Heterodimerization with Fra-1 cooperates with the ERK pathway to stabilize c-Jun in response to the RAS oncoprotein. (Q39693837)

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5 February 2020

title

Heterodimerization with Fra-1 cooperates with the ERK pathway to stabilize c-Jun in response to the RAS oncoprotein (English)

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protein heterodimerization activity

5 February 2020

main subject

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3

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5 February 2020

Jihane Basbous

5

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5 February 2020

author name string

F Talotta

1

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5 February 2020

T Mega

2

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5 February 2020

L Casalino

4

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5 February 2020

I Jariel-Encontre

6

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5 February 2020

M Piechaczyk

7

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5 February 2020

P Verde

8

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5 February 2020

language of work or name

English

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publication date

14 June 2010

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5 February 2020

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5 February 2020

volume

29

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issue

33

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page(s)

4732-4740

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https://scigraph.springernature.com/pub.10.1038/onc.2010.211

5 February 2020

exact match

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cites work

Transcriptional activation of the fra-1 gene by AP-1 is mediated by regulatory sequences in the first intron

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Ubiquitination and degradation of ATF2 are dimerization dependent

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Fra-1 induces morphological transformation and increases in vitro invasiveness and motility of epithelioid adenocarcinoma cells

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Deciphering AP-1 function in tumorigenesis: fra-ternizing on target promoters

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ERK signaling regulates tumor promoter induced c-Jun recruitment at the Fra-1 promoter

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Critical regulation of genes for tumor cell migration by AP-1.

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Promoter specificity and biological activity of tethered AP-1 dimers

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Ubiquitin-independent proteasomal degradation of Fra-1 is antagonized by Erk1/2 pathway-mediated phosphorylation of a unique C-terminal destabilizer

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FRA-1 expression level regulates proliferation and invasiveness of breast cancer cells.

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c-Fos Proto-Oncoprotein Is Degraded by the Proteasome Independently of Its Own Ubiquitinylation In Vivo

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Fra-1 promotes growth and survival in RAS-transformed thyroid cells by controlling cyclin A transcription

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Accumulation of Fra-1 in ras-transformed cells depends on both transcriptional autoregulation and MEK-dependent posttranslational stabilization

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Close encounters of many kinds: Fos-Jun interactions that mediate transcription regulatory specificity.

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Dose-dependent inhibition of thyroid differentiation by RAS oncogenes

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AP-1: a double-edged sword in tumorigenesis

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The structural determinants responsible for c-Fos protein proteasomal degradation differ according to the conditions of expression.

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Jun turnover is controlled through JNK-dependent phosphorylation of the E3 ligase Itch

31 March 2020

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c-Jun can recruit JNK to phosphorylate dimerization partners via specific docking interactions

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Mutual regulation of c-Jun and ATF2 by transcriptional activation and subcellular localization

31 March 2020

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Heterodimerization with Jun family members regulates c-Fos nucleocytoplasmic traffic.

31 March 2020

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Heterodimerization with different Jun proteins controls c-Fos intranuclear dynamics and distribution

31 March 2020

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JUN oncogene amplification and overexpression block adipocytic differentiation in highly aggressive sarcomas

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A reinvestigation of the multisite phosphorylation of the transcription factor c-Jun

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Reduced ubiquitin-dependent degradation of c-Jun after phosphorylation by MAP kinases

31 March 2020

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The ubiquitin ligase SCFFbw7 antagonizes apoptotic JNK signaling

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Yeast GCN4 as a probe for oncogenesis by AP-1 transcription factors: transcriptional activation through AP-1 sites is not sufficient for cellular transformation

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Transcription factors control invasion: AP-1 the first among equals

31 March 2020

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Targeted degradation of c-Fos, but not v-Fos, by a phosphorylation-dependent signal on c-Jun

31 March 2020

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Distinct roles for JNK1 and JNK2 in regulating JNK activity and c-Jun-dependent cell proliferation

31 March 2020

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An autoregulatory loop mediated by miR-21 and PDCD4 controls the AP-1 activity in RAS transformation

31 March 2020

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Ubiquitin-dependent c-Jun degradation in vivo is mediated by the delta domain

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Neoplastic transformation of rat thyroid cells requires the junB and fra-1 gene induction which is dependent on the HMGI-C gene product

31 March 2020

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ERK-MAPK signaling coordinately regulates activity of Rac1 and RhoA for tumor cell motility

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Classification of human B-ZIP proteins based on dimerization properties

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