(Q40589278)

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Molecular pathways executing the "trophic sentinel" response in HPV-16 E7-expressing normal human diploid fibroblasts upon growth factor deprivation

scientific article published on February 2004

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scholarly article

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Europe PubMed Central

PubMed publication ID

21 September 2017

Molecular pathways executing the "trophic sentinel" response in HPV-16 E7-expressing normal human diploid fibroblasts upon growth factor deprivation (English)

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Europe PubMed Central

PubMed publication ID

21 September 2017

6

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Europe PubMed Central

PubMed publication ID

21 September 2017

author name string

Alexandra Eichten

1

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Europe PubMed Central

PubMed publication ID

21 September 2017

Debrah S Rud

2

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Europe PubMed Central

PubMed publication ID

21 September 2017

Miranda Grace

3

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Europe PubMed Central

PubMed publication ID

21 September 2017

Siribang-On Piboonniyom

4

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Europe PubMed Central

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21 September 2017

Valerie Zacny

5

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21 September 2017

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publication date

1 February 2004

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Europe PubMed Central

PubMed publication ID

21 September 2017

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13

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21 September 2017

319

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Europe PubMed Central

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21 September 2017

1

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Europe PubMed Central

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21 September 2017

81-93

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Europe PubMed Central

PubMed publication ID

21 September 2017

Suppression of TNF-alpha-induced apoptosis by NF-kappaB

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p14ARF links the tumour suppressors RB and p53.

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Apoptotic cell death induced by c-myc is inhibited by bcl-2.

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The evolution of a mechanism of cell suicide

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Induction of the growth inhibitor IGF-binding protein 3 by p53

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Insulin-like growth factor-binding protein-5 inhibits the growth of human breast cancer cells in vitro and in vivo

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Role for NF-kappa B in mediating the effects of hyperoxia on IGF-binding protein 2 promoter activity in lung alveolar epithelial cells

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Cellular survival: a play in three Akts

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Wild-type p53 mediates apoptosis by E1A, which is inhibited by E1B.

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Elevated wild-type p53 protein levels in human epithelial cell lines immortalized by the human papillomavirus type 16 E7 gene

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Stabilization and functional impairment of the tumor suppressor p53 by the human papillomavirus type 16 E7 oncoprotein

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Induction of apoptosis in fibroblasts by c-myc protein

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Cooperative interaction between c-myc and bcl-2 proto-oncogenes

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Cellular actions of the insulin-like growth factor binding proteins

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p63 and p73 are required for p53-dependent apoptosis in response to DNA damage

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Degradation of the retinoblastoma tumor suppressor by the human papillomavirus type 16 E7 oncoprotein is important for functional inactivation and is separable from proteasomal degradation of E7.

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Down-regulation of wild-type p53 activity interferes with apoptosis of IL-3-dependent hematopoietic cells following IL-3 withdrawal.

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The central executioners of apoptosis: caspases or mitochondria?

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The Hallmarks of Cancer

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Mediation of c-Myc-induced apoptosis by p53.

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NF-kappaB function in growth control: regulation of cyclin D1 expression and G0/G1-to-S-phase transition

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Requirement for the CD95 receptor-ligand pathway in c-Myc-induced apoptosis

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Regulation of the specific DNA binding function of p53

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Destabilization of the RB tumor suppressor protein and stabilization of p53 contribute to HPV type 16 E7-induced apoptosis

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Expression of the HPV E7 oncoprotein mimics but does not evoke a p53-dependent cellular DNA damage response pathway

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c-Myc-induced sensitization to apoptosis is mediated through cytochrome c release

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Requirement for caspase-2 in stress-induced apoptosis before mitochondrial permeabilization

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The insulin-like growth factor system and cancer

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Cytochrome c and dATP-dependent formation of Apaf-1/caspase-9 complex initiates an apoptotic protease cascade

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Human papillomavirus type 16 E7 oncoprotein binds and inactivates growth-inhibitory insulin-like growth factor binding protein 3

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Death signal-induced localization of p53 protein to mitochondria. A potential role in apoptotic signaling

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Insulin-like growth factor binding protein 5 and apoptosis in mammary epithelial cells

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Requirement of NF-kappaB activation to suppress p53-independent apoptosis induced by oncogenic Ras.

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Signalling pathways involved in the direct effects of IGFBP-5 on breast epithelial cell attachment and survival

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Inhibition of Ced-3/ICE-related proteases does not prevent cell death induced by oncogenes, DNA damage, or the Bcl-2 homologue Bak

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Overexpression of insulin-like growth factor binding protein-5 helps accelerate progression to androgen-independence in the human prostate LNCaP tumor model through activation of phosphatidylinositol 3'-kinase pathway

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Human papillomavirus immortalization and transformation functions

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PUMA, a novel proapoptotic gene, is induced by p53

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E1A-induced processing of procaspase-8 can occur independently of FADD and is inhibited by Bcl-2

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Temporally distinct patterns of p53-dependent and p53-independent apoptosis during mouse lens development.

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Suppression of Myc-induced apoptosis in beta cells exposes multiple oncogenic properties of Myc and triggers carcinogenic progression.

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E2F-1 potentiates cell death by blocking antiapoptotic signaling pathways

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E1A is sufficient by itself to induce apoptosis independent of p53 and other adenoviral gene products.

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The adenovirus E1A proteins induce apoptosis, which is inhibited by the E1B 19-kDa and Bcl-2 proteins

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Role of NF-κB in p53-mediated programmed cell death

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The E6 oncoprotein encoded by human papillomavirus types 16 and 18 promotes the degradation of p53

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The HPV-16 E6 and E6-AP complex functions as a ubiquitin-protein ligase in the ubiquitination of p53

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p53 Signaling and cell cycle checkpoints

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Differential disruption of genomic integrity and cell cycle regulation in normal human fibroblasts by the HPV oncoproteins.

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10.1016/J.VIROL.2003.11.008

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Europe PubMed Central

PubMed publication ID

21 September 2017

PubMed publication ID

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PubMed publication ID

21 September 2017

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