Quantification of cell cycle-arresting proteins

Oliver Kepp; Isabelle Martins; Laurie Menger; Mickaël Michaud; Sandy Adjemian; Abdul Qader Sukkurwala; Lorenzo Galluzzi; Guido Kroemer

doi:10.1007/978-1-62703-239-1_7

Quantification of cell cycle-arresting proteins

Oliver Kepp
, Isabelle Martins
, Laurie Menger
, Mickaël Michaud
, Sandy Adjemian
, Abdul Qader Sukkurwala
, Lorenzo Galluzzi
, Guido Kroemer

Cancer Signaling and Microenvironment (CSM)

INSERM; U848
Université Paris-Sud
Université Paris Cité
Centre de Recherche des Cordeliers
Assistance publique – Hôpitaux de Paris

Research output: Chapter in Book/Report/Conference proceeding › Chapter › peer-review

Abstract

Cellular senescence, which can be defined as a stress response preventing the propagation of cells that have accumulated potentially oncogenic alterations, is invariably associated with a permanent cell cycle arrest. Such an irreversible blockage is mainly mediated by the persistent upregulation of one or more cyclindependent kinase inhibitors (CKIs), including (though not limited to) p16^INK4A and p21^CIP1 and p27^KIP1. CKIs operate by binding to cyclin-dependent kinases (CDKs), de facto inhibiting their enzymatic activity. Here, we provide an immunoblotting-based method for the detection and quantification of CKIs in vitro and ex vivo, together with a set of guidelines for the interpretation of results.

Original language	English
Title of host publication	Cell Senescence
Subtitle of host publication	Methods and Protocols
Publisher	Humana Press Inc.
Pages	121-142
Number of pages	22
Volume	965
ISBN (Print)	9781627032384
DOIs	https://doi.org/10.1007/978-1-62703-239-1_7
State	Published - 2013

Publication series

Name	Methods in molecular biology (Clifton, N.J.)
Publisher	Humana Press Inc.
ISSN (Print)	1064-3745

UN SDGs

This output contributes to the following UN Sustainable Development Goals (SDGs)

SDG 3 Good Health and Well-being

Keywords

ARF
Cancer
DNA damage
INK

Access to Document

10.1007/978-1-62703-239-1_7

Cite this

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title = "Quantification of cell cycle-arresting proteins",

abstract = "Cellular senescence, which can be defined as a stress response preventing the propagation of cells that have accumulated potentially oncogenic alterations, is invariably associated with a permanent cell cycle arrest. Such an irreversible blockage is mainly mediated by the persistent upregulation of one or more cyclindependent kinase inhibitors (CKIs), including (though not limited to) p16INK4A and p21CIP1 and p27KIP1. CKIs operate by binding to cyclin-dependent kinases (CDKs), de facto inhibiting their enzymatic activity. Here, we provide an immunoblotting-based method for the detection and quantification of CKIs in vitro and ex vivo, together with a set of guidelines for the interpretation of results.",

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T1 - Quantification of cell cycle-arresting proteins

AU - Kepp, Oliver

AU - Martins, Isabelle

AU - Menger, Laurie

AU - Michaud, Mickaël

AU - Adjemian, Sandy

AU - Sukkurwala, Abdul Qader

AU - Galluzzi, Lorenzo

AU - Kroemer, Guido

PY - 2013

Y1 - 2013

N2 - Cellular senescence, which can be defined as a stress response preventing the propagation of cells that have accumulated potentially oncogenic alterations, is invariably associated with a permanent cell cycle arrest. Such an irreversible blockage is mainly mediated by the persistent upregulation of one or more cyclindependent kinase inhibitors (CKIs), including (though not limited to) p16INK4A and p21CIP1 and p27KIP1. CKIs operate by binding to cyclin-dependent kinases (CDKs), de facto inhibiting their enzymatic activity. Here, we provide an immunoblotting-based method for the detection and quantification of CKIs in vitro and ex vivo, together with a set of guidelines for the interpretation of results.

AB - Cellular senescence, which can be defined as a stress response preventing the propagation of cells that have accumulated potentially oncogenic alterations, is invariably associated with a permanent cell cycle arrest. Such an irreversible blockage is mainly mediated by the persistent upregulation of one or more cyclindependent kinase inhibitors (CKIs), including (though not limited to) p16INK4A and p21CIP1 and p27KIP1. CKIs operate by binding to cyclin-dependent kinases (CDKs), de facto inhibiting their enzymatic activity. Here, we provide an immunoblotting-based method for the detection and quantification of CKIs in vitro and ex vivo, together with a set of guidelines for the interpretation of results.

KW - ARF

KW - Cancer

KW - DNA damage

KW - INK

UR - https://www.scopus.com/pages/publications/84878859124

U2 - 10.1007/978-1-62703-239-1_7

DO - 10.1007/978-1-62703-239-1_7

M3 - Chapter

C2 - 23296654

AN - SCOPUS:84878859124

SN - 9781627032384

VL - 965

T3 - Methods in molecular biology (Clifton, N.J.)

SP - 121

EP - 142

BT - Cell Senescence

PB - Humana Press Inc.

ER -

Quantification of cell cycle-arresting proteins

Abstract

Publication series

UN SDGs

Keywords

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