AP-1 dimers regulate transcription of the p14/p19ARF tumor suppressor gene. (Q52058675)

20 April 2018

title

AP-1 dimers regulate transcription of the p14/p19ARF tumor suppressor gene. (English)

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20 April 2018

author

Erwin F. Wagner

4

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20 April 2018

Marta B Wisniewska

object named as

Marta B Wisniewska

2

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Jonathan B. Weitzman

object named as

Jonathan B Weitzman

6

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author name string

Maya Ameyar-Zazoua

1

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20 April 2018

Latifa Bakiri

3

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20 April 2018

Moshe Yaniv

5

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20 April 2018

language of work or name

English

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publication date

1 March 2005

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20 April 2018

published in

Oncogene

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20 April 2018

volume

24

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20 April 2018

page(s)

2298-2306

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20 April 2018

issue

14

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20 April 2018

https://scigraph.springernature.com/pub.10.1038/sj.onc.1208424

exact match

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cites work

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E2F and Ras Synergize in Transcriptionally Activating p14ARFExpression

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Induction of ARF tumor suppressor gene expression and cell cycle arrest by transcription factor DMP1.

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Functional and physical interactions of the ARF tumor suppressor with p53 and Mdm2

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Transcriptional regulation of the human tumor suppressor p14(ARF) by E2F1, E2F2, E2F3, and Sp1-like factors

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Deregulated expression of human c-jun transforms primary rat embryo cells in cooperation with an activated c-Ha-ras gene and transforms rat-1a cells as a single gene

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P19(ARF) stabilizes p53 by blocking nucleo-cytoplasmic shuttling of Mdm2

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A role for AP-1 in apoptosis: the case for and against

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p14ARF links the tumour suppressors RB and p53.

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Oncogenic transformation by ras and fos is mediated by c-Jun N-terminal phosphorylation

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Tumor suppressor p16INK4a determines sensitivity of human cells to transformation by cooperating cellular oncogenes

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Liver tumor development. c-Jun antagonizes the proapoptotic activity of p53

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Rhabdomyosarcoma development in mice lacking Trp53 and Fos

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The oncogene and Polycomb-group gene bmi-1 regulates cell proliferation and senescence through the ink4a locus

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AP-1 in mouse development and tumorigenesis

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Tumor suppression at the mouse INK4a locus mediated by the alternative reading frame product p19ARF

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Loss of p16Ink4a confers susceptibility to metastatic melanoma in mice

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Variations in Jun and Fos protein expression and AP-1 activity in cycling, resting and stimulated fibroblasts

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Transformation by ras modifies AP1 composition and activity

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The mammalian Jun proteins: redundancy and specificity.

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p19ARF links the tumour suppressor p53 to Ras

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Murine fibroblasts lacking p21 undergo senescence and are resistant to transformation by oncogenic Ras.

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Mouse JunD negatively regulates fibroblast growth and antagonizes transformation by ras.

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The Ink4a tumor suppressor gene product, p19Arf, interacts with MDM2 and neutralizes MDM2's inhibition of p53

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Alternative reading frames of the INK4a tumor suppressor gene encode two unrelated proteins capable of inducing cell cycle arrest

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Opposing effects of Ras on p53: transcriptional activation of mdm2 and induction of p19ARF.

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7 January 2021

E2F transcriptional repressor complexes are critical downstream targets of p19(ARF)/p53-induced proliferative arrest

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7 January 2021

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Role of the INK4a locus in tumor suppression and cell mortality.

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Loss of p16Ink4a with retention of p19Arf predisposes mice to tumorigenesis

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The mammalian UV response: c-Jun induction is required for exit from p53-imposed growth arrest

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c-Jun and JunB antagonistically control cytokine-regulated mesenchymal-epidermal interaction in skin

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Characterization of a transcriptional promoter of human papillomavirus 18 and modulation of its expression by simian virus 40 and adenovirus early antigens

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Distinct roles of Jun : Fos and Jun : ATF dimers in oncogenesis

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7 January 2021

Identifiers

DOI

10.1038/SJ.ONC.1208424

1 reference

20 April 2018

Dimensions Publication ID

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1 reference

20 April 2018