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Harald Von Melchner - One of the best experts on this subject based on the ideXlab platform.

  • gene trapping identifies transiently induced survival genes during programmed cell death
    Genome Biology, 2001
    Co-Authors: Frank Wempe, Jiyeon Yang, Joanna Hammann, Harald Von Melchner
    Abstract:

    The existence of a constitutively expressed machinery for death in individual cells has led to the notion that survival factors repress this machinery and, if such factors are unavailable, cells die by default. In many cells, however, mRNA and protein synthesis inhibitors induce apoptosis, suggesting that in some cases transcriptional activity might actually impede cell death. To identify transcriptional mechanisms that interfere with cell death and survival, we combined gene trap mutagenesis with site-specific recombination (Cre/loxP system) to isolate genes from cells undergoing apoptosis by growth factor deprivation. From an Integration Library consisting of approximately 2 × 106 unique proviral Integrations obtained by infecting the interleukin-3 (IL-3)-dependent hematopoietic cell line - FLOXIL3 - with U3Cre gene trap virus, we have isolated 125 individual clones that converted to factor independence upon IL-3 withdrawal. Of 102 cellular sequences adjacent to U3Cre Integration sites, 17% belonged to known genes, 11% matched single expressed sequence tags (ESTs) or full cDNAs with unknown function and 72% had no match within the public databases. Most of the known genes recovered in this analysis encoded proteins with survival functions. We have shown that hematopoietic cells undergoing apoptosis after withdrawal of IL-3 activate survival genes that impede cell death. This results in reduced apoptosis and improved survival of cells treated with a transient apoptotic stimulus. Thus, apoptosis in hematopoietic cells is the end result of a conflict between death and survival signals, rather than a simple death by default.

Frank Wempe - One of the best experts on this subject based on the ideXlab platform.

  • gene trapping identifies transiently induced survival genes during programmed cell death
    Genome Biology, 2001
    Co-Authors: Frank Wempe, Jiyeon Yang, Joanna Hammann, Harald Von Melchner
    Abstract:

    The existence of a constitutively expressed machinery for death in individual cells has led to the notion that survival factors repress this machinery and, if such factors are unavailable, cells die by default. In many cells, however, mRNA and protein synthesis inhibitors induce apoptosis, suggesting that in some cases transcriptional activity might actually impede cell death. To identify transcriptional mechanisms that interfere with cell death and survival, we combined gene trap mutagenesis with site-specific recombination (Cre/loxP system) to isolate genes from cells undergoing apoptosis by growth factor deprivation. From an Integration Library consisting of approximately 2 × 106 unique proviral Integrations obtained by infecting the interleukin-3 (IL-3)-dependent hematopoietic cell line - FLOXIL3 - with U3Cre gene trap virus, we have isolated 125 individual clones that converted to factor independence upon IL-3 withdrawal. Of 102 cellular sequences adjacent to U3Cre Integration sites, 17% belonged to known genes, 11% matched single expressed sequence tags (ESTs) or full cDNAs with unknown function and 72% had no match within the public databases. Most of the known genes recovered in this analysis encoded proteins with survival functions. We have shown that hematopoietic cells undergoing apoptosis after withdrawal of IL-3 activate survival genes that impede cell death. This results in reduced apoptosis and improved survival of cells treated with a transient apoptotic stimulus. Thus, apoptosis in hematopoietic cells is the end result of a conflict between death and survival signals, rather than a simple death by default.

Jiyeon Yang - One of the best experts on this subject based on the ideXlab platform.

