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

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

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

http://www.wikidata.org/entity/Q35196825

about

Role of the ATFa/JNK2 complex in Jun activation Vanadate induction of NF-kB involves IkB kinase B and SAPK/ERK kinasa 1 in macrophages TAF7 (TAFII55) plays a role in the transcription activation by c-Jun In situ proximity ligation detection of c-Jun/AP-1 dimers reveals increased levels of c-Jun/Fra1 complexes in aggressive breast cancer cell lines in vitro and in vivo TIP49b, a regulator of activating transcription factor 2 response to stress and DNA damage Prothymosin alpha interacts with the CREB-binding protein and potentiates transcription.c-Jun regulates cell cycle progression and apoptosis by distinct mechanisms Regulation of JNK signaling by GSTp Classification of human B-ZIP proteins based on dimerization properties A nuclear isoform of the focal adhesion LIM-domain protein Trip6 integrates activating and repressing signals at AP-1- and NF-kappaB-regulated promoters Jun blockade of erythropoiesis: role for repression of GATA-1 by HERP2.p38 protects human melanoma cells from UV-induced apoptosis through down-regulation of NF-kappaB activity and Fas expression Distinct roles of Jun : Fos and Jun : ATF dimers in oncogenesis Identification of mouse Jun dimerization protein 2 as a novel repressor of ATF-2 AP-1 and Cbfa/runt physically interact and regulate parathyroid hormone-dependent MMP13 expression in osteoblasts through a new osteoblast-specific element 2/AP-1 composite element Identification and characterization of genes upregulated in cells transformed by v-Jun.Deregulation of the signaling pathways controlling urokinase production. Its relationship with the invasive phenotype.Transcription factor ATF2 cooperates with v-Jun to promote growth factor-independent proliferation in vitro and tumor formation in vivo Inhibition of ataxia telangiectasia mutated kinase activity enhances TRAIL-mediated apoptosis in human melanoma cells Emerging roles of ATF2 and the dynamic AP1 network in cancer.The mammalian Jun proteins: redundancy and specificity.Promoter specificity and biological activity of tethered AP-1 dimers.C-Jun N-terminal kinase (JNK) isoforms play differing roles in otitis media An ATF2-derived peptide sensitizes melanomas to apoptosis and inhibits their growth and metastasis.Radiosensitization of melanoma cells through combined inhibition of protein regulators of cell survival.Opposite roles of FAP-1 and dynamin in the regulation of Fas (CD95) translocation to the cell surface and susceptibility to Fas ligand-mediated apoptosis Sequential treatment by ionizing radiation and sodium arsenite dramatically accelerates TRAIL-mediated apoptosis of human melanoma cells.Arsenite sensitizes human melanomas to apoptosis via tumor necrosis factor alpha-mediated pathway.Reduced levels of ATF-2 predispose mice to mammary tumors.JunB is required for endothelial cell morphogenesis by regulating core-binding factor beta.Aberrant expression of c-Jun in glioblastoma by internal ribosome entry site (IRES)-mediated translational activation Heparin-binding epidermal growth factor-like growth factor, a v-Jun target gene, induces oncogenic transformation.Restriction to Fos family members of Trip6-dependent coactivation and glucocorticoid receptor-dependent trans-repression of activator protein-1.Enhanceosomes as integrators of hypoxia inducible factor (HIF) and other transcription factors in the hypoxic transcriptional response.Loss of E-cadherin-mediated cell-cell contacts activates a novel mechanism for up-regulation of the proto-oncogene c-Jun MGSA/GRO-mediated melanocyte transformation involves induction of Ras expression Novel mechanism of JNK pathway activation by adenoviral E1A.Ubiquitination and degradation of ATF2 are dimerization dependent.c-Jun-dependent CD95-L expression is a rate-limiting step in the induction of apoptosis by alkylating agents GAGA can mediate enhancer function in trans by linking two separate DNA molecules.

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

http://www.wikidata.org/entity/Q35196825

description

1998 nî lūn-bûn

@nan

1998 թուականի Ապրիլին հրատարակուած գիտական յօդուած

@hyw

1998 թվականի ապրիլին հրատարակված գիտական հոդված

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1998年の論文

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1998年論文

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1998年論文

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1998年論文

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1998年論文

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1998年論文

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1998年论文

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name

Autocrine growth and anchorage ...... ms of cellular transformation.

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Autocrine growth and anchorage ...... ms of cellular transformation.

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type

label

Autocrine growth and anchorage ...... ms of cellular transformation.

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Autocrine growth and anchorage ...... ms of cellular transformation.

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prefLabel

Autocrine growth and anchorage ...... ms of cellular transformation.

@ast

Autocrine growth and anchorage ...... ms of cellular transformation.

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P1433

Genes & Development

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Autocrine growth and anchorage ...... ams of cellular transformation

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P2093

A J van der Eb

http://www.w3.org/2001/XMLSchema#string

E Vial

http://www.w3.org/2001/XMLSchema#string

J Baguet

http://www.w3.org/2001/XMLSchema#string

K Kooistra

http://www.w3.org/2001/XMLSchema#string

M Castellazzi

http://www.w3.org/2001/XMLSchema#string

P Angel

http://www.w3.org/2001/XMLSchema#string

P Herrlich

http://www.w3.org/2001/XMLSchema#string

S Huguier

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P2860

Cross-family dimerization of transcription factors Fos/Jun and ATF/CREB alters DNA binding specificity

ATF-2 is preferentially activated by stress-activated protein kinases to mediate c-jun induction in response to genotoxic agents

Targeted disruption of the c-fos gene demonstrates c-fos-dependent and -independent pathways for gene expression stimulated by growth factors or oncogenes

Avian sarcoma virus 17 carries the jun oncogene

Interaction of nuclear proteins with an AP-1/CRE-like promoter sequence in the human TNF-alpha gene

Phorbol ester-inducible genes contain a common cis element recognized by a TPA-modulated trans-acting factor

The jun proto-oncogene is positively autoregulated by its product, Jun/AP-1

Metalloproteinases and their inhibitors in matrix remodeling

The role of Jun, Fos and the AP-1 complex in cell-proliferation and transformation

GAL4-VP16 is an unusually potent transcriptional activator

P304

1227-1239

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10.1101/GAD.12.8.1227

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8

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P478

12

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51341723

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9553051

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P932

316714

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