ALBERT

All Library Books, journals and Electronic Records Telegrafenberg

X
feed icon rss

Your email was sent successfully. Check your inbox.

An error occurred while sending the email. Please try again.

Proceed reservation?

Export
Filter
  • Apoptosis  (66)
  • Springer  (46)
  • American Association for the Advancement of Science (AAAS)  (20)
  • American Meteorological Society
  • Elsevier
  • 1995-1999  (66)
  • 1990-1994
  • 1940-1944
  • 1997  (66)
  • 1944
  • 1941
Collection
Keywords
Publisher
  • Springer  (46)
  • American Association for the Advancement of Science (AAAS)  (20)
  • American Meteorological Society
  • Elsevier
  • Wiley-Blackwell  (1)
Years
  • 1995-1999  (66)
  • 1990-1994
  • 1940-1944
Year
  • 1
    Electronic Resource
    Electronic Resource
    Autoactivation ofXenopus thyroid hormone receptor β genes correlates with larval epithelial apoptosis and adult cell proliferation (1997)
    Springer
    Journal of biomedical science 4 (1997), S. 9-18 
    Details
    ISSN: 1423-0127
    Keywords: Thyroid hormone receptor ; Xenopus laevis ; Metamorphosis ; Apoptosis ; Cell proliferation
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology , Medicine
    Notes: Abstract The thyroid hormone (T3)-dependent amphibian metamorphosis involves degeneration of larval tissues through programmed cell death (apoptosis) and concurrent proliferation and differentiation of adult cell types. As the mediators of the causative effects of T3 on metamorphosis, both thyroid hormone receptor (TR) α and β genes have been found to be expressed in different tissues during this process. In particular, theXenopus TRβ genes have been shown to be regulated by T3 at the transcriptional level and their expression correlates with organ-specific metamorphosis. We demonstrate here by in situ hybridization that theXenopus TRβ genes are regulated in a cell-type specific manner that correlates with tissue transformation. In particular, they are found to be expressed in the larval intestinal epithelial cells prior to their apoptotic degeneration and in the proliferating cells of the adult epithelium, connective tissue, and muscles. However, they are repressed again upon the differentiation of these adult cells. These results implicate that TRβ participates both in inducing apoptosis and stimulating cell proliferation during development.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF02255588
    Location Call Number Expected Availability
    BibTip Others were also interested in ...
    Paper (German National Licenses)
    Fulltext
  • 2
    Electronic Resource
    Electronic Resource
    Apoptosis of L1210 leukemia cells induced by 3-deazaadenosine analogs: Differential expression of c-myc, NF-kappa B and molecular events (1997)
    Springer
    Journal of biomedical science 4 (1997), S. 83-90 
    Details
    ISSN: 1423-0127
    Keywords: Apoptosis ; Cell cycle ; 3-Deazaadenosine analogs ; L1210 lymphocytic leukemia cells ; c-myc ; NF-kappa B
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology , Medicine
    Notes: Abstract A new class of potent apogens (apoptosis-inducing agents) has been identified, consisting of 3-deazaadenosine (DZA), 3-deaza-(±)aristeromycin (DZAri) and 1-β-D-arabinofuranosyl-1H-imidazo[4,5-c]pyridine (ara-3-deazaadenine; DZAra-A). They are inhibitors ofS-adenosylhomocysteine hydrolase and indirect inhibitors of methylation. Furthermore, they have also been found to form 3-deaza-nucleotide analogs. The DZA analogs, DZA, DZAri, and DZAra-A, induced DNA fragmentation in a dose- and time-dependent manner, reaching a maximum at 250 µM after 72 h. Cycloheximide at 0.5 µg/ml completely blocked the DNA fragmentation induced by 250 µM of each of the analogs. Interestingly, exogenous 100 µM L-homocysteine thiolactone abrogated the DNA fragmentation caused by DZAri and DZAra-A, but not by DZA. Flow cytometric analysis showed that DZA arrested the cells in the G2/M phase, whereas the S phase was arrested by DZAri. Correlated with the effect of DZA was a rapid decrease in the expression of c-myc, whereasnur77 and GAPDH were unaffected. In comparison, there was an elevated expression of IFN-γ mRNA without apparent change inbax, p53 or GAPDH mRNA after 24 h. After treatment with DZA, there was an elevated expression of NF-κB DNA binding activity, which became more pronounced at 24 h. Simultaneously, there was an apparent disappearance of AP-1 activity. Thus, DZA most likely inhibited the RNA synthesis of c-myc, a reduction of which could trigger a cascade of gene transcription leading to apoptosis in L1210 cells.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF02255598
    Location Call Number Expected Availability
    BibTip Others were also interested in ...
    Paper (German National Licenses)
    Fulltext
  • 3
    Electronic Resource
    Electronic Resource
    Role of oncogenic transcription factor c-Myc in cell cycle regulation, apoptosis and metabolism (1997)
    Springer
    Journal of biomedical science 4 (1997), S. 269-278 
    Details
    ISSN: 1423-0127
    Keywords: c-Myc ; Oncogene ; Transcription ; Cancer ; Metabolism ; Apoptosis
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology , Medicine
    Notes: Abstract Themyc gene was initially discovered as a prototypical retrovirally transduced oncogene. Over the decades, abundant evidence has emerged to support a causal role for the activated cellular gene, c-myc, in animal and human tumors. The gene encodes an oncogenic helix-loop-helix leucine zipper transcription factor that acts as a heterodimer with its partner protein, Max, to activate genes regulating the cell cycle machinery as well as critical metabolic enzymes. The additional ability of c-Myc to repress transcription of differentiation-related genes suggest that c-Myc is a central and key molecular integrator of cell proliferation, differentiation and metabolism.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF02258350
    Location Call Number Expected Availability
    BibTip Others were also interested in ...
    Paper (German National Licenses)
    Fulltext
  • 4
    Electronic Resource
    Electronic Resource
    Role of the Mitochondrial Permeability Transition Pore in Apoptosis (1997)
    Springer
    Bioscience reports 17 (1997), S. 67-76 
    Details
    ISSN: 1573-4935
    Keywords: Apoptosis ; necrosis ; mitochondria ; megachannel ; permeability transition ; programmed cell death ; poteases
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology , Chemistry and Pharmacology
    Notes: Abstract Mitochondrial permeability transition (PT) involves the formation of proteaceous, regulated pores, probably by apposition of inner and outer mitochondrial membrane proteins which cooperate to form the mitochondrial megachannel (=mitochondrial PT pore). PT has important metabolic consequences, namely the collapse of the mitochondrial transmembrane potential, uncoupling of the respiratory chain, hyperproduction of superoxide anions, disruption of mitochondrial biogenesis, outflow of matrix calcium and glutathione, and release of soluble intermembrane proteins. Recent evidence suggests that PT is a critical, rate limiting event of apoptosis (programmed cell death): (i) induction of PT suffices to cause apoptosis; (ii) one of the immediate consequences of PT, disruption of the mitochondrial transmembrane potential (ΔΨm), is a constant feature of early apoptosis; (iii) prevention of PT impedes the ΔΨm collapse as well as all other features of apoptosis at the levels of the cytoplasma, the nucleus, and the plasma membrane; (iv) PT is modulated by members of the apoptosis-regulatory bcl-2 gene family. Recent data suggest that the acquisition of the apoptotic phenotype, including characteristic changes in nuclear morphology and biochemistry (chromatin condensation and DNA fragmentation), depends on the action of apoptogenic proteins released from the mitochondrial intermembrane space.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1023/A:1027339418683
    Location Call Number Expected Availability
    BibTip Others were also interested in ...
    Paper (German National Licenses)
    Fulltext
  • 5
    Electronic Resource
    Electronic Resource
    Oxidative Damage and Fragmentation of Mitochondrial DNA in Cellular Apoptosis (1997)
    Springer
    Bioscience reports 17 (1997), S. 237-250 
    Details
    ISSN: 1573-4935
    Keywords: Apoptosis ; DNA fragmentation ; mitochondrial DNA ; oxidative damage
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology , Chemistry and Pharmacology
    Notes: Abstract The molecular genetics and bioenergetics of oxidative damage, fragmentation, and fragility of mitochondrial DNA in cellular apoptosis is reviewed in connection with the “redox mechanism of ageing”.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1023/A:1027324410022
    Location Call Number Expected Availability
    BibTip Others were also interested in ...
    Paper (German National Licenses)
    Fulltext
  • 6
    Electronic Resource
    Electronic Resource
    Effects of postnatal age and of thymectomy on hamster pulmonary neuroendocrine system and aspects of programmed cell death (1997)
    Springer
    Cell & tissue research 290 (1997), S. 553-567 
    Details
    ISSN: 1432-0878
    Keywords: Key words. Neuroendocrine system ; Lung ; Neuroepithelial bodies ; Apoptosis ; Thymectomy ; Golden hamster
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology , Medicine
    Notes: Abstract. Effects of postnatal age and neonatal thymectomy on the numbers and characteristics of pulmonary neuroepithelial bodies (NEB) were investigated in 14-day- compared with 2.5-month-old hamsters. Left lung sections were stained for the marker PGP 9.5 and used for light-microscopic quantification, while the right lungs were processed for an electron-microscopic survey of the NEB ultrastructural features. For the first time, it is clearly demonstrated that, depending on the sampling method, the number of NEB may rise or fall with age; when considering the entire lung volume, the actual number of NEB doubles, whereas when studying a constant surface area, their number apparently decreases. Also, the proportion of alveolar NEB as well as luminal contact increase on normal development. In neonates, in contrast to older animals, apoptosis is clearly present in NEB, and approximately 10% of the NEB are associated with inflammatory cells. In some cases, the dead cells have properties of both apoptosis, disintegration and cytoplasmic degeneration. The presence of intracorpuscular neutrophilic granulocytes correlates with cellular death and innervation of the NEB. Thymectomy causes only minor effects on the pulmonary neuroendocrine system. It is argued that development of the NEB and of their innervation continue during the postnatal period.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/s004410050961
    Location Call Number Expected Availability
    BibTip Others were also interested in ...
    Paper (German National Licenses)
    Fulltext
  • 7
    Electronic Resource
    Electronic Resource
    Programmed cell death of plant tracheary elements differentiating in vitro (1997)
    Springer
    Protoplasma 196 (1997), S. 197-211 
    Details
    ISSN: 1615-6102
    Keywords: Apoptosis ; Programmed cell death ; Tracheary element ; Xylogenesis ; Zinnia elegans
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology
    Notes: Summary We used various microscopic and labeling techniques to examine events occurring during the programmed cell death (PCD) of plant tracheary elements (TEs) developing in vitro. TEs differentiating in vitro synthesize a secondary cell wall which is complex in composition and pattern at approximately 72 h after hormone manipulation. The timing of PCD events was established relative to this developmental marker. Cytoplasmic streaming continues throughout secondary wall synthesis, which takes 6 h to complete in a typical cell. Vital dye staining and ultrastructural analysis show that the vacuole and plasma membrane are intact during secondary cell wall synthesis, but the cytoplasm becomes less dense in appearance, most likely through the action of confined hydrolysis by small vacuoles which are seen throughout the cell at this time. The final, preeminent step of TE PCD is a rapid collapse of the vacuole occurring after completion of secondary cell wall synthesis. Vacuole collapse is an irreversible commitment to death which results in the immediate cessation of cytoplasmic streaming and leads to the complete degradation of cellular contents, which is probably accomplished by release of hydrolytic enzymes sequestered in the vacuole. This event represents a novel form of PCD. The degradation of nuclear DNA is detectable by TUNEL, an in situ labeling method, and appears to occur near or after vacuole collapse. Our observations indicate that the process of cellular degradation that produces the hollow TE cell corpse is an active and cell-autonomous process which is distinguishable morphologically and kinetically from necrosis. Although TE PCD does not resemble apoptosis morphologically, we describe the production of spherical protoplast fragments by cultured cells that resemble apoptotic bodies but which are not involved in TE PCD. We also present evidence that, unlike the hypersensitive response (HR), TE PCD does not involve an oxidative burst. While this evidence does not exclude a role for reactive oxygen intermediates in TE PCD, it does suggest TE PCD is mechanistically distinct from cell death during the HR.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF01279568
    Location Call Number Expected Availability
    BibTip Others were also interested in ...
    Paper (German National Licenses)
    Fulltext
  • 8
    Electronic Resource
    Electronic Resource
    A structural analysis of cytoskeleton components during the execution phase of apoptosis (1997)
    Springer
    Protoplasma 198 (1997), S. 163-169 
    Details
    ISSN: 1615-6102
    Keywords: Actin ; Actin-binding proteins ; Apoptosis ; F9 embryonal carcinoma cells
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology
    Notes: Summary During the execution phase of apoptosis, the cell undergoes a set of morphological changes which reveal the activation of a complex machinery leading the cell to its disruption into small, spherical, membrane-bounded fragments called apoptotic bodies. In the present study, we have focused on the implications of the micro-filament network in the early stages of the active phase of apoptosis. By using confocal microscopy, we have analysed the location of the actin microfilaments and two actin-binding proteins, α-actinin and myosin, in F9 embryonal carcinoma cells undergoing apoptosis during the stages previous to their fragmentation. Our results show that these proteins locate in the centre of the disrupting cell and form a three-dimensional structure which suggests the existence of a fully functional contractile system involved in the fragmentation of the cell and the formation of apoptotic bodies.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF01287565
    Location Call Number Expected Availability
    BibTip Others were also interested in ...
