p16INK4a, but not constitutively active pRb, can impose a sustained G1 arrest: molecular mechanisms and implications for oncogenesis.

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Standard

p16INK4a, but not constitutively active pRb, can impose a sustained G1 arrest: molecular mechanisms and implications for oncogenesis. / Lukas, J; Storgaard Sørensen, Claus; Lukas, C; Santoni-Rugiu, E; Bartek, J.

I: Oncogene, Bind 18, Nr. 27, 1999, s. 3930-5.

Publikation: Bidrag til tidsskrift › Tidsskriftartikel › Forskning › fagfællebedømt

Harvard

Lukas, J, Storgaard Sørensen, C, Lukas, C, Santoni-Rugiu, E & Bartek, J 1999, 'p16INK4a, but not constitutively active pRb, can impose a sustained G1 arrest: molecular mechanisms and implications for oncogenesis.', Oncogene, bind 18, nr. 27, s. 3930-5. https://doi.org/10.1038/sj.onc.1202777

APA

Lukas, J., Storgaard Sørensen, C., Lukas, C., Santoni-Rugiu, E., & Bartek, J. (1999). p16INK4a, but not constitutively active pRb, can impose a sustained G1 arrest: molecular mechanisms and implications for oncogenesis. Oncogene, 18(27), 3930-5. https://doi.org/10.1038/sj.onc.1202777

Vancouver

Lukas J, Storgaard Sørensen C, Lukas C, Santoni-Rugiu E, Bartek J. p16INK4a, but not constitutively active pRb, can impose a sustained G1 arrest: molecular mechanisms and implications for oncogenesis. Oncogene. 1999;18(27):3930-5. https://doi.org/10.1038/sj.onc.1202777

Author

Lukas, J ; Storgaard Sørensen, Claus ; Lukas, C ; Santoni-Rugiu, E ; Bartek, J. / p16INK4a, but not constitutively active pRb, can impose a sustained G1 arrest: molecular mechanisms and implications for oncogenesis. I: Oncogene. 1999 ; Bind 18, Nr. 27. s. 3930-5.

Bibtex

@article{eaa28150525111dd8d9f000ea68e967b,

title = "p16INK4a, but not constitutively active pRb, can impose a sustained G1 arrest: molecular mechanisms and implications for oncogenesis.",

abstract = "p16ink4 and pRb, two components of a key G1/S regulatory pathway, and tumor suppressors commonly targeted in oncogenesis, are among the candidates for gene therapy of cancer. Wild-type p16 and a constitutively active pRb(delta cdk) mutant both blocked G1 in short-term experiments, but only p16 imposed a sustained G1 arrest. Unexpectedly, cells conditionally exposed to pRb(delta cdk) entered S phase after 2 days, followed by endoreduplication between days 4-6. The distinct phenotypes evoked by p16 vs pRb(delta cdk) appear mediated by cyclin E/CDK2 which, while active in the pRb(delta cdk)-expressing cells, became rapidly inhibited through restructuring diverse cyclin/CDK/p21 complexes by p16. These results provide novel insights into the roles of p16, pRb and cyclin E in G1/S control and multistep oncogenesis, with implications for gene therapy strategies.",

author = "J Lukas and {Storgaard S{\o}rensen}, Claus and C Lukas and E Santoni-Rugiu and J Bartek",

note = "Keywords: Animals; CDC2-CDC28 Kinases; Cell Transformation, Neoplastic; Cyclin-Dependent Kinase 2; Cyclin-Dependent Kinase Inhibitor p16; Cyclin-Dependent Kinases; G1 Phase; Gene Transfer Techniques; Growth Inhibitors; Humans; Osteosarcoma; Protein-Serine-Threonine Kinases; Rats; Retinoblastoma Protein; S Phase; Tumor Cells, Cultured",

year = "1999",

doi = "10.1038/sj.onc.1202777",

language = "English",

volume = "18",

pages = "3930--5",

journal = "Oncogene",

issn = "0950-9232",

publisher = "nature publishing group",

number = "27",

}

RIS

TY - JOUR

T1 - p16INK4a, but not constitutively active pRb, can impose a sustained G1 arrest: molecular mechanisms and implications for oncogenesis.

AU - Lukas, J

AU - Storgaard Sørensen, Claus

AU - Lukas, C

AU - Santoni-Rugiu, E

AU - Bartek, J

N1 - Keywords: Animals; CDC2-CDC28 Kinases; Cell Transformation, Neoplastic; Cyclin-Dependent Kinase 2; Cyclin-Dependent Kinase Inhibitor p16; Cyclin-Dependent Kinases; G1 Phase; Gene Transfer Techniques; Growth Inhibitors; Humans; Osteosarcoma; Protein-Serine-Threonine Kinases; Rats; Retinoblastoma Protein; S Phase; Tumor Cells, Cultured

PY - 1999

Y1 - 1999

N2 - p16ink4 and pRb, two components of a key G1/S regulatory pathway, and tumor suppressors commonly targeted in oncogenesis, are among the candidates for gene therapy of cancer. Wild-type p16 and a constitutively active pRb(delta cdk) mutant both blocked G1 in short-term experiments, but only p16 imposed a sustained G1 arrest. Unexpectedly, cells conditionally exposed to pRb(delta cdk) entered S phase after 2 days, followed by endoreduplication between days 4-6. The distinct phenotypes evoked by p16 vs pRb(delta cdk) appear mediated by cyclin E/CDK2 which, while active in the pRb(delta cdk)-expressing cells, became rapidly inhibited through restructuring diverse cyclin/CDK/p21 complexes by p16. These results provide novel insights into the roles of p16, pRb and cyclin E in G1/S control and multistep oncogenesis, with implications for gene therapy strategies.

AB - p16ink4 and pRb, two components of a key G1/S regulatory pathway, and tumor suppressors commonly targeted in oncogenesis, are among the candidates for gene therapy of cancer. Wild-type p16 and a constitutively active pRb(delta cdk) mutant both blocked G1 in short-term experiments, but only p16 imposed a sustained G1 arrest. Unexpectedly, cells conditionally exposed to pRb(delta cdk) entered S phase after 2 days, followed by endoreduplication between days 4-6. The distinct phenotypes evoked by p16 vs pRb(delta cdk) appear mediated by cyclin E/CDK2 which, while active in the pRb(delta cdk)-expressing cells, became rapidly inhibited through restructuring diverse cyclin/CDK/p21 complexes by p16. These results provide novel insights into the roles of p16, pRb and cyclin E in G1/S control and multistep oncogenesis, with implications for gene therapy strategies.

U2 - 10.1038/sj.onc.1202777

DO - 10.1038/sj.onc.1202777

M3 - Journal article

C2 - 10435615

VL - 18

SP - 3930

EP - 3935

JO - Oncogene

JF - Oncogene

SN - 0950-9232

IS - 27

ER -

ID: 5015814