BIOMAT Database Logo BIOMAT Database Logo

[Analysis of transient G1/S arrest in E1A+E1B-19kDa transformed cells after ionizing radiation]. 2003

A I Brichkina, and N D Aksenov, and V A Pospelov, and T V Pospelova
Institute of Cytology RAS, St. Petersburg. aibri@mail.ru

Expression of human adenovirus type 5 E1A oncogene in normal rodent cells leads to disruption of the G1/S cell cycle arrest realization in response to DNA damage. It has been shown here that rat embryo fibroblasts transformed by E1Aad5 oncogene in complementation with E1B-19 kDa gene realize the irradiation-induced transient G1/S arrest, which depends on selective suppression of CyclinE-Cdk2 activity despite functional inactivation of p21Waf1 inhibitor. Inhibitor p21Waf1 is not revealed in complexes with cyclins E and A in E1A + E1B-19 kDa transformants, however, it is not due to p21Waf1 interaction with E1A oncoproteins, because the E1A-p21Waf1 complex formation in E1A + cHa-ras transformants does not prevent the high level of CycIE, A-p21Waf1 association. In the case of p21Waf1 inactivation, the main way of cyclin-kinase activity regulation in E1A + E1B-19 kDa cells may be Cdk2 phosphorylation. However, irradiation of E1A + E1B-19 kDa transformed cells induces no changes in CAK (Cdk7-associated) kinase activity and in the protein level of Cdc25A phosphatase, which are responsible for activating Thr160 phosphoralation and Tyr15 dephosphorylation on Cdk2. Using phospho-Tyr15-Cdk2 specific antibodies, no increase of phosphorylation at Tyr15 position on immunoprecipitated Cdk2 was detected after irradiation. It seems likely that in the case of inactivated inhibitor p21Waf1 the transient G1/S block after irradiation in E1A + E1B-19 kDa transformants depends on suppression of Cycl-E-Cdk2 activity caused by inhibition of Thr160 Cdk2 phosphorylation, but his occurs with the involvement of other kinases rather than CAK.

UI MeSH Term Description Entries
D010766 Phosphorylation The introduction of a phosphoryl group into a compound through the formation of an ester bond between the compound and a phosphorus moiety. Phosphorylations
D002461 Cell Line, Transformed Eukaryotic cell line obtained in a quiescent or stationary phase which undergoes conversion to a state of unregulated growth in culture, resembling an in vitro tumor. It occurs spontaneously or through interaction with viruses, oncogenes, radiation, or drugs/chemicals. Transformed Cell Line,Cell Lines, Transformed,Transformed Cell Lines
D002471 Cell Transformation, Neoplastic Cell changes manifested by escape from control mechanisms, increased growth potential, alterations in the cell surface, karyotypic abnormalities, morphological and biochemical deviations from the norm, and other attributes conferring the ability to invade, metastasize, and kill. Neoplastic Transformation, Cell,Neoplastic Cell Transformation,Transformation, Neoplastic Cell,Tumorigenic Transformation,Cell Neoplastic Transformation,Cell Neoplastic Transformations,Cell Transformations, Neoplastic,Neoplastic Cell Transformations,Neoplastic Transformations, Cell,Transformation, Cell Neoplastic,Transformation, Tumorigenic,Transformations, Cell Neoplastic,Transformations, Neoplastic Cell,Transformations, Tumorigenic,Tumorigenic Transformations
D004249 DNA Damage Injuries to DNA that introduce deviations from its normal, intact structure and which may, if left unrepaired, result in a MUTATION or a block of DNA REPLICATION. These deviations may be caused by physical or chemical agents and occur by natural or unnatural, introduced circumstances. They include the introduction of illegitimate bases during replication or by deamination or other modification of bases; the loss of a base from the DNA backbone leaving an abasic site; single-strand breaks; double strand breaks; and intrastrand (PYRIMIDINE DIMERS) or interstrand crosslinking. Damage can often be repaired (DNA REPAIR). If the damage is extensive, it can induce APOPTOSIS. DNA Injury,DNA Lesion,DNA Lesions,Genotoxic Stress,Stress, Genotoxic,Injury, DNA,DNA Injuries
D004622 Embryo, Mammalian The entity of a developing mammal (MAMMALS), generally from the cleavage of a ZYGOTE to the end of embryonic differentiation of basic structures. For the human embryo, this represents the first two months of intrauterine development preceding the stages of the FETUS. Embryonic Structures, Mammalian,Mammalian Embryo,Mammalian Embryo Structures,Mammalian Embryonic Structures,Embryo Structure, Mammalian,Embryo Structures, Mammalian,Embryonic Structure, Mammalian,Embryos, Mammalian,Mammalian Embryo Structure,Mammalian Embryonic Structure,Mammalian Embryos,Structure, Mammalian Embryo,Structure, Mammalian Embryonic,Structures, Mammalian Embryo,Structures, Mammalian Embryonic
D005347 Fibroblasts Connective tissue cells which secrete an extracellular matrix rich in collagen and other macromolecules. Fibroblast
D000818 Animals Unicellular or multicellular, heterotrophic organisms, that have sensation and the power of voluntary movement. Under the older five kingdom paradigm, Animalia was one of the kingdoms. Under the modern three domain model, Animalia represents one of the many groups in the domain EUKARYOTA. Animal,Metazoa,Animalia
D016193 G1 Phase The period of the CELL CYCLE preceding DNA REPLICATION in S PHASE. Subphases of G1 include "competence" (to respond to growth factors), G1a (entry into G1), G1b (progression), and G1c (assembly). Progression through the G1 subphases is effected by limiting growth factors, nutrients, or inhibitors. First Gap Phase,G1a Phase,G1b Phase,Gap Phase 1,First Gap Phases,G1 Phases,G1a Phases,G1b Phases,Gap Phase, First,Gap Phases, First,Phase 1, Gap,Phase, First Gap,Phase, G1,Phase, G1a,Phase, G1b,Phases, First Gap,Phases, G1,Phases, G1a,Phases, G1b
D016196 S Phase Phase of the CELL CYCLE following G1 and preceding G2 when the entire DNA content of the nucleus is replicated. It is achieved by bidirectional replication at multiple sites along each chromosome. S Period,Period, S,Periods, S,Phase, S,Phases, S,S Periods,S Phases
D017500 Adenovirus E1A Proteins Proteins transcribed from the E1A genome region of ADENOVIRUSES which are involved in positive regulation of transcription of the early genes of host infection. Adenovirus E1A Protein Domain 3,Adenovirus E1A Protein,E1A Protein, Adenovirus,E1A Proteins, Adenovirus