    Paper (German National Licenses)
    Fulltext
  • 9
    Electronic Resource
    Electronic Resource
    Etoposide phosphate, the water soluble prodrug of etoposide (1997)
    Springer
    Pharmacy world & science 19 (1997), S. 119-125 
    Details
    ISSN: 1573-739X
    Keywords: Apoptosis ; Chemotherapy ; Drug resistence ; Necrosis ; P53 tumor suppressor gene ; Programmed cell death
    Source: Springer Online Journal Archives 1860-2000
    Topics: Chemistry and Pharmacology
    Notes: Abstract Apoptosis, or programmed cell death, is an orderly and genetically controlled form of cell death. In a morphological sense, it differs from necrosis in that cellular shrinkage and chromatin condensation occurs, followed by fragmentation of nuclear components within membrane-bound vesicles which are cleared by phagocytosis without damage to adjacent tissue. The molecular pathway includes an initiating phase, which starts after signalling by external triggers, such as ligation to distinct receptors or by endogenous mechanisms related to aging or to exogenous irreversible cellular or nuclear damage. The initiation phase is followed by a decision phase. During this phase transduction occurs of the apoptotic signal to nuclear and cytoplasmatic target enzymes, which includes activation of endonucleases and enzymatic alterations of the cytoskeleton. There are numerous proteins and lipid–derived moieties which modulate the apoptotic mechanism in positive or negative direction. The execution phase is started when the cell has arrived at a stage of no return. The nuclear DNA is cleaved into multiples of 180–200 basepairs, the plasma membrane integrity and the mitochondria remain initially intact, the cell splits up into apoptotic bodies, small vesicles which enclose the nuclear and cellular remnants. Finally, the clearing phase is arrived, when the apoptotic bodies are phagocytosed by adjacent cells and macrophages. It is thought that the pharmacodynamics of anticancer drugs consists of two distinct steps. The first step includes the interaction with its cellular target, which is not lethal per se. The commitment of the cell to undergo apoptosis forms the second step. The efficacy of anticancer drugs is determined by the ability to selectively sensitize tumor cells to apoptosis, which depends to a large extent from the expression of various oncogenes, such as bcl–2, p53, bax, ras, c–myc and others, and from endogenous factors. It is a challenge in pharmacological research to explore apoptosis by modulating the extrinsic and intrinsic regulators in a positive or negative direction in order to improve the efficacy of anticancer treatment.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1023/A:1008654316572
    Location Call Number Expected Availability
    BibTip Others were also interested in ...
    Paper (German National Licenses)
    Fulltext
  • 10
    Electronic Resource
    Electronic Resource
    Apoptosis and mammary gland involution: reviewing the process (1997)
    Springer
    Apoptosis 2 (1997), S. 19-24 
    Details
    ISSN: 1573-675X
    Keywords: Apoptosis ; bcl-2 gene family ; hormones ; mammary gland involution ; proteinase ; tissue remodelling
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology , Medicine
    Notes: Abstract Apoptosis is a process of programmed cell death. Mammary gland involution is a tissue remodelling process. Mammary epithelial cell apoptosis is an integral component of tissue remodelling but it is only one element. Equally important are the factors which degrade basement membrane and extracellular matrix. Both operations are required for completion of mammary gland involution. The primary apoptotic process occurs first and is temporally distinct from the second stage of involution typified by lobular-alveolar collapse. Local factors related to milk accumulation trigger the first stage, but loss of systemic hormonal stimulation governs the second stage. Changes in the expression patterns of cell cycle control genes and bcl-2 family member genes are found in the first stage. Proteinase gene activation dominates the second stage. These findings support a two stage model of mammary gland involution. Both mammary epithelial cell apoptosis and mammary gland remodelling advance through a process which includes both loss of survival factors and gain of death factors. This review focuses on signalling pathways and genetic controls which are activated and repressed during mammary gland involution.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1023/A:1026454207398
    Location Call Number Expected Availability
    BibTip Others were also interested in ...
    Paper (German National Licenses)
    Fulltext
  • 11
    Electronic Resource
    Electronic Resource
    HIV-gp120 induced cell death in hematopoietic progenitor CD34+ cells (1997)
    Springer
    Apoptosis 2 (1997), S. 61-68 
    Details
    ISSN: 1573-675X
    Keywords: Apoptosis ; bone marrow ; cord blood ; CD34+CD4+ cells ; fas antigen ; HIV-1 infection
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology , Medicine
    Notes: Abstract Haematologic abnormalities accompany the majority of HIV-1 infections. At present it is unclear whether this is due directly to HIV infection of hematopoietic progenitor cells, or whether this results from an indirect mechanism secondary to HIV infection. Here we provide evidence for an indirect mechanism, whereby hematopoietic progenitor cells undergo HIV gp120-induced apoptosis (programmed cell death) even in the absence of HIV infection. Freshly isolated, purified human hematopoietic progenitor CD34+ cells, derived from both umbilical cord blood and bone marrow, co-expressed the CD4 marker at low density on their surface. Although these CD34+CD4+ cells theoretically should be capable of productive infection by HIV, we found that HIV-IIIB could not establish productive infection in these cells. Nonetheless, gp120 from IIIB could bind the cells. Thus, binding of gp120 did not correlate with infectivity. Furthermore, binding of gp120 was a specific event, leading to apoptosis upon crosslinking with anti-gp120 through a fas-dependent mechanism. If apoptosis is also observed in vivo even in uninfected hematopoietic cells, this could contribute significantly to the impairment in hematopoietic cell number and function. Our data suggest a novel indirect mechanism for depletion of CD34+ and CD34+-derived cells even in the absence of productive viral infection of these cells.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1023/A:1026439726053
    Location Call Number Expected Availability
    BibTip Others were also interested in ...
    Paper (German National Licenses)
    Fulltext
  • 12
    Electronic Resource
    Electronic Resource
    HIV-1 envelope glycoproteins-mediated apoptosis is regulated by CD4 dependent and independent mechanisms (1997)
    Springer
    Apoptosis 2 (1997), S. 47-60 
    Details
    ISSN: 1573-675X
    Keywords: Apoptosis ; CD4 ; HIV ; PMA
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology , Medicine
    Notes: Abstract The progressive loss of CD4 T lymphocytes is one of the hallmarks of HIV infection. The reverse correlation observed in vivo, between plasmatic HIV levels and CD4 T lymphocyte counts, supports the concept that direct HIV-mediated cell death contributes to this depletion. Previously, we and others have demonstrated, in vitro, that interactions between membrane-expressed HIV-envelope glycoprotein complexes and CD4 ecto-molecules are critical to cell killing which occurs mainly by apoptosis. Here, by the use of a co-culture model, in which chronically HIV-1 infected cells trigger apoptosis in uninfected CD4+ target cells, we have investigated the role of different CD4 domains in HIV envelope-mediated apoptosis. Target cells were A201 lymphoblastoid cell lines expressing wild-type CD4 or mutant forms of CD4. We show that the cytoplasmic domain of CD4 was not required for apoptosis induction. In contrast, the HIV permissive cell line expressing a CD4/CD8 chimeric molecule which contains only the first 171 amino acids of CD4, appeared to be resistant to HIV-induced apoptosis; thus suggesting that the D3-D4 CD4 module plays somewhat a regulatory role. Pre-treatment of wild-type CD4 expressing target cells by the phorbol ester PMA which leads to down-regulation of CD4, completely abolished apoptosis. Interestingly, in cells expressing CD4 devoid of its cytoplasmic domain, PMA blocked partially cell death without affecting, as expected, the CD4 expression. Taken together, these results demonstrate that although CD4 expression is essential for HIV envelope induced apoptosis, the apoptotic signal could be delivered in the absence of its cytoplasmic domain. Consistent with this, we suggest that other membrane associated molecule(s) are recruited for the signalling to initiate apoptosis.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1023/A:1026435625144
    Location Call Number Expected Availability
    BibTip Others were also interested in ...
    Paper (German National Licenses)
    Fulltext
  • 13
    Electronic Resource
    Electronic Resource
    Serum withdrawal and etoposide induce apoptosis in human lung carcinoma cell line A549 via distinct pathways (1997)
    Springer
    Apoptosis 2 (1997), S. 199-206 
    Details
    ISSN: 1573-675X
    Keywords: Apoptosis ; ERK ; JNK ; p53 ; Rb
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology , Medicine
    Notes: Abstract The molecular events associated with apoptosis induced by two distinct triggers (1) serum withdrawal and (2) etoposide treatment were investigated in the human lung carcinoma cell line A549. Although both serum withdrawal and etoposide treatment resulted in internucleosomal DNA fragmentation, the morphologic features were distinct. Serum deprived apoptotic cells appeared small, round and refractile, with little evidence of nuclear fragmentation; etoposide-induced apoptotic cells appeared enlarged and flattened and displayed prominent nuclear fragmentation. p53 and p21/waf1 protein levels were elevated in etoposide-treated cells, but not in cells subjected to serum with-drawal. Apoptosis induced by both treatments was accompanied by a significant reduction in Rb protein levels. However, etoposide treatment led to hypo-phosphorylation of Rb, while serum withdrawal did not alter the Rb phosphorylation pattern. Serum withdrawal-induced apoptosis was correlated with activation of JNK and suppression of ERK activities, while both JNK and ERK activities were slightly elevated during etoposid- induced apoptosis. Together, these results support the hypothesis that apoptosis induced by serum withdrawal and etoposide treatment occurs through different pathways and involves distinct mediators.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1023/A:1026420616484
    Location Call Number Expected Availability
    BibTip Others were also interested in ...
    Paper (German National Licenses)
    Fulltext
  • 14
    Electronic Resource
    Electronic Resource
    Apoptotic and necrotic cell death are both induced by electroporation in HL60 human promyeloid leukaemia cells (1997)
    Springer
    Apoptosis 2 (1997), S. 330-336 
    Details
    ISSN: 1573-675X
    Keywords: Apoptosis ; electroporation ; HL-60
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology , Medicine
    Notes: Abstract Cell death was induced by electroporation in HL60 cells, a human promyeloid leukaemia strain, in order to determine by both morphological and biochemical criteria whether necrotic or apoptotic processes occurred. Cells sampled at several times after electroporation were analyzed for the assessment of the following end-points: (i) chromosomal DNA fragmentation; (ii) cell viability; (iii) mono- and oligonucleosomes in the cytoplasmic fraction; (iv) apoptotic index; and (v) morphology of treated cells. The results indicate that about 50% of the cells killed by electroporation die through necrosis, while the remaining 50% of the cells undergo apoptosis. Chromosome damage was also studied by cytogenetic analysis at metaphase. The possibility of killing tumour cells by electroporation, as a variant of electrotherapy, constitutes, in our opinion, a promising procedure in cancer therapy, avoiding the undesirable side effects normally derived from treatment with cytotoxic drugs.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1023/A:1026497306006
    Location Call Number Expected Availability
    BibTip Others were also interested in ...
    Paper (German National Licenses)
    Fulltext
  • 15
    Electronic Resource
    Electronic Resource
    Apoptosis induced by cadmium (1997)
    Springer
    Apoptosis 2 (1997), S. 359-367 
    Details
    ISSN: 1573-675X
    Keywords: Apoptosis ; cadmium ; metallothionein ; superoxide ; zinc-finger
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology , Medicine
    Notes: Abstract Cell death resulting from cadmium (Cd) intoxication has been confirmed to occur through apoptosis by morphological and biochemical studies. However it is still not clear whether Cd itself or metallothionein (MT) induced by Cd is the major factor responsible for the apoptosis. Although apoptosis is inducible by exposure of cells to various stimuli, the common pathway involved is generally accepted to be activation of endonucleases that induce internucleosomal cleavage of DNA, resulting in the ‘ladder’ formation observed upon agarose gel electrophoresis and the chromatin condensation seen by electron microscopy. Cd does not seem to activate the endonuclease in vitro. However, Cd itself can be associated with apoptosis through indirect oxidative stress by inhibition of antioxidant enzymes and possible interaction with zinc finger protein. In addition to the direct effect of Cd, MT appears to play dual roles in apoptosis induction: one as a Cd carrier by which Cd accumulates in the nucleus, and the other as an inhibitor of zinc finger proteins, which include transcriptional factors related to apoptosis such as the product of the apoptosis resistance gene A20. In this review, we demonstrated that the mode of cell death following Cd exposure is associated with intracellular movement of Cd and MT. A possible mechanism for Cd-induced apoptosis is also discussed.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1023/A:1026401506914
    Location Call Number Expected Availability
    BibTip Others were also interested in ...
    Paper (German National Licenses)
    Fulltext
  • 16
    Electronic Resource
    Electronic Resource
    Apoptosis induced in L1210 leukaemia cells by an inhibitor of the chymotrypsin-like activity of the proteasome (1997)
    Springer
    Apoptosis 2 (1997), S. 455-462 
    Details
    ISSN: 1573-675X
    Keywords: Apoptosis ; experimental cancer therapy ; L1210 leukaemia ; proteasome ; proteasome inhibitor ; TNF
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology , Medicine
    Notes: Abstract Of a number of factors involved in apoptosis, protease activity may play a crucial role. We show that N-benzyloxycarbonyl-Ile-Glu( O-t-butyl)-Ala-leucinal (PSI), a selective inhibitor of the chymotrypsin-like activity of the proteasome, induces massive apoptosis in murine leukaemia L1210 cells. At 50 nM concentration, PSI induces a block of cytokinesis, while higher concentrations (500 nM) cause S phase block and massive apoptosis. Z-Leu-leucinal, a specific calpain inhibitor, did not induce apoptosis. In contrast to previous reports, TNF-α did not enhance apoptosis when combined with PSI. Our results suggest that proteasome inhibitors may be considered as potential anti-neoplastic agents.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1023/A:1026470027387
    Location Call Number Expected Availability
    BibTip Others were also interested in ...
