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150325s1992 xx |||||o 00| ||eng c |
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|a (DE-627)JST069891060
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|a (JST)2359853
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|a DE-627
|b ger
|c DE-627
|e rakwb
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|a eng
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|a Chen, Yunn-Yi
|e verfasserin
|4 aut
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|a Lymphoid Cells Transformed by Abelson Virus Require the v-abl Protein- Tyrosine Kinase Only During Early G<sub>1</sub>
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|c 1992
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|a Text
|b txt
|2 rdacontent
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|a Computermedien
|b c
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|a Online-Ressource
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|a Cells infected with temperature-sensitive transformation mutants of the Abelson murine leukemia virus express low levels of kinase activity at the nonpermissive temperature, causing transformed pre-B cells to die under these conditions. Examination of cell cycle profiles of such populations prior to cell death reveals that the cells accumulate in the G<sub>1</sub> phase of the cell cycle. Following G<sub>1</sub> arrest, the cells die via apoptosis, an active process of cell elimination. Cell synchronization and temperature-shift experiments show that G<sub>1</sub> arrest reflects the requirement for a functional v-abl protein during early G<sub>1</sub> and that the molecule is not required at other phases of the cell cycle. These data indicate that the substrate(s) critical to v-abl-mediated transformation is involved in regulating G<sub>1</sub> transit and that these interactions are dominant over all other changes required for the multistep process that results in the fully malignant phenotype associated with v-abl expression in lymphoid cells.
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|a Copyright 1992 The National Academy of Sciences of the United States of America
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|a Genetics
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|a Apoptosis
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|a Transformation
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|a v-abl Oncogene
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|a Cell Cycle
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|a Biological sciences
|x Biology
|x Cytology
|x Cell biology
|x Cell physiology
|x Cell cycle
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|a Biological sciences
|x Biology
|x Physiology
|x Body composition
|x Body fluids
|x Blood
|x Blood cells
|x Leukocytes
|x Mononuclear leukocytes
|x Lymphocytes
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|a Biological sciences
|x Biology
|x Cytology
|x Cell biology
|x Cell physiology
|x Cell death
|x Apoptosis
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|a Biological sciences
|x Biology
|x Cytology
|x Cell biology
|x Cell physiology
|x Cell growth
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|a Physical sciences
|x Chemistry
|x Chemical compounds
|x Chemicals
|x Acids
|x Nucleic acids
|x DNA
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|a Biological sciences
|x Biology
|x Cytology
|x Cell biology
|x Cells
|x Cultured cells
|x Cell lines
|x Transformed cell line
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|a Biological sciences
|x Biology
|x Microbiology
|x Microorganisms
|x Viruses
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|a Physical sciences
|x Physics
|x Microphysics
|x Molecular physics
|x Molecules
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|a Biological sciences
|x Biology
|x Cytology
|x Cell biology
|x Cell physiology
|x Cell cycle
|x Interphase
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|a Health sciences
|x Medical sciences
|x Immunology
|x Immune system
|x Immune response
|x Adaptive immunity
|x Active immunity
|x Humoral immunity
|x Antibodies
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|a research-article
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|a Rosenberg, Naomi
|e verfasserin
|4 aut
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0 |
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|i Enthalten in
|t Proceedings of the National Academy of Sciences of the United States of America
|d National Academy of Sciences of the United States of America
|g 89(1992), 15, Seite 6683-6687
|w (DE-627)254235379
|w (DE-600)1461794-8
|x 10916490
|7 nnns
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|g volume:89
|g year:1992
|g number:15
|g pages:6683-6687
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|u https://www.jstor.org/stable/2359853
|3 Volltext
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|a GBV_ILN_105
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|a GBV_ILN_110
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|a GBV_ILN_602
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|a GBV_ILN_702
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|a GBV_ILN_2001
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|a GBV_ILN_2003
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|a GBV_ILN_2005
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|a GBV_ILN_2006
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|a GBV_ILN_2011
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|a GBV_ILN_2021
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|a GBV_ILN_2026
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|a GBV_ILN_2027
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|a GBV_ILN_2044
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|a GBV_ILN_2050
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|a GBV_ILN_2057
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|a GBV_ILN_2061
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|a GBV_ILN_2088
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|a GBV_ILN_2107
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|a GBV_ILN_2110
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|a GBV_ILN_2190
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|a GBV_ILN_2943
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|a GBV_ILN_2949
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|a GBV_ILN_2951
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|a GBV_ILN_4012
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|a GBV_ILN_4035
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912 |
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|a GBV_ILN_4037
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912 |
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|a GBV_ILN_4046
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|a GBV_ILN_4126
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|a GBV_ILN_4249
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|a GBV_ILN_4251
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|a GBV_ILN_4305
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|
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|a GBV_ILN_4313
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|a GBV_ILN_4322
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|a GBV_ILN_4323
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|a GBV_ILN_4324
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|a GBV_ILN_4325
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|a GBV_ILN_4335
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|a GBV_ILN_4338
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|a GBV_ILN_4346
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|a GBV_ILN_4367
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|a GBV_ILN_4700
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|a AR
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|d 89
|j 1992
|e 15
|h 6683-6687
|