MEKK1 regulates the AP-1 dimer repertoire via control of JunB transcription and Fra-2 protein stability (Q38333982)

2 September 2017

MEKK1 regulates the AP-1 dimer repertoire via control of JunB transcription and Fra-2 protein stability (English)

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2 September 2017

Bruce D Cuevas

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2 September 2017

Mark T Uhlik

series ordinal

2

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2 September 2017

Timothy P Garrington

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3

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2 September 2017

Gary L Johnson

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4

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2 September 2017

language of work or name

English

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publication date

1 January 2005

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2 September 2017

24

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801-809

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https://scigraph.springernature.com/pub.10.1038/sj.onc.1208239

2 September 2017

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cites work

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

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Role of distinct mitogen-activated protein kinase pathways and cooperation between Ets-2, ATF-2, and Jun family members in human urokinase-type plasminogen activator gene induction by interleukin-1 and tetradecanoyl phorbol acetate

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c-Jun NH2-terminal kinases target the ubiquitination of their associated transcription factors

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

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The stromal proteinase MMP3/stromelysin-1 promotes mammary carcinogenesis

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Transactivation of Fra-1 and consequent activation of AP-1 occur extracellular signal-regulated kinase dependently

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MEK kinase 1 gene disruption alters cell migration and c-Jun NH2-terminal kinase regulation but does not cause a measurable defect in NF-kappa B activation

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c-Jun regulates eyelid closure and skin tumor development through EGFR signaling

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

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Identifiers

DOI

10.1038/SJ.ONC.1208239

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Dimensions Publication ID

2 September 2017

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1 reference