    Paper (German National Licenses)
    Fulltext
  • 17
    Electronic Resource
    Electronic Resource
    Expression of Bax, Bcl-2, Waf-1, and PCNA gene products in an immortalized human endothelial cell line undergoing p53-mediated apoptosis (1997)
    Springer
    Apoptosis 2 (1997), S. 442-454 
    Details
    ISSN: 1573-675X
    Keywords: Apoptosis ; endothelial ; p53
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology , Medicine
    Notes: Abstract Transfection of the wild-type p53 gene into an immortalized human endothelial cell line (ECV-304) by recombinant adenoviral delivery resulted in high level expression of the wild-type p53 protein and induction of apoptosis. Increases in the number of apoptotic cells were observed within 12 h after infection of ECV-304 cells with recombinant p53 adenovirus, as deter-mined by the appearance of internucleosomal DNA fragmentation ladders and by TUNEL and electron microscopic analyses. Control cells infected with a β-galactosidase recombinant adenovirus exhibited little or no increase in apoptosis over uninfected cells. The expression of Waf-1 and Bax gene products were in-creased substantially in apoptotic ECV-304 cells as determined by Northern blot, reverse transcription-PCR and immunoblotting analyses. Lesser increases in the expression of the PCNA gene were detected in ECV-304 cells undergoing apoptosis. Both control and apoptotic ECV-304 cells did not express detectable levels of Bcl-2 mRNA or protein in Northern blotting and immunoblotting analyses, respectively. The data suggest a role for the Bax gene product in p53-mediated apoptosis of endothelial cells.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1023/A:1026418010549
    Location Call Number Expected Availability
    BibTip Others were also interested in ...
    Paper (German National Licenses)
    Fulltext
  • 18
    Electronic Resource
    Electronic Resource
    Life and death decisions: the role of the IAPs in modulating programmed cell death (1997)
    Springer
    Apoptosis 2 (1997), S. 423-441 
    Details
    ISSN: 1573-675X
    Keywords: Apoptosis ; IAP ; NAIP ; TNF
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology , Medicine
    Notes: Abstract Multicellular organisms have evolved elaborate signal transduction pathways for maintaining homeostasis through the control of cell proliferation and death. The recent surge of interest in the regulation of programmed cell death has led to the rapid identification of many proteins involved in controlling and executing apoptosis. The inhibitors of apoptosis proteins (IAPs) constitute a family of highly conserved death suppressing proteins that were first identified in baculoviruses, and that has recently expanded to include at least two homologues in Drosophila melanogaster and four in rodents and humans. In this article we review the current state of IAP research. Two of the IAPs, HIAP-1 and HIAP-2, have been placed within the TNFα induced cell death pathway which involves two receptors for TNFα and multiple, overlapping signal transduction proteins. A third, X-linked gene termed XIAP, is ubiquitously expressed and appears to have a broad range of suppressor activity to a variety of apoptotic triggers. The fourth member, NAIP, has been identified as the protein product of a candidate gene for the inherited neuromuscular disorder, spinal muscular atrophy (SMA). The neuroprotective activity of NAIP in an in vivo model of cerebral ischemia has also been demonstrated.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1023/A:1026465926478
    Location Call Number Expected Availability
    BibTip Others were also interested in ...
    Paper (German National Licenses)
    Fulltext
  • 19
    Electronic Resource
    Electronic Resource
    Effects of BCL-2 overexpression on the sensitivity of MCF-7 breast cancer cells to ricin, diphtheria and Pseudomonas toxin and immunotoxins (1997)
    Springer
    Apoptosis 2 (1997), S. 192-198 
    Details
    ISSN: 1573-675X
    Keywords: Apoptosis ; cancer therapy ; drug resistance ; LMB-7
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology , Medicine
    Notes: Abstract Immunotoxins are presently being evaluated as novel agents for cancer therapy. The direct mechanism by which immunotoxins kill cancer cells is inhibition of protein synthesis, but cytotoxicity due to induction of apoptosis has also been observed with these agents. Some cancers that express high levels of BCL-2 are relatively resistant to apoptosis inducing agents. It is therefore important to determine to what degree the toxicity of ricin, diphtheria toxin, Pseudomonas exotoxin and Pseudomonas exotoxin derived immunotoxins towards cancer cells can be attributed to inhibition of protein synthesis, and to what degree to subsequent induction of apoptosis. We compared the sensitivity of MCF-7 breast cancer cells that were stably transfected with a BCL-2 expression plasmid and thus protected against apoptosis and of MCF-7 cells transfected with a control plasmid towards ricin, diphtheria and Pseudomonas toxin, a Pseudomonas toxin-derived immunotoxin (LMB-7) and tumour necrosis factor α (TNF). We found that BCL-2 mediated inhibition of apoptosis renders the cells almost completely resistant (1000-fold) to tumour necrosis factor, but the same cells were only 3–10 fold more resistant to cytotoxicity induced by immunotoxin LMB-7 as well as Pseudo-monas exotoxin, diphtheria toxin and ricin. We next studied several leukaemia cell lines with variable levels of BCL-2 expression and found them quite sensitive to a Pseudomonas exotoxin containing immunotoxin independent of the level of BCL-2. Our data indicate that although BCL-2 overexpression can have a modest effect on sensitivity to an immunotoxin, cell lines derived from patients are still very sensitive to immunotoxins.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1023/A:1026468532413
    Location Call Number Expected Availability
    BibTip Others were also interested in ...
    Paper (German National Licenses)
    Fulltext
  • 20
    Electronic Resource
    Electronic Resource
    Therapy for oral squamous cell carcinoma by tegafur and streptococcal agent OK-432 in combination with radiotherapy: Association of the therapeutic effect with differentiation and apoptosis in the cancer cells (1997)
    Springer
    Apoptosis 2 (1997), S. 227-238 
    Details
    ISSN: 1573-675X
    Keywords: Apoptosis ; differentiation ; OK-432 ; oral squamous cell carcinoma ; radiotherapy ; tegafur
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology , Medicine
    Notes: Abstract Twenty patients with oral squamous cell carcinoma having mainly stage II or III lesions without distant metastasis, were treated with tegafur and streptococcal agent, OK-432, in combination with radiotherapy. As a consequence, 16 cases among the treated 20 cases showed complete remission by this therapy alone. Especially, we have found that the squamous cell carcinoma arising in non-keratinizing oral epithelium rather than in keratinizing oral epithelium has better response to this therapy. Among the 16 cases with complete remission (CR) by the current therapy, 10 cases were histopathologically diagnosed as well-differentiated squamous cell carcinoma and six cases as moderately differentiated squamous cell carcinoma. When we examined immunohistochemically the expres-sion of various antigens such as proliferating cell nuclear antigen (PCNA), p53 and LeY or the presence of DNA fragmentation by nick-end labelling in the biopsy materials taken at the first visit to our clinic from 20 patients treated with the current therapy, the CR group showed a significantly increased LeY expres-sion level ( p〈 0.05) and DNA fragmentation rate ( p〈 0.05) as compared with the partial response (PR, n= 3) + no change (NC, n= 1) group. On the other hand, the CR group with respect to PCNA expression level was significantly decreased as compared with the PR + NC group ( p〈 0.05). From these findings, it can be considered that the therapy for oral squamous cell carcinoma by UFT and OK-432 in combination with radiotherapy is very effective, which may be associated with differentiation or apoptosis in oral squamous carcinoma cells. In addition, we present the clinical findings and results of immunohistochemical staining for the biopsy materials obtained from four CR cases treated with the current therapeutic method.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1023/A:1026428918301
    Location Call Number Expected Availability
    BibTip Others were also interested in ...
    Paper (German National Licenses)
    Fulltext
  • 21
    Electronic Resource
    Electronic Resource
    Role of apoptosis and apoptosis-related proteins in the cisplatin-resistant phenotype of human tumor cell lines (1997)
    Springer
    Apoptosis 2 (1997), S. 540-548 
    Details
    ISSN: 1573-675X
    Keywords: Apoptosis ; bcl-2 ; cisplatin resistance ; p53
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology , Medicine
    Notes: Abstract Since apoptosis is the primary mode of cell death induced by cisplatin, the role of apoptosis and apoptosis-related gene products in cisplatin resistance was investigated in four human cisplatin-resistant cell lines of different tumour type. A common feature of the resistant sublines was a reduced susceptibility to drug-induced apoptosis compared to parental sensitive lines. Loss of wild-type p53 function was not a general event associated with the development of drug resistance. An increased bcl-2 expression was found in resistant cells characterized by mutant p53 (A431/Pt and IGROV-1/Pt), whereas in osteosarcoma (U2-OS/Pt) and in ovarian carcinoma (A2780/CP) cells with wild-type p53, bcl-2 levels were markedly reduced. U2-OS/Pt cells had a 16-fold increase in the level of Bcl-xL protein. Stable transfection of U2-OS cells with bcl-xL cDNA conferred a low level of drug resistance to cisplatin, suggesting that overexpression of this gene contributes to the ci splatin-resistant phenotype of this osteosarcoma cell system. In conclusion, these observations suggest a variable contribution of apoptosis-related genes to cisplatin resistance depending on the biological background of the cell system and presumably reflecting different pathways of apoptosis.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1023/A:1026442716000
    Location Call Number Expected Availability
    BibTip Others were also interested in ...
    Paper (German National Licenses)
    Fulltext
  • 22
    Electronic Resource
    Electronic Resource
    A C-terminal domain of HIV-1 accessory protein Vpr is involved in penetration, mitochondrial dysfunction and apoptosis of human CD4+ lymphocytes (1997)
    Springer
    Apoptosis 2 (1997), S. 69-76 
    Details
    ISSN: 1573-675X
    Keywords: Apoptosis ; CD4+ lymphocytes ; cell penetration ; HIV-1 ; mitochondrial dysfunction ; Vpr
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology , Medicine
    Notes: Abstract We have previously shown that expression of HIV-1 vpr in yeast results in cell growth arrest and structural defects, and identified a C-terminal domain of Vpr as being responsible for these effects in yeast.1 In this report we show that recombinant Vpr and C-terminal peptides of Vpr containing the conserved sequence HFRIGCRHSRIG caused permeabilization of CD4+ T lymphocytes, a dramatic reduction of mitochondrial membrane potential and finally cell death. Vpr and Vpr peptides containing the conserved sequence rapidly penetrated cells, co-localized with the DNA, and caused increased granularity and formation of dense apoptotic bodies. The above results suggest that Vpr treated cells undergo apoptosis and this was confirmed by demonstration of DNA fragmentation by the highly sensitive TUNEL assay. Our results, together with the demonstration of extracellular Vpr in HIV infected individuals,2,3 suggest the possibility that extracellular Vpr could contribute to the apoptotic death and depletion of bystander cells in lymphoid tissues4,5 during HIV infection.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1023/A:1026487609215
    Location Call Number Expected Availability
    BibTip Others were also interested in ...
    Paper (German National Licenses)
    Fulltext
  • 23
    Electronic Resource
    Electronic Resource
    The restrictive proteolysis of α-fodrin to a 120 kDa fragment is not catalyzed by calpains during thymic apoptosis (1997)
    Springer
    Apoptosis 2 (1997), S. 84-90 
    Details
    ISSN: 1573-675X
    Keywords: Apoptosis ; α-fodrin ; calpain ; thymocytes ; x-irradiation
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology , Medicine
    Notes: Abstract The α-subunit (240 kDa) of fodrin was found to be digested selectively to a 120 kDa fragment during apoptosis of rat thymocytes in vivo and in vitro. This fragment was detected by an antibody (Ab) against full length α-fodrin, but not by the anti-N-terminal sequence (GMMPR) of the μ-calpain-generated 150 kDa fragment Ab or the anti-PEST sequence of α-fodrin Ab. On the other hand, basal levels of the 150 kDa fragment were constantly recognized by these three antibodies during apoptosis. The production of the 120 kDa fragment during apoptosis was not affected by the addition of calpain inhibitors such as Ac-LLLnal and E-64d, despite inhibition of the generation of the 150 kDa fragment. When x-irradiated thymocytes were incubated in the presence of N-tosyl-L-phenylalanyl chloromethyl ketone (TPCK), both production of the 120 kDa fragment and apoptosis were suppressed. Purified μ- and m-calpain did not catalyze the formation of the 120 kDa fragment from purified α-fodrin in vitro. These results suggest that a protease different from calpains is involved in the major process of α-fodrin proteolysis to a 120 kDa fragment during thymic apoptosis.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1023/A:1026443926962
    Location Call Number Expected Availability
    BibTip Others were also interested in ...
    Paper (German National Licenses)
    Fulltext
  • 24
    Electronic Resource
    Electronic Resource
    Activation of a CPP32-like protease during L1210 cell apoptosis induced by thiol deprivation (1997)
    Springer
    Apoptosis 2 (1997), S. 77-83 
    Details
    ISSN: 1573-675X
    Keywords: Apoptosis ; bcl-2 ; CPP32 ; thiol
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology , Medicine
    Notes: Abstract Reduced thiols (e.g., cysteine) are important in the maintenance of lymphocyte cell viability and growth. L1210 monocytic leukaemia cells were known to have a limited ability to uptake cystine, and they require cysteine for cell growth. L1210 cells underwent apoptosis when cultured without thiol-bearing and dithiol-cleaving compounds, adding thiols suppressed the apoptosis and promoted cell growth. A specific inhibitor of interleukin-1 β-converting enzyme (ICE)-like and CPP32-like proteases could suppress L1210 cell apoptosis induced by thiol deprivation. The cell lysates of apoptotic L1210 cells exhibited protease activity that could cleave DEVD-AMC, but not YVAD-AMC, and so CPP32-like proteases, but not ICE-like proteases, were activated and participated in apoptosis. The addition of thiols could suppress CPP32-like protease activation. Although the cell death-suppressor bcl-2-family proteins (bcl-2 and bcl-XL) were recently found to suppress the activation of CPP32-like proteases, the expression levels of death-suppressor bcl-2-family proteins did not change when thiols were added. These results suggest that reduced thiols maintain L1210 cell survival by inhibiting the activation of CPP32-like proteases without changing the anti-apoptotic bcl-2-family protein expression.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1023/A:1026491810123
    Location Call Number Expected Availability
    BibTip Others were also interested in ...