Related Publications

A I Brichkina, and N D Aksenov, and V A Pospelov, and T V Pospelova
[Transfection with the E1A and E1B-19kDa oncogenes does not prevent rat embryo fibroblasts from cell cycle arrest after gamma-radiation].
January 2002, Molekuliarnaia biologiia,
A I Brichkina, and N D Aksenov, and V A Pospelov, and T V Pospelova
Restoration of G1/S arrest in E1A+c-Ha-ras-transformed cells by Bcl-2 overexpression.
November 2004, Cell cycle (Georgetown, Tex.),
A I Brichkina, and N D Aksenov, and V A Pospelov, and T V Pospelova
Adenovirus E1A/E1B Transformed Amniotic Fluid Cells Support Human Cytomegalovirus Replication.
February 2016, Viruses,
A I Brichkina, and N D Aksenov, and V A Pospelov, and T V Pospelova
Inhibition of G1-phase arrest induced by ionizing radiation in hematopoietic cells by overexpression of genes involved in the G1/S-phase transition.
September 1995, Radiation research,
A I Brichkina, and N D Aksenov, and V A Pospelov, and T V Pospelova
Activation of adenovirus 5 E1A transcription by region E1B in transformed primary rat cells.
November 1987, The EMBO journal,
A I Brichkina, and N D Aksenov, and V A Pospelov, and T V Pospelova
Restoration of an absent G1 arrest and protection from apoptosis in embryonic stem cells after ionizing radiation.
October 2004, Proceedings of the National Academy of Sciences of the United States of America,
A I Brichkina, and N D Aksenov, and V A Pospelov, and T V Pospelova
[E1A oncogene effect on the ability of p21(Waf1) to regulate G1/S arrest in E1A-expressing transformants following irradiation].
January 2005, Tsitologiia,
A I Brichkina, and N D Aksenov, and V A Pospelov, and T V Pospelova
Induction of integrated adenovirus E1A and E1B genes in transformed human cells by phorbol ester tumor promoters.
February 1987, Cancer research,
A I Brichkina, and N D Aksenov, and V A Pospelov, and T V Pospelova
Drosophila Caliban mediates G1-S transition and ionizing radiation induced S phase checkpoint.
January 2018, Cell cycle (Georgetown, Tex.),
A I Brichkina, and N D Aksenov, and V A Pospelov, and T V Pospelova
G1/S arrest induced by histone deacetylase inhibitor sodium butyrate in E1A + Ras-transformed cells is mediated through down-regulation of E2F activity and stabilization of beta-catenin.
July 2006, The Journal of biological chemistry,
Copied contents to your clipboard!