High levels of phosphorylated c-Jun, Fra-1, Fra-2 and ATF-2 proteins correlate with malignant phenotypes in the multistage mouse skin carcinogenesis model. (Q53406451)

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English	High levels of phosphorylated c-Jun, Fra-1, Fra-2 and ATF-2 proteins correlate with malignant phenotypes in the multistage mouse skin carcinogenesis model.	scientific article

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scholarly article

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Europe PubMed Central

14 May 2018

http://europepmc.org/abstract/MED/10962557

High levels of phosphorylated c-Jun, Fra-1, Fra-2 and ATF-2 proteins correlate with malignant phenotypes in the multistage mouse skin carcinogenesis model. (English)

1 reference

Europe PubMed Central

14 May 2018

http://europepmc.org/abstract/MED/10962557

phosphorylation

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Spiros Linardopoulos

3

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Europe PubMed Central

14 May 2018

http://europepmc.org/abstract/MED/10962557

author name string

Zoumpourlis V

1

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Europe PubMed Central

14 May 2018

http://europepmc.org/abstract/MED/10962557

Papassava P

2

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Europe PubMed Central

14 May 2018

http://europepmc.org/abstract/MED/10962557

Gillespie D

4

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Europe PubMed Central

14 May 2018

http://europepmc.org/abstract/MED/10962557

Balmain A

5

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Europe PubMed Central

14 May 2018

http://europepmc.org/abstract/MED/10962557

Pintzas A

6

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14 May 2018

http://europepmc.org/abstract/MED/10962557

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1 August 2000

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http://europepmc.org/abstract/MED/10962557

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Europe PubMed Central

14 May 2018

http://europepmc.org/abstract/MED/10962557

19

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Europe PubMed Central

14 May 2018

http://europepmc.org/abstract/MED/10962557

35

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Europe PubMed Central

14 May 2018

http://europepmc.org/abstract/MED/10962557

4011-4021

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Europe PubMed Central

14 May 2018

http://europepmc.org/abstract/MED/10962557

https://scigraph.springernature.com/pub.10.1038/sj.onc.1203732

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Transforming p21ras mutants and c-Ets-2 activate the cyclin D1 promoter through distinguishable regions

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12-O-tetradecanoyl-phorbol-13-acetate induction of the human collagenase gene is mediated by an inducible enhancer element located in the 5'-flanking region

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

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Ha-Ras augments c-Jun activity and stimulates phosphorylation of its activation domain

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Human proto-oncogene c-jun encodes a DNA binding protein with structural and functional properties of transcription factor AP-1

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A rapid and sensitive method for the quantitation of microgram quantities of protein utilizing the principle of protein-dye binding

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Genetic changes in skin tumor progression: correlation between presence of a mutant ras gene and loss of heterozygosity on mouse chromosome 7.

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Increasing complexity of Ras signaling.

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High-efficiency transformation of mammalian cells by plasmid DNA

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Jun-B differs in its biological properties from, and is a negative regulator of, c-Jun

1 reference

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fra-1: a serum-inducible, cellular immediate-early gene that encodes a fos-related antigen.

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JNK1: a protein kinase stimulated by UV light and Ha-Ras that binds and phosphorylates the c-Jun activation domain

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Constitutive AP-1 DNA binding and transactivating ability of malignant but not benign mouse epidermal cells

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A gel electrophoresis method for quantifying the binding of proteins to specific DNA regions: application to components of the Escherichia coli lactose operon regulatory system

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Harvey and Kirsten sarcoma viruses promote the growth and differentiation of erythroid precursor cells in vitro

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Rescue of cells from ras oncogene-induced growth arrest by a second, complementing, oncogene

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STATs: signal transducers and activators of transcription

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Cellular transformation and malignancy induced by ras require c-jun

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AP-1 function and regulation

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ATF-2 has intrinsic histone acetyltransferase activity which is modulated by phosphorylation

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Reduction of p53 gene dosage does not increase initiation or promotion but enhances malignant progression of chemically induced skin tumors.

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

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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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Stress-activated protein kinases are negatively regulated by cell density.

1 reference

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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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Transformation suppressor activity of a Jun transcription factor lacking its activation domain

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Transformation by ras modifies AP1 composition and activity

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Phosphorylation and high level expression of Fra-2 in v-src transformed cells: a pathway of activation of endogenous AP-1.

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Isolation and characterization of fra-2, an additional member of the fos gene family

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

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Phosphorylation of c-jun mediated by MAP kinases.

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Comparison of ras activation during epidermal carcinogenesis in vitro and in vivo

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Carcinogen-specific mutation and amplification of Ha-ras during mouse skin carcinogenesis

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A gene activated by growth factors is related to the oncogene v-jun

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c-fos is required for malignant progression of skin tumors.

1 reference

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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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jun-B inhibits and c-fos stimulates the transforming and trans-activating activities of c-jun

1 reference

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Mammalian G1 cyclins

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Oncogenic and transcriptional cooperation with Ha-Ras requires phosphorylation of c-Jun on serines 63 and 73

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The conversion of mouse skin squamous cell carcinomas to spindle cell carcinomas is a recessive event

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Ternary complex factors: growth factor regulated transcriptional activators

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Autocrine growth and anchorage independence: two complementing Jun-controlled genetic programs of cellular transformation.

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Stepwise transformation of rat embryo fibroblasts: c-Jun, JunB, or JunD can cooperate with Ras for focus formation, but a c-Jun-containing heterodimer is required for immortalization

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Oncogenic Ras activates c-Jun via a separate pathway from the activation of extracellular signal-regulated kinases

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Microinjection of the oncogene form of the human H-ras (T-24) protein results in rapid proliferation of quiescent cells

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The product of a novel growth factor activated gene, fos B, interacts with JUN proteins enhancing their DNA binding activity

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Identifiers

10.1038/SJ.ONC.1203732

1 reference

Europe PubMed Central

14 May 2018

http://europepmc.org/abstract/MED/10962557

1 reference

Europe PubMed Central

14 May 2018

http://europepmc.org/abstract/MED/10962557

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