    Paper (German National Licenses)
    Fulltext
  • 25
    Electronic Resource
    Electronic Resource
    Cytokeratin-19 associated with apoptosis and chemosensitivity in human cervical cancer cells (1997)
    Springer
    Apoptosis 2 (1997), S. 101-105 
    Details
    ISSN: 1573-675X
    Keywords: Apoptosis ; cytokeratin ; drug resistance
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology , Medicine
    Notes: Abstract Cytokeratins are one group of intermediate filament proteins responsible for the integrity of cell structure, and have been recently reported to play a role in conferring a drug resistance phenotype. MAb Cx-99 is a monoclonal antibody exhibiting the specificity toward its corresponding antigen which was recently identified as the cytokeratin-19 protein. In the present study, we found that the level of cytokeratin-19 in cervical cancer cells could be decreased by incubation of cancer cells with MAb Cx-99. The reduction of cytokeratin-19 level had a killing effect on cervical carcinoma SIHA and HeLa S3 cell lines. The DNA ladder pattern, convoluted nuclei and blebbing morphology were observed with these cells after exposure to MAb Cx-99 for 72 h, suggesting that the cytotoxic mechanism of reduced cytokeratin-19 was mediated by induction of apoptosis. Moreover, the MAb Cx-99 treatment could increase the cytotoxicities of cancer chemotherapeutic agents such as cisplatin and vinblastine to both cervical carcinoma cell lines. The LD80 values were at least 15-fold reduced when cancer cells were treated with cisplatin or vinblastine in the presence of MAb Cx-99. These results suggest that the functional role of cytokeratin-19 was associated with the apoptosis prevention and drug resistance of cervical cancer cells.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1023/A:1026448027870
    Location Call Number Expected Availability
    BibTip Others were also interested in ...
    Paper (German National Licenses)
    Fulltext
  • 26
    Electronic Resource
    Electronic Resource
    Evidence for an interleukin-1β converting enzyme (ICE)-like activity distinct from ICE and responsible for ICE and CPP32 cleavage during apoptosis (1997)
    Springer
    Apoptosis 2 (1997), S. 125-135 
    Details
    ISSN: 1573-675X
    Keywords: Apoptosis ; CPP32 ; ICE ; ICE inhibitors ; ICE-related protease
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology , Medicine
    Notes: Abstract IL-1β converting enzyme (ICE) and ICE-related proteases (IRPs) have been suggested to play a central role in apoptosis. We report the use of peptidic ICE inhibitors to reassess the role of this enzyme in the apoptosis induced by Fas or TNFα receptor ligation in Jurkat cells, U937 cells or monocytes. Our results show that inhibition of IL-1β processing can be dissociated from inhibition of apoptosis. Indeed, two out of three com-pounds active on ICE are not inhibitory for apoptosis. This shows that ICE is not required for progression in the apoptotic pathway, but that one or several IRPs are necessary. In addition, Western blot analysis of cell lysates shows that both ICE and CPP32 precursors disappear rapidly after apoptosis induction, while ICH-1L precursor remains intact. Concomitant appearance of cleavage products can be visualized for CPP32, but not for ICE, suggesting that the former is proteolytically activated. In addition, this precursor cleavage can be blocked by an ICE inhibitor active on apoptosis. Altogether, our data support the hypothesis that one or several IRPs are necessary for apoptosis and are responsible for ICE and CPP32 cleavage during this process.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1023/A:1026404212849
    Location Call Number Expected Availability
    BibTip Others were also interested in ...
    Paper (German National Licenses)
    Fulltext
  • 27
    Electronic Resource
    Electronic Resource
    The proto-oncogene Bcl-2 inhibits cellular toxicity of dopamine: possible implications for Parkinson's Disease (1997)
    Springer
    Apoptosis 2 (1997), S. 149-155 
    Details
    ISSN: 1573-675X
    Keywords: Apoptosis ; bcl-2 ; dopamine ; Parkinson's disease ; PC-12 ; proto-oncogene
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology , Medicine
    Notes: Abstract It is currently believed that excessive oxidant stress induced by metabolism of dopamine (DA), plays a major role in the pathogenesis of the selective nigrostriatal neuronal loss in Parkinson's disease. We recently showed that the neurotransmitter DA, in physiological concentrations, is capable of initiating apoptosis in cultured, post-mitotic sympathetic neurons. Bcl-2 is a proto-oncogene that blocks apoptosis. We now report that Bcl-2 is a powerful inhibitor of DA toxicity in PC-12 pheochromocytoma cells. We induced stable expression of Bcl-2 in PC-12 cells by transfection with recombinant pCMV5 expression vector, containing mouse bcl-2 (coding-sequence) cDNA. Cells expressing Bcl-2 manifested marked resistance to otherwise lethal (300 uM) in vitroconcentrations of DA. This protective effect was reflected in the trypan-blue test of cell survival, 3 H-thymidine incorporation and inhibition of the characteristic apoptotic morphologic alterations in scanning electron microscopic studies. Bcl-2 and associated control systems of apoptosis may have an important physiological role in restraining the apop-tosis-triggering potential of DA in nigrostriatal neurons. This novel field of research may yield insights into the pathogenesis of Parkinson's disease and lead to development of novel therapeutic approaches.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1023/A:1026408313758
    Location Call Number Expected Availability
    BibTip Others were also interested in ...
    Paper (German National Licenses)
    Fulltext
  • 28
    Electronic Resource
    Electronic Resource
    Superoxide, nitric oxide, peroxynitrite and cytokine combinations all cause functional impairment and morphological changes in rat islets of Langerhans and insulin secreting cell lines, but dictate cell death by different mechanisms (1997)
    Springer
    Apoptosis 2 (1997), S. 164-177 
    Details
    ISSN: 1573-675X
    Keywords: Apoptosis ; beta cells ; cytokines ; Islets of Langerhans ; nitric oxide ; peroxynitrite ; superoxide
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology , Medicine
    Notes: Abstract We have shown that nitric oxide treatment for 30–90 min causes inhibition of insulin secretion, DNA damage and disturbs sub-cellular organization in rat and human islets of Langerhans and HIT-T15 cells. Here rat islets and beta-cell lines were treated with various free radical generating systems S-nitrosoglutathione (nitric oxide), xanthine oxidase plus hypoxanthine (reactive oxygen species), 3-morpholinosydnonimine (nitric oxide, super-oxide, peroxynitrite, hydrogen peroxide) and peroxynitrite and their effects over 4 h to 3 days compared with those of the cytokine combination interleukin-1β, tumour necrosis factor-α and interferon-γ. End points examined were de novo protein synthesis, cellular reducing capacity, morphological changes and apoptosis by acridine orange cytochemistry, DNA gel electrophoresis and electron microscopy. Treatment (24–72 h) with nitric oxide, superoxide, peroxynitrite or combined cytokines differentially decreased redox function and inhibited protein synthesis in rat islets of Langerhans and in insulin-containing cell lines; cytokine effects were arginine and nitric oxide dependent. Peroxynitrite gave rare apoptosis in HIT-T15 cells and superoxide gave none in any cell type, but caused the most beta cell-specific damage in islets. S-nitroso-glutathione was the most effective agent at causing DNA laddering or chromatin margination characteristic of apoptotic cell death in insulin-containing cells. Cytokine-induced apoptosis was observed specifically in islet beta cells, combined cytokine effects on islet function and death most resembled those of the mixed radical donor SIN-1.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1023/A:1026412414666
    Location Call Number Expected Availability
    BibTip Others were also interested in ...
    Paper (German National Licenses)
    Fulltext
  • 29
    Electronic Resource
    Electronic Resource
    Spontaneous death of isolated adult rat cardiocytes in culture in association with internucleosomal cleavage of genomic DNA (1997)
    Springer
    Apoptosis 2 (1997), S. 178-188 
    Details
    ISSN: 1573-675X
    Keywords: Apoptosis ; enzyme immunoassay ; gel electrophoresis ; growth factor ; immunohistochemistry
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology , Medicine
    Notes: Abstract Many isolated adult cardiocytes do not survive beyond the early days of culture, but why they die has not been defined. We examined the possibility of apoptosis as the mechanism of death in cultured atrial and ventricular rat cardiocytes. Calcium-tolerant cardiocytes isolated by enzymatic dissociation were cultured with a medium containing FBS. Nucleosomal DNA fragmentation was detected by electrophoresis of DNA extracted from the cardiocytes, by immunohistochemical in situ DNA nick-end labelling of single cells, and by enzyme immunoassay for in vitro quantification in cytoplasmic fraction. Electrophoresis on the 5th to 14th day of culture revealed the ladder appearance characteristic of internucleosomal DNA cleavage in apoptosis with a consistent single peak of increased cytoplasmic DNA fragments. After the 14th day, the cytoplasmic DNA fragments decreased, and the ladder appearance could no longer be detected by electrophoresis. Cardiocytes positive with nick-end labelling were seen by the 5th day, and then increased in number over the remaining days. These results indicate that many isolated cardiocytes die spontaneously by apoptosis within the first 2 weeks of culture, suggesting a possible signal dependence for survival of adult cardiocytes. In addition to chemical signal depletion in culture, other possible explanations for this apoptosis include the absence of an electric signal during culture, lack of contractile activity, and initial loss of intercellular connections.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1023/A:1026464431505
    Location Call Number Expected Availability
    BibTip Others were also interested in ...
    Paper (German National Licenses)
    Fulltext
  • 30
    Electronic Resource
    Electronic Resource
    Radiation-induced apoptosis and its relationship to loss of clonogenic survival (1997)
    Springer
    Apoptosis 2 (1997), S. 265-282 
    Details
    ISSN: 1573-675X
    Keywords: Apoptosis ; cell cycle ; clonogenicity ; p53 ; radiation
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology , Medicine
    Notes: Abstract Ionizing radiation can be an effective inducer of apoptosis and studies of many aspects of the pathways and mechanisms involved in this apoptosis induction have been published. This review stresses two aspects: the relationship between apoptosis and loss of clonogenic ability in irradiated cells and the time course for the appearance of apoptosis after radiation exposure. Although it was initially assumed that apoptosis occurred relatively quickly (within hours) after irradiation, evidence is presented and discussed here showing that apoptosis can occur at long times after irradiation (out to 20 days) in some cell types. This late, or delayed, apoptosis occurs after the cells have divided once or several times. The impact of delayed apoptosis on loss of clonogenicity after irradiation remains unclear. It seems likely that in some cell types, e.g., fibroblasts, the occurrence of late apoptosis is minimal and may have little impact on long term cell survival of the population, but in at least one instance, with a cell line of hematopoietic origin, it appears that late apoptosis can account for all the loss of clonogenicity in irradiated cells. The role of p53 in radiation-induced apoptosis is also discussed, with data presented showing that both p53-dependent and independent pathways for radiation-induced apoptosis exist, depending on the cell type.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1023/A:1026485003280
    Location Call Number Expected Availability
    BibTip Others were also interested in ...
    Paper (German National Licenses)
    Fulltext
  • 31
    Electronic Resource
    Electronic Resource
    Butyrate-induced reversal of dexamethasone resistance in autonomous rat Nb2 lymphoma cells (1997)
    Springer
    Apoptosis 2 (1997), S. 518-528 
    Details
    ISSN: 1573-675X
    Keywords: Apoptosis ; Bcl-2 ; dexamethasone ; Nb2 lymphoma ; Pim-1 ; prolactin
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology , Medicine
    Notes: Abstract The parental rat Nb2 lymphoma is a prolactin (PRL)-dependent T cell line. Exposure of a PRL-independent subline, Nb2-SFJCD1, to sodium butyrate (NaBT) causes transient reversal of their growth factor-independent proliferation in association with constitutive expression of protooncogenes pim-1and c-myc. In the present study, we investigated the effect of NaBT treatment on the sensitivity of Nb2-SFJCD1 cells to dexamethasone (DEX)-induced apoptosis. Pretreatment with NaBT (2 mM, 72 h) partially reversed resistance to apoptosis in Nb2-SFJCD1 cells exposed to DEX (100 nM) for 12 h, assessed by flow cytometric analyses of DNA fragmentation. However, the cytolytic effect of DEX was abrogated by PRL i n a time- and concentration-dependent manner. Eval uati on of apoptosis-associated gene expression in NaBT-pre-treated cultures incubated with DEX or DEX+PRL indicated that the apoptosis resistance did not stem from altered bcl-2 or bax expression. However, there was a strong correlation between the resistance to DEX-activated apoptosis and their enhanced expression of pim-1 mRNA and protein. The results show that it is possible to reverse DEX-induced apoptosis of Nb2 pre-T cells and suggest the pim-1 gene product has an important role as a suppressor of this process, perhaps functioning as a mediator of PRL action.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1023/A:1026438615092
    Location Call Number Expected Availability
    BibTip Others were also interested in ...
    Paper (German National Licenses)
    Fulltext
  • 32
    Electronic Resource
    Electronic Resource
    Accumulation of major stress protein 70kDa protects myeloid and lymphoid cells from death by apoptosis (1997)
    Springer
    Apoptosis 2 (1997), S. 156-163 
    Details
    ISSN: 1573-675X
    Keywords: Apoptosis ; hsp70 ; liposomes ; quercetin
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology , Medicine
    Notes: Abstract The major heat shock protein, hsp70, is known to contribute to the mechanisms of cell protection against a variety of stress and cytotoxic factors, providing an increase of cell survival. Whether hsp70 could be implicated in the rescue of cells from stress-induced death proceeding on apoptotic pathway is not well established. Here we report that susceptibility of myeloid and lymphoid cell lines to apoptosis induced by heat shock or ethanol coincides with hsp70 content and can be modulated by changes in expression of this protein. Cells of lymphoid and myeloid lines differing in basal and inducible level of the protein were tested. The cells containing higher amounts of hsp70 (U937, Jurkat, Molt4) were more resistant to the apoptosis-inducing stimuli then cells which accumu-late lower amounts of the protein (HL60) and especially those lacking the protein (NSO). Inhibition of hsp70 accumulation by quercetin made cells more susceptible to the same apoptotic inducer. Enhancement of hsp70 expression by previous heating or by liposomal delivery of the exogenic protein to the cells lacking hsp70 made them more resistant to apoptosis. The possible mechanisms of the hsp70 protective effect in apoptosis are discussed.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1023/A:1026460330596
    Location Call Number Expected Availability
    BibTip Others were also interested in ...
