Deficiency of G1 regulators P53, P21Cip1 and/or pRb decreases hepatocyte sensitivity to TGFbeta cell cycle arrest

Sharon Sheahan; Christopher O Bellamy; Donald R Dunbar; David J Harrison; Sandrine Prost

doi:10.1186/1471-2407-7-215

Deficiency of G1 regulators P53, P21Cip1 and/or pRb decreases hepatocyte sensitivity to TGFbeta cell cycle arrest

Sharon Sheahan, Christopher O Bellamy, Donald R Dunbar, David J Harrison, Sandrine Prost

School of Medicine

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

Abstract

TGFbeta is critical to control hepatocyte proliferation by inducing G1-growth arrest through multiple pathways leading to inhibition of E2F transcription activity. The retinoblastoma protein pRb is a key controller of E2F activity and G1/S transition which can be inhibited in viral hepatitis. It is not known whether the impairment of pRb would alter the growth inhibitory potential of TGFbeta in disease. We asked how Rb-deficiency would affect responses to TGFbeta-induced cell cycle arrest.

Original language	English
Article number	215
Number of pages	10
Journal	BMC Cancer
Volume	7
DOIs	https://doi.org/10.1186/1471-2407-7-215
Publication status	Published - 19 Nov 2007

Keywords

Animals
Cell cycle
Cell proliferation
Cyclin-dependent kinase Inhibitor p16
Cyclin-dependent kinase Inhibitor p21
E2F transcription factors
Fluorescent antibody technique
Hepatocytes
Male
Mice
Mice, Knockout
Proto-oncogene proteins c-myc
Retinoblastoma protein
Signal transduction
Transforming growth factor beta
Tumor suppressor protein p53

UN SDGs

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

Access to Document

10.1186/1471-2407-7-215

sheahan2007bmccancer215
© 2007 Sheahan et al; licensee BioMed Central Ltd. This is an Open Access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/2.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.
Final published version, 749 KB

Cite this

@article{bcb80305da074c01a23aff451bcdfd5a,

title = "Deficiency of G1 regulators P53, P21Cip1 and/or pRb decreases hepatocyte sensitivity to TGFbeta cell cycle arrest",

abstract = "TGFbeta is critical to control hepatocyte proliferation by inducing G1-growth arrest through multiple pathways leading to inhibition of E2F transcription activity. The retinoblastoma protein pRb is a key controller of E2F activity and G1/S transition which can be inhibited in viral hepatitis. It is not known whether the impairment of pRb would alter the growth inhibitory potential of TGFbeta in disease. We asked how Rb-deficiency would affect responses to TGFbeta-induced cell cycle arrest.",

keywords = "Animals, Cell cycle, Cell proliferation, Cyclin-dependent kinase Inhibitor p16, Cyclin-dependent kinase Inhibitor p21, E2F transcription factors, Fluorescent antibody technique, Hepatocytes, Male, Mice, Mice, Knockout, Proto-oncogene proteins c-myc, Retinoblastoma protein, Signal transduction, Transforming growth factor beta, Tumor suppressor protein p53",

author = "Sharon Sheahan and Bellamy, {Christopher O} and Dunbar, {Donald R} and Harrison, {David J} and Sandrine Prost",

year = "2007",

month = nov,

day = "19",

doi = "10.1186/1471-2407-7-215",

language = "English",

volume = "7",

journal = "BMC Cancer",

issn = "1471-2407",

publisher = "BioMed Central",

}

TY - JOUR

T1 - Deficiency of G1 regulators P53, P21Cip1 and/or pRb decreases hepatocyte sensitivity to TGFbeta cell cycle arrest

AU - Sheahan, Sharon

AU - Bellamy, Christopher O

AU - Dunbar, Donald R

AU - Harrison, David J

AU - Prost, Sandrine

PY - 2007/11/19

Y1 - 2007/11/19

N2 - TGFbeta is critical to control hepatocyte proliferation by inducing G1-growth arrest through multiple pathways leading to inhibition of E2F transcription activity. The retinoblastoma protein pRb is a key controller of E2F activity and G1/S transition which can be inhibited in viral hepatitis. It is not known whether the impairment of pRb would alter the growth inhibitory potential of TGFbeta in disease. We asked how Rb-deficiency would affect responses to TGFbeta-induced cell cycle arrest.

AB - TGFbeta is critical to control hepatocyte proliferation by inducing G1-growth arrest through multiple pathways leading to inhibition of E2F transcription activity. The retinoblastoma protein pRb is a key controller of E2F activity and G1/S transition which can be inhibited in viral hepatitis. It is not known whether the impairment of pRb would alter the growth inhibitory potential of TGFbeta in disease. We asked how Rb-deficiency would affect responses to TGFbeta-induced cell cycle arrest.

KW - Animals

KW - Cell cycle

KW - Cell proliferation

KW - Cyclin-dependent kinase Inhibitor p16

KW - Cyclin-dependent kinase Inhibitor p21

KW - E2F transcription factors

KW - Fluorescent antibody technique

KW - Hepatocytes

KW - Male

KW - Mice

KW - Mice, Knockout

KW - Proto-oncogene proteins c-myc

KW - Retinoblastoma protein

KW - Signal transduction

KW - Transforming growth factor beta

KW - Tumor suppressor protein p53

UR - http://www.biomedcentral.com/1471-2407/7/215

U2 - 10.1186/1471-2407-7-215

DO - 10.1186/1471-2407-7-215

M3 - Article

SN - 1471-2407

VL - 7

JO - BMC Cancer

JF - BMC Cancer

M1 - 215

ER -

Deficiency of G1 regulators P53, P21Cip1 and/or pRb decreases hepatocyte sensitivity to TGFbeta cell cycle arrest

Abstract

Keywords

UN SDGs

Access to Document

Other files and links

Fingerprint

Cite this