Inhibition of pRb phosphorylation and cell-cycle progression by a 20-residue peptide derived from p16CDKN2/INK4A

R Fåhraeus; J M Paramio; K L Ball; S Laín; D P Lane

doi:10.1016/S0960-9822(02)00425-6

Inhibition of pRb phosphorylation and cell-cycle progression by a 20-residue peptide derived from p16CDKN2/INK4A

R Fåhraeus, J M Paramio, K L Ball, S Laín, D P Lane

Research output: Contribution to journal › Article › peer-review

Abstract

The CDKN2/INK4A tumour suppressor gene is deleted or mutated in a large number of human cancers. Overexpression of its product, p16, has been shown to block the transition through the G1/S phase of the cell cycle in a pRb-dependent fashion by inhibiting the cyclin D-dependent kinases cdk4 and cdk6. Reconstitution of p16 function in transformed cells is therefore an attractive target for anti-cancer drug design.

Original language	English
Pages (from-to)	84-91
Number of pages	8
Journal	Current biology : CB
Volume	6
Issue number	1
DOIs	https://doi.org/10.1016/S0960-9822(02)00425-6
Publication status	Published - 1 Jan 1996

Keywords

Amino Acid Sequence
Carrier Proteins
Cell Cycle
Cyclin-Dependent Kinase 4
Cyclin-Dependent Kinase 6
Cyclin-Dependent Kinase Inhibitor p16
Cyclin-Dependent Kinases
Molecular Sequence Data
Peptides
Phosphorylation
Protein-Serine-Threonine Kinases
Proto-Oncogene Proteins
Retinoblastoma Protein
S Phase

Access to Document

10.1016/S0960-9822(02)00425-6

Inhibition of pRb phosphorylation and cell-cycle progression
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http://www.sciencedirect.com/science/article/pii/S0960982202004256

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@article{9e95b5ccbe554c50bfd904eb51b3e3f9,

title = "Inhibition of pRb phosphorylation and cell-cycle progression by a 20-residue peptide derived from p16CDKN2/INK4A",

abstract = "The CDKN2/INK4A tumour suppressor gene is deleted or mutated in a large number of human cancers. Overexpression of its product, p16, has been shown to block the transition through the G1/S phase of the cell cycle in a pRb-dependent fashion by inhibiting the cyclin D-dependent kinases cdk4 and cdk6. Reconstitution of p16 function in transformed cells is therefore an attractive target for anti-cancer drug design.",

keywords = "Amino Acid Sequence, Carrier Proteins, Cell Cycle, Cyclin-Dependent Kinase 4, Cyclin-Dependent Kinase 6, Cyclin-Dependent Kinase Inhibitor p16, Cyclin-Dependent Kinases, Molecular Sequence Data, Peptides, Phosphorylation, Protein-Serine-Threonine Kinases, Proto-Oncogene Proteins, Retinoblastoma Protein, S Phase",

author = "R F{\aa}hraeus and Paramio, {J M} and Ball, {K L} and S La{\'i}n and Lane, {D P}",

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T1 - Inhibition of pRb phosphorylation and cell-cycle progression by a 20-residue peptide derived from p16CDKN2/INK4A

AU - Fåhraeus, R

AU - Paramio, J M

AU - Ball, K L

AU - Laín, S

AU - Lane, D P

PY - 1996/1/1

Y1 - 1996/1/1

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AB - The CDKN2/INK4A tumour suppressor gene is deleted or mutated in a large number of human cancers. Overexpression of its product, p16, has been shown to block the transition through the G1/S phase of the cell cycle in a pRb-dependent fashion by inhibiting the cyclin D-dependent kinases cdk4 and cdk6. Reconstitution of p16 function in transformed cells is therefore an attractive target for anti-cancer drug design.

KW - Amino Acid Sequence

KW - Carrier Proteins

KW - Cell Cycle

KW - Cyclin-Dependent Kinase 4

KW - Cyclin-Dependent Kinase 6

KW - Cyclin-Dependent Kinase Inhibitor p16

KW - Cyclin-Dependent Kinases

KW - Molecular Sequence Data

KW - Peptides

KW - Phosphorylation

KW - Protein-Serine-Threonine Kinases

KW - Proto-Oncogene Proteins

KW - Retinoblastoma Protein

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