    Paper (German National Licenses)
    Fulltext
  • 33
    Electronic Resource
    Electronic Resource
    Human keratinocytes maintain reversible anti-apoptotic defenses in vivo and in vitro (1997)
    Springer
    Apoptosis 2 (1997), S. 136-148 
    Details
    ISSN: 1573-675X
    Keywords: Apoptosis ; bcl-2 ; keratinocytes ; proto-oncogene ; ultraviolet radiation
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology , Medicine
    Notes: Abstract Human keratinocytes proliferate and differentiate in an epidermal environment where induction of apoptosis can be triggered by ultraviolet radiation (UVR), activated lymphocytes and cytokines. The purpose of this study was to determine whether keratinocytes were susceptible to apoptosis induced by ionophore, ultra-violet radiation, cytokines or crosslinking of CD95 (Fas/APO-1). In normal human skin exposed to two minimal erythema doses of ultraviolet radiation, suprabasal cells were the first keratinocytes to demonstrate apoptotic nuclei, and by 48 h apoptotic cells were identified throughout the mid to upper epidermis. However, most keratinocytes resisted apoptosis and UVR-induced apoptosis was not observed in basal cells, or in the most differentiated epidermis. Human keratinocytes and keratinocyte cell lines cultured in vitro developed maximal apoptosis 48 h after radiation. Human keratinocytes cultured in full growth factor supplements were resistant to UVR-induced apoptosis compared to keratinocyte cell lines or to a lymphoid cell line (HL60) susceptible to apoptosis. Keratinocyte cell lines were completely resistant to apoptosis induced by interferon-γ, interferon-α, IL-2, IL-6, TNF-α, IL-1Ra, and GM-CSF. A subset of the cells in cultures of keratinocytes and transformed keratinocyte cell lines died by apoptosis in response to anti-Fas, IL-1α and TNF-α plus IFN-γ and ionophore. Second passage freshly isolated human keratinocytes were much more resistant to apoptosis induced by ionophore, anti-Fas and cytokines than were transformed keratinocyte cell lines. Calcium shift to induce differentiation in second-passage keratinocyte cultures made keratino-cytes even more resistant to UVR-induced apoptosis. This parallels the lack of UVR-induced apoptosis observed in the most differentiated keratinocytes in irradiated human skin. Both keratinocytes and kerati-nocyte cell lines express rather low levels of the anti-apoptotic proteins bcl-2 and bcl-x compared to other apoptosis-resistant cell types. The differences between keratinocytes and keratinocyte cell lines in suscepti-bility to apoptosis are not explained by difference in expression of bcl-2 or bcl-x. Finally, withdrawal of growth factors from keratinocytes decreased cell survival following UVR and increased the induction of apoptosis. Inhibition of protein synthesis with cyclo-heximide also made keratinocytes more susceptible to UVR-induced apoptosis, indicating that anti-apop-totic defences in cultured keratinocytes are dependent on active protein synthesis. These experiments show that the strong keratinocyte defences against apoptosis are stratified within the epidermis, and can be altered by differentiation and growth factor withdrawal.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1023/A:1026456229688
    Location Call Number Expected Availability
    BibTip Others were also interested in ...
    Paper (German National Licenses)
    Fulltext
  • 34
    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
    Location Call Number Expected Availability
    BibTip Others were also interested in ...
    Paper (German National Licenses)
    Fulltext
  • 35
    Electronic Resource
    Electronic Resource
    Intraepithelial lymphocytes vs. colorectal neoplastic cells: Who is winning the apoptotic battle? (1997)
    Springer
    Apoptosis 2 (1997), S. 489-493 
    Details
    ISSN: 1573-675X
    Keywords: Apoptosis ; intraepithelial lymphocytes ; colorectal adenomas
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology , Medicine
    Notes: Abstract Intraepithelial lymphocytes (IELs) and Intraepithelial apoptotic granules (AGs) are found in the vast majority of colorectal adenomas, less frequently in incipient carcinomas and occasionally in advanced colorectal carcinomas. In colorectal adenomas, the activated and cytotoxic IELs undergo apoptosis by a Fas-FasL mechanism. In advanced invasive carcinomas lacking IELs, that mechanism cannot be activated. On the other hand, the peritumoural lymphocytes which surround some advanced invasive carcinomas may abrogate to-be-metastatic tumor cells, as treated cancer patients with peritumoural lymphocytes have a better 5-years' survival than those without that peritumoural barrier. In colorectal adenomas the host reaction (IELs) dysplastic cells Fas-dependent confrontation seems to prevent rapidly proliferating adenomas from becoming rapidly invasive carcinomas, since that process takes 10 to 20 years to evolve.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1023/A:1026430313275
    Location Call Number Expected Availability
    BibTip Others were also interested in ...
    Paper (German National Licenses)
    Fulltext
  • 36
    Electronic Resource
    Electronic Resource
    Intracellular alkalinization in dexamethasone-induced thymocyte apoptosis (1997)
    Springer
    Apoptosis 2 (1997), S. 304-312 
    Details
    ISSN: 1573-675X
    Keywords: Apoptosis ; intracellular pH ; ion transporter ; thymocytes
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology , Medicine
    Notes: Abstract Glucocorticoid can induce apoptosis of thymocytes, but its mechanism is not clear yet. In this study, we reported that dexamethasone-induced apoptosis was associated with intracellular alkalinization. Dexamethasone induced a higher percentage of apoptosis in 138 mM than in 50 mM NaCl, total abrogation of apoptosis was noted in NaCl-depleted culture medium. Highest apoptotic rate was observed in medium with pH 7.2, whereas it was partially and completely inhibited at pH 6.5 and pH 6.0, respectively. Intracellular pH was higher in pre-apoptotic thymocytes than non-apoptotic ones. The Na+ /H+ antiporter inhibitor of 5-(N,N'-dimethyl)-amiloride inhibited the dexamethasone-induced increase in pHi and apoptosis of thymocytes. Glucocorticoid antagonist RU486 also blocked the dexamethasone-induced effect. Furthermore, the apoptosis and increase in intracellular pH induced by dexamethasone were inhibited by cycloheximide, actinomycin D. It seems that intracellular pH is increased during the development of thymocyte apoptosis and inhibiting its increment would retard the rate of progression to cell death.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1023/A:1026441221027
    Location Call Number Expected Availability
    BibTip Others were also interested in ...
    Paper (German National Licenses)
    Fulltext
  • 37
    Electronic Resource
    Electronic Resource
    The treatment with differentiation- and apoptosis-inducing agent, vesnarinone, of a patient with oral squamous cell carcinoma (1997)
    Springer
    Apoptosis 2 (1997), S. 313-318 
    Details
    ISSN: 1573-675X
    Keywords: Apoptosis ; differentiation ; oral squamous cell carcinoma ; vesnarinone
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology , Medicine
    Notes: Abstract A patient with histopathological recurrent oral cancer with well-differentiated squamous cell carcinoma, was treated with differentiation- and apoptosis-inducing agent, vesnarinone, per os at a dose of 180 mg/day for 56 days and then at a dose of 60 mg/day for 93 days. The vesnarinone administration caused complete remission of the tumour. It has been found by immunohistochemical staining and PCR-SSCP analysis that the recurrent tumour has wild type p53 gene and relative high level of LeY expression as well as DNA fragmentation in the cancer cells, as assessed by nick-end labelling. These findings suggest that the cure of oral squamous cell carcinoma observed in this case might be associated with induction of differentiation and apoptosis of cancer cells by vesnarinone.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1023/A:1026493205097
    Location Call Number Expected Availability
    BibTip Others were also interested in ...
    Paper (German National Licenses)
    Fulltext
  • 38
    Electronic Resource
    Electronic Resource
    Regulation of apoptosis-associated proteins in cell death following transient focal ischemia in rat pups (1997)
    Springer
    Apoptosis 2 (1997), S. 368-376 
    Details
    ISSN: 1573-675X
    Keywords: Apoptosis ; Bax ; Bcl2 ; cerebral neonatal ischemia ; hsp72 ; immunohistochemistry ; p53
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology , Medicine
    Notes: Abstract Apoptosis is a process whereby developmental or environmental stimuli activate a genetic programme to execute a specific series of events that culminate in the death and efficient disposal of a cell. Although a series of recent data suggested that neuronal death following cerebral ischemia occurs through an apoptotic pathway, additional work is needed to establish the existence of a causal relationship between gene expression and DNA breaks in neuronal death. We investigate the role of p53 and Bax proteins in the induction of apoptosis induced by a new transient focal ischemia model in the rat pup. Our results show that wild-type p53 exerts a significant and time-dependent effect in the initiation of apoptosis, and that apoptosis is induced via DNA-strand breakage. Subsequently, increased Bax expression was observed in the cytoplasm of dying cells located in the infarct, whereas an increased Bcl-2 and hsp72 staining was detectable in survival cells and reactive glia present at the periphery of the lesion.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1023/A:1026453623753
    Location Call Number Expected Availability
    BibTip Others were also interested in ...
    Paper (German National Licenses)
    Fulltext
  • 39
    Electronic Resource
    Electronic Resource
    BAG-1 inhibits p53-induced but not apoptin-induced apoptosis (1997)
    Springer
    Apoptosis 2 (1997), S. 395-402 
    Details
    ISSN: 1573-675X
    Keywords: Apoptosis ; apoptin ; BAG-1 ; Bcl-2 ; p53 ; programmed cell death
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology , Medicine
    Notes: Abstract BAG-1 has been identified as a Bcl-2-binding protein that inhibits apoptosis, either alone or in co-operation with Bcl-2. Here we show that BAG-1 inhibits p53- induced apoptosis in the human tumour cell line Saos-2. In contrast, BAG-1 was unable to inhibit the p53-independent pathway induced by apoptin, an apoptosis-inducing protein derived from chicken anaemia virus. Whereas BAG-1 seemed to co-operate with Bcl-2 to repress p53-induced apoptosis, co-expression of these proteins had no inhibitory effect on apoptin-induced apoptosis. Moreover, Bcl-2, and to some extent also BAG-1, paradoxically enhanced the apoptotic activity of apoptin. These results demonstrate that p53 and apoptin induce apoptosis through independent pathways, which are differentially regulated by BAG-1 and Bcl-2.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1023/A:1026409808732
    Location Call Number Expected Availability
    BibTip Others were also interested in ...
    Paper (German National Licenses)
    Fulltext
  • 40
    Electronic Resource
    Electronic Resource
    Apoptotic myocardial degeneration in thrombotic thrombocytopenic purpura (1997)
    Springer
    Apoptosis 2 (1997), S. 384-394 
    Details
    ISSN: 1573-675X
    Keywords: Apoptosis ; cardiac conduction system ; cardiogenic hypertensive chemoreflex ; myocardial ischemia ; platelets ; thrombotic thrombocytopenic purpura
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology , Medicine
    Notes: Abstract The objective of this study was to determine whether the known myocardial degeneration in TTP is due to apoptosis. In TTP the heart is often involved, including the cardiac conduction system. Despite many platelet occlusions of small coronary arteries, there is little myocardial necrosis. Why the intermittent clinical episodes begin or end is unknown. Six hearts of patients dying with TTP were examined with routine and immunohistochemical stains. In addition to ventricular and atrial myocardium we examined the cardiac conduction system and coronary chemoreceptor. Numerous small coronary arteries were occluded with platelet thrombi in all these sites, including especially the sinus node, AV node and His bundle. The myocardial degeneration we found was conspicuously devoid of inflammation and the myocytes were relatively intact. These characteristics combined with TUNEL-positivity in the degenerating cells are typical of apoptosis. The focal degeneration in TTP is primarily apoptotic. Because circulating serotonin is carried by platelets and is released during aggregation, and because serotonin can cause a powerful cardiogenic hypertensive chemoreflex, we suggest that such a response may dislodge early platelet aggregations. Lessons from TTP may have special relevance for better understanding of myocardial reperfusion problems associated with angioplasty, thrombolysis and ischemic preconditioning.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1023/A:1026457724661
    Location Call Number Expected Availability
    BibTip Others were also interested in ...
    Paper (German National Licenses)
    Fulltext
  • 41
    Electronic Resource
    Electronic Resource
    Oestradiol inhibits spontaneous and cisplatin-induced apoptosis in epithelial ovarian cancer cells: relationship to DNA repair capacity (1997)
    Springer
    Apoptosis 2 (1997), S. 478-484 
    Details
    ISSN: 1573-675X
    Keywords: Apoptosis ; cisplatin ; DNA repair ; epithelial ovarian cancer cells ; oestradiol
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology , Medicine
    Notes: Abstract A prospective role of sex steroid hormones in the pathogenesis of common epithelial ovarian cancer remains equivocal. We hypothesized that oestradiol can protect ovarian cells from apoptosis by augmenting their DNA repair capacity. Two established oestrogen receptor-positive human cancer cell lines of ovarian surface epithelial origin (OVCAR-3, SKOV-3) were studied during short-term (24 h) subculture in the absence or presence of oestradiol-17β and/or the DNA-damaging chemotherapeutic agent cisplatin. Apoptosis was monitored among individual cells by in situ DNA fragmentation analysis. Basal rates of apoptosis were diminished by exposure to oestradiol (progesterone or testosterone were without effect). Oestradiol also suppressed apoptosis induced by cisplatin and enhanced the repair of a cisplatin-damaged reporter chloramphenicol-O-acetyltransferase gene transfected into ovarian cells. The ability of oestrogen-responsive ovarian cancer cells to efficiently repair DNA and thereby avoid apoptosis may be related to propensity for clonal expansion and drug resistance.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1023/A:1026426212366
    Location Call Number Expected Availability
    BibTip Others were also interested in ...
