principal bases for future therapeutic application of this potential anti-cancer agent.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF01321105
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  • 4
    Electronic Resource
    Electronic Resource
    Cell cycle G2/M arrest and activation of cyclin-dependent kinases associated with low-dose paclitaxel-induced sub-G1 apoptosis (1997)
    Springer
    Apoptosis 2 (1997), S. 463-470 
    Details
    ISSN: 1573-675X
    Keywords: Apoptosis ; CDC 2 (CDK 1) ; CDK 7 ; cyclin B1 ; G2/M arrest ; paclitaxel (Taxol(tm))
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology , Medicine
    Notes: Abstract Paclitaxel is a potential anti-cancer agent for several malignancies including ovary, breast, and head and neck cancers. This study investigated the kinetics of paclitaxel-induced cell cycle perturbation in two human nasopharyngeal carcinoma (NPC) cell lines, NPC-TW01 and NPC-TW04. NPC cells treated with higher concentrations (0.1 or 1 µM) of paclitaxel showed obvious G2/M arrest and then converted to a cell population with reduced DNA content, which was detected as a sub-G2 peak in the flow cytometric histographs. If a low concentration (5 nM) of paclitaxel was used instead, transient G2/M arrest was observed in NPC cells, which subsequently converted to a sub-G1 form during the treatment period. Internucleosomal fragmentation and chromatin condensation were detectable in these sub-G1 and sub-G2 cells, suggesting that persistent or transient G2/M arrest is a prerequisite step for apoptosis elicited by varying doses of paclitaxel. The levels of cyclins A, B1, D1, E, CDK 1 (CDC 2), CDK 2 and proliferating cell nuclear antigen (PCNA) were unchanged in NPC cells following treatment with any concentration of paclitaxel; however, apoptosis-related cyclin B1-associated CDC 2 kinase was highly activated by paclitaxel even at concentrations as low as 5 nM, which is consistent with the finding that low-dose paclitaxel is also able to induce apoptosis in NPC cells. Activation of cyclin B1-associated CDC 2 kinase seems to be an important G2/M event required for paclitaxel-induced apoptosis, and this activation of cyclin B1/CDC 2 kinase could be attributed to the increased activity of CDK 7 kinase.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1023/A:1026422111457
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  • 5
    Electronic Resource
    Electronic Resource
    Differential inducibilities of GFAP expression, cytostasis and apoptosis in primary cultures of human astrocytic tumours (1998)
    Springer
    Apoptosis 3 (1998), S. 171-182 
    Details
    ISSN: 1573-675X
    Keywords: 12-O-tetradecanoylphorbol-13-acetate (TPA) ; BiCNUTM ; differentiation ; glial fibrillary acidic protein (GFAP) ; phenylacetate ; sodium butyrate
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology , Medicine
    Notes: Abstract Glial fibrillary acidic protein (GFAP) is an astrocytic lineage-specific intermediate filament protein, and its expression or non-expression is inversely correlated with the tumourigenecity of astrocytoma cells. To estimate the GFAP levels of astrocytes in intracranial tumour tissues, we established primary cultures from six astrocytic tumour specimens and used a double-staining flow cytometric method to detect the different levels of GFAP among these primary cultures. Although these primary cultures exhibited the same Matrigel invasiveness, their GFAP expression is inversely related to the rate of cell growth and the histologic grade of the original tumour. Phenylacetate, 12-O-tetradecanoylphorbol-13-acetate (TPA) and sodium butyrate, which are potent inducers of differentiation in various cancer cells, have been examined for their effects on these primary cultures. Cytostasis was more or less caused by these compounds in all six primary cultures, but induction of GFAP was observed only in the primary culture derived from a less malignant astrocytoma specimen having the highest intrinsic GFAP level. Interestingly, this primary culture, but not others, also exhibited increased HRG-α expression after phenylacetate or sodium butyrate treatment. Loss of the inducibility of differentiation-related gene expression could be one of the events involved in the malignant progression of astrocytomas. In addition, the chemotherapeutic agent BiCNU has a killing effect on all six primary culture cells, with LD50 less than 60nM. The underlying mechanism was through the induction of apoptosis in these primary culture cells regardless of their varying malignancies of original tumours. However, unlike colon cancer and leukaemia cells, sodium butyrate could not induce apoptosis within 4 days in these astrocytic tumour cells, indicating that the cell context of different cell types indeed determined the ability of sodium butyrate to induce apoptosis.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1023/A:1009698822305
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  • 6
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    Structure and analysis of the mouse Na+/H+ exchanger (NHE1) gene: Homology and conservation of splice sites (1996)
    Springer
    Details
    Publication Date: 1996-12-01
    Print ISSN: 0300-8177
    Electronic ISSN: 1573-4919
    Topics: Biology , Chemistry and Pharmacology , Medicine
    Published by Springer
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