Loss of p21WAF1/CIP1 accelerates Ras oncogenesis in a transgenic/knockout mammary cancer model (Q73263614)

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2 November 2019

title

Loss of p21WAF1/CIP1 accelerates Ras oncogenesis in a transgenic/knockout mammary cancer model (English)

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2 November 2019

author name string

Adnane J

1

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2 November 2019

Jackson RJ

2

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2 November 2019

Nicosia SV

3

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2 November 2019

Cantor AB

4

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2 November 2019

Pledger WJ

5

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2 November 2019

Sebti SM

6

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2 November 2019

language of work or name

English

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publication date

1 November 2000

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2 November 2019

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2 November 2019

volume

19

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2 November 2019

issue

47

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2 November 2019

page(s)

5338-5347

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https://scigraph.springernature.com/pub.10.1038/sj.onc.1203956

2 November 2019

exact match

0 references

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p21(WAF1/CIP1) is upregulated by the geranylgeranyltransferase I inhibitor GGTI-298 through a transforming growth factor beta- and Sp1-responsive element: involvement of the small GTPase rhoA.

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Ha-ras oncogene expression directed by a milk protein gene promoter: tissue specificity, hormonal regulation, and tumor induction in transgenic mice

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Ha-ras and c-myc oncogene expression interferes with morphological and functional differentiation of mammary epithelial cells in single and double transgenic mice

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Susceptibility to apoptosis is differentially regulated by c-myc and mutated Ha-ras oncogenes and is associated with endonuclease availability

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Functional analysis of a p21WAF1,CIP1,SDI1 mutant (Arg94 --> Trp) identified in a human breast carcinoma. Evidence that the mutation impairs the ability of p21 to inhibit cyclin-dependent kinases.

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MMTV-Fgf8 transgenic mice develop mammary and salivary gland neoplasia and ovarian stromal hyperplasia

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H-, K- and N-Ras inhibit myeloid leukemia cell proliferation by a p21WAF1-dependent mechanism

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Mice lacking p21CIP1/WAF1 undergo normal development, but are defective in G1 checkpoint control

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Cell cycle: routine role for Ras.

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Diabetes induced in male transgenic mice by expression of human H-ras oncoprotein in pancreatic beta cells

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Relationship between Ras pathways and cell cycle control.

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In vitro establishment is not a sufficient prerequisite for transformation by activated ras oncogenes.

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Cellular ras and cyclin D1 are required during different cell cycle periods in cycling NIH 3T3 cells

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Activated H-ras rescues E1A-induced apoptosis and cooperates with E1A to overcome p53-dependent growth arrest

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Ras transformation results in an elevated level of cyclin D1 and acceleration of G1 progression in NIH 3T3 cells

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Cooperating oncogenes converge to regulate cyclin/cdk complexes.

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The absence of p21Cip1/WAF1 alters keratinocyte growth and differentiation and promotes ras-tumor progression.

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7 January 2021

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7 January 2021

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7 January 2021

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7 January 2021

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7 January 2021

Tyrosine phosphorylation of the proto-oncoprotein Raf-1 is regulated by Raf-1 itself and the phosphatase Cdc25A

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7 January 2021

N-myc can cooperate with ras to transform normal cells in culture

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7 January 2021

Increased susceptibility to carcinogen-induced mammary tumors in MMTV-Cdc25B transgenic mice

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7 January 2021

Proliferating cell nuclear antigen and p21 are components of multiple cell cycle kinase complexes

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7 January 2021