    Paper (German National Licenses)
    Fulltext
  • 42
    Electronic Resource
    Electronic Resource
    Role of XIAP protein, a human member of the inhibitor of apoptosis (IAP) protein family, in phytohemagglutinin-induced apoptosis of human T cell lines (1997)
    Springer
    Apoptosis 2 (1997), S. 501-509 
    Details
    ISSN: 1573-675X
    Keywords: Apoptosis ; human T cells ; signal transduction
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology , Medicine
    Notes: Abstract A new family of human genes xiap, hiap-1 and hiap-2, which are homologous to the baculovirus iap (inhibitor of apoptosis) genes cp-iap and op-iap, has been recently cloned and shown to suppress apoptosis after serum withdrawal or exposure to a free radical inducer. In order to examine the role of one of these human genes, namely xiap, in lymphoid cells, we studied XIAP expression, after PHA stimulation in three different human T cell lines. We report here that stimulation with PHA resulted in the human T cell lines undergoing apoptosis, as assessed by DNA fragmentation and by propidiumiodide (PI) staining and flow cytometry. When XIAP protein expression was evaluated by Western blot, we observed that the induction of apoptosis by PHA was associated with a parallel decrease of XIAP expression. We also provide evidence that stably transfected Jurkat cells containing the xiap open reading frame became resistant to PHA-induced apoptosis. These data suggest a role for XIAP protein in the regulation of apoptosis in lymphoid cells.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1023/A:1026434514183
    Location Call Number Expected Availability
    BibTip Others were also interested in ...
    Paper (German National Licenses)
    Fulltext
  • 43
    Electronic Resource
    Electronic Resource
    Inhibition of protein synthesis sensitizes thermotolerant cells to heat shock induced apoptosis (1997)
    Springer
    Apoptosis 2 (1997), S. 510-517 
    Details
    ISSN: 1573-675X
    Keywords: Apoptosis ; comet assay ; hyperthermia ; thermotolerance
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology , Medicine
    Notes: Abstract Hyperthermia is a potent inducer of apoptosis in many cell lines. A brief exposure to mildly elevated temperatures elicits a transient state of augmented resistance to subsequent thermal stress. Here we show that a hyperthermic treatment of 43°C for 1 h is sufficient to induce apoptosis in the cell line HL-60. This observation is based on morphologic evaluation and on comet assay results (an extremely sensitive method of detecting and quantifying apoptotic DNA fragmentation in individual cells). The thermotolerance phenomenon was also verified in the same manner by giving the cells a brief 30 min sub-lethal heat conditioning treatment at 43°C followed by a 6 h incubation time prior to the administration of a lethal heat load (43°C for 1 h). We observed a dramatic decrease in resultant apoptoses in the thermotolerized cells in comparison to unconditioned cells. We assessed the necessity of de novo protein synthesis in the protective phenomenon. When the conditioned cells were given a cycloheximide treatment prior to heat conditioning we saw a sensitization of the conditioned cells to secondary thermal injury.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1023/A:1026486531021
    Location Call Number Expected Availability
    BibTip Others were also interested in ...
    Paper (German National Licenses)
    Fulltext
  • 44
    Electronic Resource
    Electronic Resource
    Apoptosis Dependent Decrease of the Intramembrane Ion Traffic in Cultured Mouse Fibroblasts Shown by Conductivity Dispersion (1997)
    Springer
    Bioscience reports 17 (1997), S. 547-556 
    Details
    ISSN: 1573-4935
    Keywords: Apoptosis ; conductivity ; dielectric ; fibroblast
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology , Chemistry and Pharmacology
    Notes: Abstract We have investigated the intramembranal ion traffic in apoptotic 3T6 cells in culture. Apoptosis was induced by various treatments, such as serum deprivation, high density growth and hydrogen peroxide at subnecrotic doses. Cell death was assessed by nucleosomal DNA fragmentation, single cell electrophoresis, immunofluorescence and histological staining. To study the modifications of membrane structure and function, we adopted a well established biophysical strategy based on the measurement of the electrical conductivity of cell suspensions, as a function of the frequency of the electrical field applied to the sample. A comparison between the conductivity of normal and apoptotic cell suspensions shows that programmed cell death causes a decrease of membrane conductivity which indicates a diminished intramembranal ion traffic. Our results strongly suggest that one of the early events in the triggering of apoptosis is represented by an overall reduction of plasma membrane function. Finally, our results are in agreement with the idea that the nucleus is not the sole target of the apoptotic process.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1023/A:1027364308147
    Location Call Number Expected Availability
    BibTip Others were also interested in ...
    Paper (German National Licenses)
    Fulltext
  • 45
    Electronic Resource
    Electronic Resource
    Induction of apoptosis by protein kinase C pseudosubstrate lipopeptides in several human cells (1997)
    Springer
    International journal of peptide research and therapeutics 4 (1997), S. 397-402 
    Details
    ISSN: 1573-3904
    Keywords: Apoptosis ; Protein kinase C ; Pseudosubstrate sequence ; Lipopeptide
    Source: Springer Online Journal Archives 1860-2000
    Topics: Chemistry and Pharmacology
    Notes: Abstract Intracellular enzymes or receptors are interesting targets for thepharmacomodulation of cellular metabolism. We have previously shown thatmodification of relatively long peptides by a palmitoyl-lysine residue couldfacilitate their delivery into the cytoplasm of living cells. Severalpeptides containing pseudosubstrate sequences of protein kinase C (PKC) havebeen evaluated for their ability to modulate phosphorylation of modelsubstrate, neuronal morphology or tumor necrosis factor secretion. In thiswork we have evaluated the effect of palmitoyl-modified PKC-pseudosubstratepeptides on induction of apoptosis. We have established that these peptidesare able to induce apoptosis in different human cell types (primaryfibroblasts, T- and B-lymphocyte cell lines) as assessed by (terminal deoxynucleotidyl transferase dUTP nick-end labelling) and DNAfragmentation. In contrast, control peptides (non-lipidicPKC-pseudosubstrate peptides and irrelevant lipopeptides) had no or littleeffect on programmed cell death. This work highlights the pharmacologicalinterest of lipopeptides and argues in favor of the potential role of PKC(s)in the cell death machinery.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1023/A:1008833929317
    Location Call Number Expected Availability
    BibTip Others were also interested in ...
    Paper (German National Licenses)
    Fulltext
  • 46
    Electronic Resource
    Electronic Resource
    Induction of apoptosis by protein kinase C pseudosubstrate lipopeptides in several human cells (1997)
    Springer
    International journal of peptide research and therapeutics 4 (1997), S. 397-402 
    Details
    ISSN: 1573-3904
    Keywords: Apoptosis ; Protein kinase C ; Pseudosubstrate sequence ; Lipopeptide
    Source: Springer Online Journal Archives 1860-2000
    Topics: Chemistry and Pharmacology
    Notes: Summary Intracellular enzymes or receptors are interesting targets for the pharmacomodulation of cellular metabolism. We have previously shown that modification of relatively long peptides by a palmitoyl-lysine residue could facilitate their delivery into the cytoplasm of living cells. Several peptides containing pseudosubstrate sequences of protein kinase C (PKC) have been evaluated for their ability to modulate phosphorylation of model substrate, neuronal morphology or tumor necrosis factor secretion. In this work we have evaluated the effect of palmitoyl-modified PKC-pseudosubstrate peptides on induction of apoptosis. We have established that these peptides are able to induce apoptosis in different human cell types (primary fibroblasts, T- and B-lymphocyte cell lines) as assessed by (terminal deoxynucleotidyl transferase dUTP nick-end labelling) and DNA fragmentation. In contrast, control peptides (non-lipidic PKC-pseudosubstrate peptides and irrelevant lipopeptides) had no or little effect on programmed cell death. This work highlights the pharmacological interest of lipopeptides and argues in favor of the potential role of PKC(s) in the cell death machinery.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF02442906
    Location Call Number Expected Availability
    BibTip Others were also interested in ...
    Paper (German National Licenses)
    Fulltext
  • 47
    facet.materialart.
    Unknown
    Oncogenic transcription factors in the human acute leukemias (1997)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1997-11-14
    Description: Chromosomal translocations in the human acute leukemias rearrange the regulatory and coding regions of a variety of transcription factor genes. The resultant protein products can interfere with regulatory cascades that control the growth, differentiation, and survival of normal blood cell precursors. Support for this interpretation comes from the results of gene manipulation studies in mice, as well as the sequence homology of oncogenic transcription factors with proteins known to regulate embryonic development in primitive organisms, including the nematode Caenorhabditis elegans and the fruit fly Drosophila melanogaster. Many of these genetic alterations have important prognostic implications that can guide the selection of therapy. The insights gained from studies of translocation-generated oncogenes and their protein products should hasten the development of highly specific, and hence less toxic, forms of leukemia therapy.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Look, A T -- CA-20180/CA/NCI NIH HHS/ -- CA-21765/CA/NCI NIH HHS/ -- CA-59571/CA/NCI NIH HHS/ -- New York, N.Y. -- Science. 1997 Nov 7;278(5340):1059-64.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Experimental Oncology, St. Jude Children's Research Hospital, Memphis, TN 38105, USA. 38163, USA. thomas.look@stjude.org〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9353180" target="_blank"〉PubMed〈/a〉
    Keywords: Acute Disease ; Animals ; Apoptosis ; Cell Transformation, Neoplastic ; *Gene Expression Regulation, Leukemic ; Genes, Homeobox ; Humans ; Leukemia, Myeloid/*genetics/pathology/therapy ; Precursor Cell Lymphoblastic Leukemia-Lymphoma/*genetics/pathology/therapy ; Prognosis ; Transcription Factors/*genetics ; *Translocation, Genetic
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
    Published by American Association for the Advancement of Science (AAAS)
    Location Call Number Expected Availability
    BibTip Others were also interested in ...
    PAPER CURRENT
  • 48
    facet.materialart.
    Unknown
    Exploitation of mammalian host cell functions by bacterial pathogens (1997)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1997-05-02
    Description: Interest in bacterial pathogenesis has recently increased because of antibiotic resistance, the emergence of new pathogens and the resurgence of old ones, and the lack of effective therapeutics. The molecular and cellular mechanisms of microbial pathogenesis are currently being defined, with precise knowledge of both the common strategies used by multiple pathogenic bacteria and the unique tactics evolved by individual species to help establish infection. What is emerging is a new appreciation of how bacterial pathogens interact with host cells. Many host cell functions, including signal transduction pathways, cytoskeletal rearrangements, and vacuolar trafficking, are exploited, and these are the focus of this review. A bonus of this work is that bacterial virulence factors are providing new tools to study various aspects of mammalian cell functions, in addition to mechanisms of bacterial disease. Together these developments may lead to new therapeutic strategies.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Finlay, B B -- Cossart, P -- New York, N.Y. -- Science. 1997 May 2;276(5313):718-25.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Biotechnology Laboratory, University of British Columbia, Vancouver, B.C., Canada, V6T-1Z3. bfinlay@unixg.ubc.ca〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9115192" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Apoptosis ; Bacteria/genetics/*pathogenicity ; *Bacterial Adhesion ; Bacterial Infections/*microbiology ; Bacterial Physiological Phenomena ; Bacterial Toxins/toxicity ; Cells, Cultured ; Cytoskeleton/physiology ; Epithelial Cells ; Epithelium/microbiology ; Humans ; Phagocytosis ; Signal Transduction ; Vacuoles/microbiology ; Virulence/genetics
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
    Published by American Association for the Advancement of Science (AAAS)
    Location Call Number Expected Availability
    BibTip Others were also interested in ...
    PAPER CURRENT
  • 49
    facet.materialart.
    Unknown
    Immune response and myoblasts that express Fas ligand (1997)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1997-12-31
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Kang, S M -- Hoffmann, A -- Le, D -- Springer, M L -- Stock, P G -- Blau, H M -- F32 HL08991/HL/NHLBI NIH HHS/ -- R01-CA59717/CA/NCI NIH HHS/ -- R01-HD18179/HD/NICHD NIH HHS/ -- etc. -- New York, N.Y. -- Science. 1997 Nov 14;278(5341):1322-4.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9411754" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Antigens, CD95/biosynthesis ; Apoptosis ; Cell Differentiation ; Cell Transplantation ; Fas Ligand Protein ; *Graft Rejection ; Immune Tolerance ; Islets of Langerhans/cytology ; *Islets of Langerhans Transplantation ; Membrane Glycoproteins/genetics/*physiology ; Mice ; Mice, Inbred C3H ; Mice, Inbred C57BL ; Muscle Fibers, Skeletal/*cytology/metabolism ; Muscle, Skeletal/*cytology/metabolism ; Neutrophils/*immunology ; Transfection
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
    Published by American Association for the Advancement of Science (AAAS)
    Location Call Number Expected Availability
    BibTip Others were also interested in ...
    PAPER CURRENT
  • 50
    facet.materialart.
    Unknown
    Lymphocyte survival: a red queen hypothesis (1997)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1997-10-23
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Freitas, A A -- Rocha, B -- New York, N.Y. -- Science. 1997 Sep 26;277(5334):1950.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Laboratoire des Dynamiques Lymphocytaires, Institut Pasteur CNRS URA 1961, 75015 Paris, France. afreitas@pasteur.fr〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9333949" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Apoptosis ; CD8-Positive T-Lymphocytes/cytology/immunology ; Cell Survival ; Histocompatibility Antigens Class I/physiology ; Histocompatibility Antigens Class II/physiology ; Immunologic Memory ; Kruppel-Like Transcription Factors ; Lymphocyte Activation ; Mice ; T-Lymphocytes/*cytology/*immunology/metabolism ; Trans-Activators/*physiology ; Zinc Fingers
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
    Published by American Association for the Advancement of Science (AAAS)
    Location Call Number Expected Availability
    BibTip Others were also interested in ...
    PAPER CURRENT
  • 51
    facet.materialart.
