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

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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

Cite this

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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.",

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

year = "1996",

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doi = "10.1016/S0960-9822(02)00425-6",

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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

N2 - 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.

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

KW - S Phase

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DO - 10.1016/S0960-9822(02)00425-6

M3 - Article

C2 - 8805225

VL - 6

SP - 84

EP - 91

JO - Current Biology

JF - Current Biology

SN - 0960-9822

IS - 1

ER -

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

Abstract

Keywords

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