Growth inhibition of astrocytoma cells by farnesyl transferase inhibitors is mediated by a combination of anti-proliferative, pro-apoptotic and anti-angiogenic effects. (Q55476334)

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scientific article published in December 1999

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English	Growth inhibition of astrocytoma cells by farnesyl transferase inhibitors is mediated by a combination of anti-proliferative, pro-apoptotic and anti-angiogenic effects.	scientific article published in December 1999

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scholarly article

1 reference

Europe PubMed Central

PubMed publication ID

12 July 2018

http://europepmc.org/abstract/MED/10602510

Growth inhibition of astrocytoma cells by farnesyl transferase inhibitors is mediated by a combination of anti-proliferative, pro-apoptotic and anti-angiogenic effects. (English)

1 reference

Europe PubMed Central

PubMed publication ID

12 July 2018

http://europepmc.org/abstract/MED/10602510

angiogenesis inhibitor

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based on heuristic

inferred from title

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based on heuristic

inferred from title

apoptotic process

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author name string

Feldkamp MM

1

1 reference

Europe PubMed Central

PubMed publication ID

12 July 2018

http://europepmc.org/abstract/MED/10602510

Lau N

2

1 reference

Europe PubMed Central

PubMed publication ID

12 July 2018

http://europepmc.org/abstract/MED/10602510

Guha A

3

1 reference

Europe PubMed Central

PubMed publication ID

12 July 2018

http://europepmc.org/abstract/MED/10602510

language of work or name

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publication date

1 December 1999

1 reference

Europe PubMed Central

PubMed publication ID

12 July 2018

http://europepmc.org/abstract/MED/10602510

1 reference

Europe PubMed Central

PubMed publication ID

12 July 2018

http://europepmc.org/abstract/MED/10602510

18

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Europe PubMed Central

PubMed publication ID

12 July 2018

http://europepmc.org/abstract/MED/10602510

52

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Europe PubMed Central

PubMed publication ID

12 July 2018

http://europepmc.org/abstract/MED/10602510

7514-7526

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Europe PubMed Central

PubMed publication ID

12 July 2018

http://europepmc.org/abstract/MED/10602510

1 reference

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Activation of mitogen-activated protein kinase kinase by v-Raf in NIH 3T3 cells and in vitro

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Regulation of p21ras by GTPase activating proteins and guanine nucleotide exchange proteins

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Cell growth inhibition by farnesyltransferase inhibitors is mediated by gain of geranylgeranylated RhoB.

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Inhibition of NIH 3T3 cell proliferation by a mutant ras protein with preferential affinity for GDP.

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Normoxic and hypoxic regulation of vascular endothelial growth factor (VEGF) by astrocytoma cells is mediated by Ras.

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Hypoxia-induced transcription of the vascular endothelial growth factor gene is independent of functional AP-1 transcription factor

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Identification of programmed cell death in situ via specific labeling of nuclear DNA fragmentation

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Both v-Ha-Ras and v-Raf Stimulate Expression of the Vascular Endothelial Growth Factor in NIH 3T3 Cells

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Expression of PDGF and PDGF receptors in human astrocytoma operation specimens supports the existence of an autocrine loop.

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Proliferation of human malignant astrocytomas is dependent on Ras activation

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Expression of platelet derived growth factor and platelet derived growth factor receptor mRNA in a glioblastoma from a patient with Li-Fraumeni syndrome

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A polybasic domain or palmitoylation is required in addition to the CAAX motif to localize p21ras to the plasma membrane

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Activation of the MAP kinase pathway by the protein kinase raf

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Phosphorylation of neurofibromatosis type 1 gene product (neurofibromin) by cAMP-dependent protein kinase

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Resistance of K-RasBV12 proteins to farnesyltransferase inhibitors in Rat1 cells

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Bcl-2 and Bax function independently to regulate cell death

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Selective inhibition of ras-dependent transformation by a farnesyltransferase inhibitor

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Protein farnesyltransferase inhibitors block the growth of ras-dependent tumors in nude mice

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Raf-1 activates MAP kinase-kinase

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Inhibition of DNA synthesis by a farnesyltransferase inhibitor involves inhibition of the p70(s6k) pathway

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Evidence that farnesyltransferase inhibitors suppress Ras transformation by interfering with Rho activity

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Ras CAAX Peptidomimetic FTI-277 Selectively Blocks Oncogenic Ras Signaling by Inducing Cytoplasmic Accumulation of Inactive Ras-Raf Complexes

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Disruption of Oncogenic K-Ras4B Processing and Signaling by a Potent Geranylgeranyltransferase I Inhibitor

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Post-transcriptional regulation of vascular endothelial growth factor by hypoxia

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Specificity of receptor tyrosine kinase signaling: transient versus sustained extracellular signal-regulated kinase activation

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Unfarnesylated transforming Ras mutant inhibits the Ras-signaling pathway by forming a stable Ras.Raf complex in the cytosol

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Signals from Ras and Rho GTPases interact to regulate expression of p21Waf1/Cip1.

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Vascular endothelial growth factor is a potential tumour angiogenesis factor in human gliomas in vivo.

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Farnesyltransferase inhibition causes morphological reversion of ras-transformed cells by a complex mechanism that involves regulation of the actin cytoskeleton

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The small GTP-binding protein rac regulates growth factor-induced membrane ruffling

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The SH2 and SH3 domains of mammalian Grb2 couple the EGF receptor to the Ras activator mSos1

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A farnesyl-protein transferase inhibitor induces p21 expression and G1 block in p53 wild type tumor cells

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Dominant-negative mutants of platelet-derived growth factor revert the transformed phenotype of human astrocytoma cells

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Requirement for c-ras proteins during viral oncogene transformation

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Inhibition of farnesyltransferase induces regression of mammary and salivary carcinomas in ras transgenic mice

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10.1038/SJ.ONC.1203105

1 reference

Europe PubMed Central

PubMed publication ID

12 July 2018

http://europepmc.org/abstract/MED/10602510

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PubMed publication ID

1 reference

Europe PubMed Central

PubMed publication ID

12 July 2018

http://europepmc.org/abstract/MED/10602510

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