    Unknown
    Signaling vascular morphogenesis and maintenance (1997)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1997-07-04
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Hanahan, D -- New York, N.Y. -- Science. 1997 Jul 4;277(5322):48-50.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Biochemistry, University of California at San Francisco, San Francisco, CA 94143-0534, USA. dougvhanahan@biochem.ucsf.edu〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9229772" target="_blank"〉PubMed〈/a〉
    Keywords: Angiopoietin-1 ; Angiopoietin-2 ; Animals ; Apoptosis ; Blood Vessels/*embryology/growth & development/metabolism ; Cell Division ; Endothelial Growth Factors/metabolism ; Endothelium, Vascular/*cytology/metabolism ; Lymphokines/metabolism ; Membrane Glycoproteins/metabolism ; Mice ; Mice, Knockout ; Morphogenesis ; *Neovascularization, Physiologic ; Phosphorylation ; Proteins/metabolism ; Proto-Oncogene Proteins/metabolism ; Receptor Protein-Tyrosine Kinases/*metabolism ; Receptor, TIE-2 ; Receptors, Growth Factor/metabolism ; Receptors, Vascular Endothelial Growth Factor ; *Signal Transduction ; Vascular Endothelial Growth Factor A ; Vascular Endothelial Growth Factor Receptor-1 ; Vascular Endothelial Growth Factors
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
    Published by American Association for the Advancement of Science (AAAS)
    Location Call Number Expected Availability
    BibTip Others were also interested in ...
    PAPER CURRENT
  • 52
    facet.materialart.
    Unknown
    Somatic frameshift mutations in the BAX gene in colon cancers of the microsatellite mutator phenotype (1997)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1997-02-14
    Description: Cancers of the microsatellite mutator phenotype (MMP) show exaggerated genomic instability at simple repeat sequences. More than 50 percent (21 out of 41) of human MMP+ colon adenocarcinomas examined were found to have frameshift mutations in a tract of eight deoxyguanosines [(G)8] within BAX, a gene that promotes apoptosis. These mutations were absent in MMP- tumors and were significantly less frequent in (G)8 repeats from other genes. Frameshift mutations were present in both BAX alleles in some MMP+ colon tumor cell lines and in primary tumors. These results suggest that inactivating BAX mutations are selected for during the progression of colorectal MMP+ tumors and that the wild-type BAX gene plays a suppressor role in a p53-independent pathway for colorectal carcinogenesis.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Rampino, N -- Yamamoto, H -- Ionov, Y -- Li, Y -- Sawai, H -- Reed, J C -- Perucho, M -- CA38579/CA/NCI NIH HHS/ -- CA63585/CA/NCI NIH HHS/ -- New York, N.Y. -- Science. 1997 Feb 14;275(5302):967-9.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉The Burnham Institute, La Jolla Cancer Research Center, 10901 North Torrey Pines Road, La Jolla, CA 92037, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9020077" target="_blank"〉PubMed〈/a〉
    Keywords: Adenocarcinoma/*genetics ; Alleles ; Apoptosis ; Base Sequence ; Colonic Neoplasms/*genetics ; *Frameshift Mutation ; Gene Expression ; *Genes, Tumor Suppressor ; Humans ; Microsatellite Repeats/*genetics ; Molecular Sequence Data ; Mutation ; Phenotype ; Polymerase Chain Reaction ; Proto-Oncogene Proteins/*genetics ; *Proto-Oncogene Proteins c-bcl-2 ; Sequence Deletion ; Tumor Cells, Cultured ; bcl-2-Associated X Protein
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
    Published by American Association for the Advancement of Science (AAAS)
    Location Call Number Expected Availability
    BibTip Others were also interested in ...
    PAPER CURRENT
  • 53
    facet.materialart.
    Unknown
    Interleukin-3-induced phosphorylation of BAD through the protein kinase Akt (1997)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1997-10-24
    Description: BAD is a distant member of the Bcl-2 family that promotes cell death. Phosphorylation of BAD prevents this. BAD phosphorylation induced by interleukin-3 (IL-3) was inhibited by specific inhibitors of phosphoinositide 3-kinase (PI 3-kinase). Akt, a survival-promoting serine-threonine protein kinase, was activated by IL-3 in a PI 3-kinase-dependent manner. Active, but not inactive, forms of Akt were found to phosphorylate BAD in vivo and in vitro at the same residues that are phosphorylated in response to IL-3. Thus, the proapoptotic function of BAD is regulated by the PI 3-kinase-Akt pathway.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉del Peso, L -- Gonzalez-Garcia, M -- Page, C -- Herrera, R -- Nunez, G -- CA-64556/CA/NCI NIH HHS/ -- New York, N.Y. -- Science. 1997 Oct 24;278(5338):687-9.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Pathology and Comprehensive Cancer Center, University of Michigan Medical School, Ann Arbor, MI 48109, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9381178" target="_blank"〉PubMed〈/a〉
    Keywords: Androstadienes/pharmacology ; Animals ; Apoptosis ; Carrier Proteins/*metabolism ; Cell Line ; Chromones/pharmacology ; Enzyme Activation ; Enzyme Inhibitors/pharmacology ; Humans ; Interleukin-3/*pharmacology ; Mice ; Morpholines/pharmacology ; Phosphatidylinositol 3-Kinases/antagonists & inhibitors/*metabolism ; Phosphorylation ; Phosphoserine/metabolism ; Protein-Serine-Threonine Kinases/*metabolism ; Proto-Oncogene Proteins/*metabolism ; Proto-Oncogene Proteins c-akt ; Proto-Oncogene Proteins c-bcl-2/metabolism ; Recombinant Proteins/metabolism ; Signal Transduction ; bcl-Associated Death Protein ; bcl-X Protein
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
    Published by American Association for the Advancement of Science (AAAS)
    Location Call Number Expected Availability
    BibTip Others were also interested in ...
    PAPER CURRENT
  • 54
    facet.materialart.
    Unknown
    Activation of SAPK/JNK by TNF receptor 1 through a noncytotoxic TRAF2-dependent pathway (1997)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1997-01-10
    Description: Interaction of the p55 tumor necrosis factor receptor 1 (TNF-R1)-associated signal transducer TRADD with FADD signals apoptosis, whereas the TNF receptor-associated factor 2 protein (TRAF2) is required for activation of the nuclear transcription factor nuclear factor kappa B. TNF-induced activation of the stress-activated protein kinase (SAPK) was shown to occur through a noncytotoxic TRAF2-dependent pathway. TRAF2 was both sufficient and necessary for activation of SAPK by TNF-R1; conversely, expression of a dominant-negative FADD mutant, which blocks apoptosis, did not interfere with SAPK activation. Therefore, SAPK activation occurs through a pathway that is not required for TNF-R1-induced apoptosis.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Natoli, G -- Costanzo, A -- Ianni, A -- Templeton, D J -- Woodgett, J R -- Balsano, C -- Levrero, M -- New York, N.Y. -- Science. 1997 Jan 10;275(5297):200-3.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Fondazione Andrea Cesalpino and Istituto di I Clinica Medica, Policlinico Umberto I, Viale del Policlinico 155, 00161 Rome, Italy.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8985011" target="_blank"〉PubMed〈/a〉
    Keywords: Acetylcysteine/pharmacology ; *Adaptor Proteins, Signal Transducing ; Apoptosis ; Calcium-Calmodulin-Dependent Protein Kinases/*metabolism ; Carrier Proteins/metabolism ; Cell Line ; Dactinomycin/pharmacology ; Enzyme Activation ; Fas-Associated Death Domain Protein ; Free Radical Scavengers/pharmacology ; HeLa Cells ; Humans ; JNK Mitogen-Activated Protein Kinases ; *MAP Kinase Kinase Kinase 1 ; *Mitogen-Activated Protein Kinases ; NF-kappa B/metabolism ; Protein-Serine-Threonine Kinases/metabolism ; Proteins/*metabolism ; Reactive Oxygen Species/metabolism ; Receptors, Tumor Necrosis Factor/*metabolism ; Recombinant Proteins/pharmacology ; Signal Transduction ; TNF Receptor-Associated Factor 1 ; TNF Receptor-Associated Factor 2 ; Transfection ; Tumor Necrosis Factor-alpha/*pharmacology
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
    Published by American Association for the Advancement of Science (AAAS)
    Location Call Number Expected Availability
    BibTip Others were also interested in ...
    PAPER CURRENT
  • 55
    facet.materialart.
    Unknown
    Expression cloning in the test tube (1997)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1997-08-15
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉King, R W -- Lustig, K D -- Stukenberg, P T -- McGarry, T J -- Kirschner, M W -- New York, N.Y. -- Science. 1997 Aug 15;277(5328):973-4.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Cell Biology, Harvard Medical School, Boston, MA 02115, USA. king@bcmp.med.harvard.edu〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9281074" target="_blank"〉PubMed〈/a〉
    Keywords: Apoptosis ; Cloning, Molecular/*methods ; DNA, Complementary/genetics ; Enzymes/metabolism ; Gene Expression ; Mitosis ; Phosphorylation ; Plasmids ; Protein Processing, Post-Translational ; Proteins/genetics/*metabolism
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
    Published by American Association for the Advancement of Science (AAAS)
    Location Call Number Expected Availability
    BibTip Others were also interested in ...
    PAPER CURRENT
  • 56
    facet.materialart.
    Unknown
    LKLF: A transcriptional regulator of single-positive T cell quiescence and survival (1997)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1997-09-26
    Description: Mature single-positive (SP) T lymphocytes enter a "resting" state in which they are proliferatively quiescent and relatively resistant to apoptosis. The molecular mechanisms regulating this quiescent phenotype were unknown. Here it was found that the expression of a Kruppel-like zinc finger transcription factor, lung Kruppel-like factor (LKLF), is developmentally induced during the maturation of SP quiescent T cells and rapidly extinguished after SP T cell activation. LKLF-deficient T cells produced by gene targeting had a spontaneously activated phenotype and died in the spleen and lymph nodes from Fas ligand-induced apoptosis. Thus, LKLF is required to program the quiescent state of SP T cells and to maintain their viability in the peripheral lymphoid organs and blood.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Kuo, C T -- Veselits, M L -- Leiden, J M -- AI29637/AI/NIAID NIH HHS/ -- New York, N.Y. -- Science. 1997 Sep 26;277(5334):1986-90.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Medicine, University of Chicago, Chicago, IL 60637, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9302292" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Antigens, CD95/biosynthesis ; Apoptosis ; B-Lymphocytes/metabolism ; Cell Survival ; Chimera ; Fas Ligand Protein ; Gene Deletion ; Gene Targeting ; *Interphase ; Kruppel-Like Transcription Factors ; Lymph Nodes/cytology ; Lymphocyte Activation ; Membrane Glycoproteins/biosynthesis ; Mice ; Mice, Inbred C57BL ; Spleen/cytology ; T-Lymphocyte Subsets/metabolism ; T-Lymphocytes/*cytology/*immunology/metabolism ; Trans-Activators/biosynthesis/genetics/*physiology ; Transfection ; *Zinc Fingers
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
    Published by American Association for the Advancement of Science (AAAS)
    Location Call Number Expected Availability
    BibTip Others were also interested in ...
    PAPER CURRENT
  • 57
    facet.materialart.
    Unknown
    Beta-catenin as oncogene: the smoking gun (1997)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1997-03-21
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Peifer, M -- New York, N.Y. -- Science. 1997 Mar 21;275(5307):1752-3.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Biology, University of North Carolina at Chapel Hill, Chapel Hill, NC 27599-3280, USA. peifer@unc.edu〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9122680" target="_blank"〉PubMed〈/a〉
    Keywords: Adenomatous Polyposis Coli Protein ; Animals ; Apoptosis ; Cell Division ; Cell Movement ; Colon/cytology/metabolism ; Colonic Neoplasms/*genetics/metabolism ; Cytoskeletal Proteins/*genetics/*metabolism ; DNA-Binding Proteins/metabolism ; *Drosophila Proteins ; Gene Expression Regulation, Neoplastic ; Genes, APC ; Humans ; Insect Proteins/metabolism ; Intestinal Mucosa/cytology/metabolism ; Lymphoid Enhancer-Binding Factor 1 ; Melanoma/*genetics/metabolism ; Mutation ; *Oncogenes ; *Repressor Proteins ; Signal Transduction ; *Trans-Activators ; Transcription Factors/metabolism ; Tumor Cells, Cultured ; beta Catenin
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
    Published by American Association for the Advancement of Science (AAAS)
    Location Call Number Expected Availability
    BibTip Others were also interested in ...
    PAPER CURRENT
  • 58
    facet.materialart.
    Unknown
    Amphibian limb regeneration: rebuilding a complex structure (1997)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1997-04-04
    Description: The ability to regenerate complex structures is widespread in metazoan phylogeny, but among vertebrates the urodele amphibians are exceptional. Adult urodeles can regenerate their limbs by local formation of a mesenchymal growth zone or blastema. The generation of blastemal cells depends not only on the local extracellular environment after amputation or wounding but also on the ability to reenter the cell cycle from the differentiated state. The blastema replaces structures appropriate to its proximodistal position. Axial identity is probably encoded as a graded property that controls cellular growth and movement through local cell interactions. The molecular basis is not understood, but proximodistal identity in newt blastemal cells may be respecified by signaling through a retinoic acid receptor isoform. The possibility of inducing a blastema on a mammalian limb cannot be discounted, although the molecular constraints are becoming clearer as we understand more about the mechanisms of urodele regeneration.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Brockes, J P -- New York, N.Y. -- Science. 1997 Apr 4;276(5309):81-7.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Ludwig Institute for Cancer Research and Department of Biochemistry and Molecular Biology, University College London, 91 Riding House Street, London W1P 8BT, UK. jerbro@ludwig.ucl.ac.uk〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9082990" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Apoptosis ; Cell Cycle ; Cell Differentiation ; Extremities/*physiology ; Mesoderm/cytology/*physiology ; Morphogenesis ; Muscle, Skeletal/cytology/physiology ; Neoplasms/pathology ; *Regeneration ; Urodela/*physiology
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
    Published by American Association for the Advancement of Science (AAAS)
    Location Call Number Expected Availability
    BibTip Others were also interested in ...
    PAPER CURRENT
  • 59
    facet.materialart.