  • gene trapping identifies transiently induced survival genes during programmed cell death
    Genome Biology, 2001
    Co-Authors: Frank Wempe, Jiyeon Yang, Joanna Hammann, Harald Von Melchner
    Abstract:

    The existence of a constitutively expressed machinery for death in individual cells has led to the notion that survival factors repress this machinery and, if such factors are unavailable, cells die by default. In many cells, however, mRNA and protein synthesis inhibitors induce apoptosis, suggesting that in some cases transcriptional activity might actually impede cell death. To identify transcriptional mechanisms that interfere with cell death and survival, we combined gene trap mutagenesis with site-specific recombination (Cre/loxP system) to isolate genes from cells undergoing apoptosis by growth factor deprivation. From an Integration Library consisting of approximately 2 × 106 unique proviral Integrations obtained by infecting the interleukin-3 (IL-3)-dependent hematopoietic cell line - FLOXIL3 - with U3Cre gene trap virus, we have isolated 125 individual clones that converted to factor independence upon IL-3 withdrawal. Of 102 cellular sequences adjacent to U3Cre Integration sites, 17% belonged to known genes, 11% matched single expressed sequence tags (ESTs) or full cDNAs with unknown function and 72% had no match within the public databases. Most of the known genes recovered in this analysis encoded proteins with survival functions. We have shown that hematopoietic cells undergoing apoptosis after withdrawal of IL-3 activate survival genes that impede cell death. This results in reduced apoptosis and improved survival of cells treated with a transient apoptotic stimulus. Thus, apoptosis in hematopoietic cells is the end result of a conflict between death and survival signals, rather than a simple death by default.

Joanna Hammann - One of the best experts on this subject based on the ideXlab platform.

  • gene trapping identifies transiently induced survival genes during programmed cell death
    Genome Biology, 2001
    Co-Authors: Frank Wempe, Jiyeon Yang, Joanna Hammann, Harald Von Melchner
    Abstract:

    The existence of a constitutively expressed machinery for death in individual cells has led to the notion that survival factors repress this machinery and, if such factors are unavailable, cells die by default. In many cells, however, mRNA and protein synthesis inhibitors induce apoptosis, suggesting that in some cases transcriptional activity might actually impede cell death. To identify transcriptional mechanisms that interfere with cell death and survival, we combined gene trap mutagenesis with site-specific recombination (Cre/loxP system) to isolate genes from cells undergoing apoptosis by growth factor deprivation. From an Integration Library consisting of approximately 2 × 106 unique proviral Integrations obtained by infecting the interleukin-3 (IL-3)-dependent hematopoietic cell line - FLOXIL3 - with U3Cre gene trap virus, we have isolated 125 individual clones that converted to factor independence upon IL-3 withdrawal. Of 102 cellular sequences adjacent to U3Cre Integration sites, 17% belonged to known genes, 11% matched single expressed sequence tags (ESTs) or full cDNAs with unknown function and 72% had no match within the public databases. Most of the known genes recovered in this analysis encoded proteins with survival functions. We have shown that hematopoietic cells undergoing apoptosis after withdrawal of IL-3 activate survival genes that impede cell death. This results in reduced apoptosis and improved survival of cells treated with a transient apoptotic stimulus. Thus, apoptosis in hematopoietic cells is the end result of a conflict between death and survival signals, rather than a simple death by default.

Johan H. Huijsing - One of the best experts on this subject based on the ideXlab platform.

  • Compact low-voltage power-efficient operational amplifier cells for VLSI
    IEEE Journal of Solid-State Circuits, 1998
    Co-Authors: Klaas-jan Langen, Johan H. Huijsing
    Abstract:

    Compact low-voltage power-efficient operational amplifiers are\ndescribed that are very suitable as very-large-scale-Integration Library\ncells because of the small die area of 0.08 mm2 and the\nminimum supply voltage of 1.8 V. A key part of the circuit is the\nrail-to-rail class-AB output stage with folded mesh feedback control\nthat combines power efficiency with operation down to 1.8 V and allows\nsufficient gain in a compact two-stage topology. A version with\nrail-to-rail input stage features a rail-to-rail input range for supply\nvoltages down to 2.5 V. The dc gain of the op amps is more than 80 db\nwhile driving 10 kΩ, and the unity-gain frequency is 4 MHz with\nphase margin of 67° while driving 5 pF. The equivalent input noise\nvoltage is 38 nV/√(Hz) at a frequency of 100 kHz. The amplifiers\nhave been implemented in a standard digital 1.6-μm complementary\nmetal-oxide-semiconductor process