    Unknown
    Bypass of senescence after disruption of p21CIP1/WAF1 gene in normal diploid human fibroblasts (1997)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1997-08-08
    Description: Most somatic cells die after a finite number of cell divisions, a phenomenon described as senescence. The p21(CIP1/WAF1) gene encodes an inhibitor of cyclin-dependent kinases. Inactivation of p21 by two sequential rounds of targeted homologous recombination was sufficient to bypass senescence in normal diploid human fibroblasts. At the checkpoint between the prereplicative phase of growth and the phase of chromosome replication, cells lacking p21 failed to arrest the cell cycle in response to DNA damage, but their apoptotic response and genomic stability were unaltered. These results establish the feasibility of using gene targeting for genetic studies of normal human cells.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Brown, J P -- Wei, W -- Sedivy, J M -- GM41690/GM/NIGMS NIH HHS/ -- New York, N.Y. -- Science. 1997 Aug 8;277(5327):831-4.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Molecular Biology, Cell Biology, and Biochemistry, Brown University, Providence, RI 02912, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9242615" target="_blank"〉PubMed〈/a〉
    Keywords: Apoptosis ; Aspartate Carbamoyltransferase/genetics ; Carbamoyl-Phosphate Synthase (Glutamine-Hydrolyzing)/genetics ; Cell Aging/*genetics ; Cell Division ; Cells, Cultured ; Cyclin-Dependent Kinase Inhibitor p21 ; Cyclins/*genetics/physiology ; DNA Damage ; Dihydroorotase/genetics ; Electroporation ; Fibroblasts ; G1 Phase ; *Gene Deletion ; Gene Targeting ; Genetic Vectors ; Humans ; Multienzyme Complexes/genetics ; Telomere/physiology
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
    Published by American Association for the Advancement of Science (AAAS)
    Location Call Number Expected Availability
    BibTip Others were also interested in ...
    PAPER CURRENT
  • 60
    facet.materialart.
    Unknown
    Transmission of the BSE agent to mice in the absence of detectable abnormal prion protein (1997)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1997-01-17
    Description: The agent responsible for transmissible spongiform encephalopathies (TSEs) is thought to be a malfolded, protease-resistant version (PrPres) of the normal cellular prion protein (PrP). The interspecies transmission of bovine spongiform encephalopathy (BSE) to mice was studied. Although all of the mice injected with homogenate from BSE-infected cattle brain exhibited neurological symptoms and neuronal death, more than 55 percent had no detectable PrPres. During serial passage, PrPres appeared after the agent became adapted to the new host. Thus, PrPres may be involved in species adaptation, but a further unidentified agent may actually transmit BSE.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Lasmezas, C I -- Deslys, J P -- Robain, O -- Jaegly, A -- Beringue, V -- Peyrin, J M -- Fournier, J G -- Hauw, J J -- Rossier, J -- Dormont, D -- New York, N.Y. -- Science. 1997 Jan 17;275(5298):402-5.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Commissariat a l'Energie Atomique, Service de Neurovirologie, DSV/DRM/SSA, B.P. 6, 60-68 avenue du General Leclerc, 92265 Fontenay-aux-Roses Cedex, France. CORINNE.LASMEZAS@cea.fr〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8994041" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Apoptosis ; Astrocytes/pathology ; Brain/pathology ; *Brain Chemistry ; Cattle ; Encephalopathy, Bovine Spongiform/metabolism/pathology/*transmission ; Endopeptidases/metabolism ; Mice ; Mice, Inbred C57BL ; Nerve Tissue Proteins/*analysis ; Phenotype ; Prions/*analysis ; Purkinje Cells/pathology ; Serial Passage ; Time Factors ; Vacuoles/pathology
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
    Published by American Association for the Advancement of Science (AAAS)
    Location Call Number Expected Availability
    BibTip Others were also interested in ...
    PAPER CURRENT
  • 61
    facet.materialart.
    Unknown
    Drosophila mitotic domain boundaries as cell fate boundaries (1997)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1997-08-08
    Description: Fate determination in Drosophila embryos is evidenced by the appearance of mitotic domains. To identify fate or fates of cells, individual cells in mitotic domains 2, 8, and 15 were marked and monitored through development. Comparison of the different fates indicated that domain boundaries are cell fate boundaries. Cells were marked by expression of GAL4-dependent transgenes after photoactivation of a caged GAL4VP16 analog that had its DNA binding activity inhibited with a photolabile blocking reagent. Caged GAL4VP16 was also used to induce gene expression in Xenopus embryos. Thus, photoactivated gene expression is a versatile tool for spatiotemporal control of gene expression.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Cambridge, S B -- Davis, R L -- Minden, J S -- New York, N.Y. -- Science. 1997 Aug 8;277(5327):825-8.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Biological Sciences and Center for Light Microscope Imaging and Biotechnology, Carnegie Mellon University, Pittsburgh, PA 15213, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9242613" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Apoptosis ; Cell Differentiation ; *Cell Lineage ; Drosophila/cytology/*embryology/*genetics/metabolism ; Fungal Proteins/*metabolism ; Gastrula/cytology ; *Gene Expression Regulation, Developmental ; Light ; *Mitosis ; Trans-Activators/*metabolism ; *Transcriptional Activation ; Transgenes ; Xenopus/embryology/genetics
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
    Published by American Association for the Advancement of Science (AAAS)
    Location Call Number Expected Availability
    BibTip Others were also interested in ...
    PAPER CURRENT
  • 62
    facet.materialart.
    Unknown
    Inhibition of Bax channel-forming activity by Bcl-2 (1997)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1997-07-18
    Description: Proteins of the Bcl-2 family are intracellular membrane-associated proteins that regulate programmed cell death (apoptosis) either positively or negatively by as yet unknown mechanisms. Bax, a pro-apoptotic member of the Bcl-2 family, was shown to form channels in lipid membranes. Bax triggered the release of liposome-encapsulated carboxyfluorescein at both neutral and acidic pH. At physiological pH, release could be blocked by Bcl-2. Bcl-2, in contrast, triggered carboxyfluorescein release at acidic pH only. In planar lipid bilayers, Bax formed pH- and voltage-dependent ion-conducting channels. Thus, the pro-apoptotic effects of Bax may be elicited through an intrinsic pore-forming activity that can be antagonized by Bcl-2.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Antonsson, B -- Conti, F -- Ciavatta, A -- Montessuit, S -- Lewis, S -- Martinou, I -- Bernasconi, L -- Bernard, A -- Mermod, J J -- Mazzei, G -- Maundrell, K -- Gambale, F -- Sadoul, R -- Martinou, J C -- New York, N.Y. -- Science. 1997 Jul 18;277(5324):370-2.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Geneva Biomedical Research Institute, Glaxo Wellcome R&D S. A., 1288 Plan les Ouates, Geneva, Switzerland. beau6063@ggr.co.uk〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9219694" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Apoptosis ; Cell Membrane Permeability ; Cells, Cultured ; Erythrocytes/cytology ; Fluoresceins/metabolism ; Hemolysis ; Humans ; Hydrogen-Ion Concentration ; Ion Channels/*physiology ; Lipid Bilayers ; Liposomes ; Membrane Potentials ; Neurons/cytology ; Patch-Clamp Techniques ; Proto-Oncogene Proteins/pharmacology/*physiology ; Proto-Oncogene Proteins c-bcl-2/antagonists & inhibitors/pharmacology/*physiology ; Sheep ; Sympathetic Nervous System/cytology ; bcl-2-Associated X Protein
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
    Published by American Association for the Advancement of Science (AAAS)
    Location Call Number Expected Availability
    BibTip Others were also interested in ...
    PAPER CURRENT
  • 63
    facet.materialart.
    Unknown
    First p53 relative may be a new tumor suppressor (1997)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1997-10-06
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Dickman, S -- New York, N.Y. -- Science. 1997 Sep 12;277(5332):1605-6.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9312855" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Apoptosis ; Cell Division ; Chromosome Mapping ; Chromosomes, Human, Pair 1 ; Cyclin-Dependent Kinase Inhibitor p21 ; Cyclins/biosynthesis ; DNA-Binding Proteins/*genetics/physiology ; *Genes, Tumor Suppressor ; *Genes, p53 ; Genomic Imprinting ; Humans ; Mice ; Neuroblastoma/*genetics ; Nuclear Proteins/*genetics/physiology ; Tumor Cells, Cultured ; Tumor Suppressor Protein p53/physiology ; Tumor Suppressor Proteins
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
    Published by American Association for the Advancement of Science (AAAS)
    Location Call Number Expected Availability
    BibTip Others were also interested in ...
    PAPER CURRENT
  • 64
    facet.materialart.
    Unknown
    Structure of Bcl-xL-Bak peptide complex: recognition between regulators of apoptosis (1997)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1997-02-14
    Description: Heterodimerization between members of the Bcl-2 family of proteins is a key event in the regulation of programmed cell death. The molecular basis for heterodimer formation was investigated by determination of the solution structure of a complex between the survival protein Bcl-xL and the death-promoting region of the Bcl-2-related protein Bak. The structure and binding affinities of mutant Bak peptides indicate that the Bak peptide adopts an amphipathic alpha helix that interacts with Bcl-xL through hydrophobic and electrostatic interactions. Mutations in full-length Bak that disrupt either type of interaction inhibit the ability of Bak to heterodimerize with Bcl-xL.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Sattler, M -- Liang, H -- Nettesheim, D -- Meadows, R P -- Harlan, J E -- Eberstadt, M -- Yoon, H S -- Shuker, S B -- Chang, B S -- Minn, A J -- Thompson, C B -- Fesik, S W -- P01 A135294/PHS HHS/ -- R37 CA48023/CA/NCI NIH HHS/ -- New York, N.Y. -- Science. 1997 Feb 14;275(5302):983-6.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Pharmaceutical Discovery Division, Abbott Laboratories, Abbott Park, IL 60064, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9020082" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Apoptosis ; Crystallography, X-Ray ; Dimerization ; Magnetic Resonance Spectroscopy ; Membrane Proteins/*chemistry/genetics/metabolism ; Models, Molecular ; Molecular Sequence Data ; *Protein Conformation ; Protein Structure, Secondary ; Proto-Oncogene Proteins/*chemistry/metabolism ; *Proto-Oncogene Proteins c-bcl-2 ; Sequence Deletion ; bcl-2 Homologous Antagonist-Killer Protein ; bcl-X Protein
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
    Published by American Association for the Advancement of Science (AAAS)
    Location Call Number Expected Availability
    BibTip Others were also interested in ...
    PAPER CURRENT
  • 65
    facet.materialart.
    Unknown
    The homeotic gene lin-39 and the evolution of nematode epidermal cell fates (1997)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1997-10-23
    Description: The fate of ventral epidermal cells differs among nematode species. Nonvulval cells fuse with the epidermis in Caenorhabditis elegans, whereas the homologous cells undergo apoptosis in Pristionchus pacificus. The homeotic gene lin-39 is involved in the regulation of these epidermal cell fates. In Caenorhabditis, lin-39 prevents cell fusion of potential vulval cells and specifies the vulva equivalence group. Pristionchus vulvaless mutants that displayed apoptosis of the vulval precursor cells were isolated, and point mutations in lin-39 were identified. Thus, the evolution of these epidermal cell fates is driven by different intrinsic properties of homologous cells.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Eizinger, A -- Sommer, R J -- New York, N.Y. -- Science. 1997 Oct 17;278(5337):452-5.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Max-Planck Institut fur Entwicklungsbiologie, Abteilung Zellbiologie, Spemannstrasse 35, 72076 Tubingen, Germany.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9334302" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Animals ; Apoptosis ; Base Sequence ; *Biological Evolution ; Caenorhabditis elegans/cytology/genetics/growth & development ; Cell Fusion ; Cell Lineage ; Epidermis/cytology ; Exons ; Female ; *Genes, Helminth ; *Genes, Homeobox ; Molecular Sequence Data ; Mutation ; Phenotype ; Rhabditida/*cytology/*genetics ; Stem Cells/cytology ; Vulva/cytology
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
    Published by American Association for the Advancement of Science (AAAS)
    Location Call Number Expected Availability
    BibTip Others were also interested in ...
    PAPER CURRENT
  • 66
    facet.materialart.
    Unknown
    Repression of c-myc transcription by Blimp-1, an inducer of terminal B cell differentiation (1997)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1997-04-25
    Description: Transcription of c-myc in plasma cells, which are terminally differentiated B cells, is repressed by plasmacytoma repressor factor. This factor was identified as Blimp-1, known for its ability to induce B cell differentiation. Blimp-1 repressed c-myc promoter activity in a binding site-dependent manner. Treatment of BCL1 lymphoma cells with interleukin-2 (IL-2) plus IL-5 induced Blimp-1 and caused a subsequent decline in c-Myc protein. Ectopic expression of Blimp-1 in Abelson-transformed precursor B cells repressed endogenous c-Myc and caused apoptosis; Blimp-1-induced death was partially overcome by ectopic expression of c-Myc. Thus, repression of c-myc is a component of the Blimp-1 program of terminal B cell differentiation.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Lin, Y -- Wong, K -- Calame, K -- New York, N.Y. -- Science. 1997 Apr 25;276(5312):596-9.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Microbiology, Columbia University College of Physicians and Surgeons, New York, NY 10032, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9110979" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Apoptosis ; B-Lymphocytes/*cytology/metabolism ; Binding Sites ; Cell Differentiation ; Cell Line ; Gene Expression Regulation ; *Genes, myc ; Interleukin-2/pharmacology ; Interleukin-5/pharmacology ; Mice ; Mutagenesis, Site-Directed ; Plasmacytoma ; Promoter Regions, Genetic ; *Repressor Proteins ; Transcription Factors/genetics/*metabolism ; *Transcription, Genetic ; Transfection ; Tumor Cells, Cultured ; Zinc Fingers
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
    Published by American Association for the Advancement of Science (AAAS)
    Location Call Number Expected Availability
    BibTip Others were also interested in ...
    PAPER CURRENT
Close ⊗
This website uses cookies and the analysis tool Matomo. More information can be found here...