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The ALK inhibitor PF-06463922 is effective as a single agent in neuroblastoma driven by expression of ALK and MYCN

Disease models & mechanisms, 2016-09, Vol.9 (9), p.941-952

2016

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Activation of cAMP and mitogen responsive genes relies on a common nuclear factor

Nature (London), 1994-07, Vol.370 (6486), p.226-229

1994

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c-Jun N-terminal phosphorylation correlates with activation of the JNK subgroup but not the ERK subgroup of mitogen-activated protein kinases

Molecular and Cellular Biology, 1994-10, Vol.14 (10), p.6683-6688

1994

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397P Early decreases in KRAS mutant allele frequency (MAF) predicts clinical benefit to the PLK1 inhibitor onvansertib in combination with FOLFIRI/bev in 2L treatment of metastatic colorectal carcinoma (mCRC)

Annals of oncology, 2022-09, Vol.33, p.S718-S719

2022

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Altering the specificity of signal transduction cascades: positive regulation of c‐Jun transcriptional activity by protein kinase A

The EMBO journal, 1994-12, Vol.13 (24), p.6006-6010

1994

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366P The PLK1 inhibitor onvansertib overcomes irinotecan resistance in RAS-mutated (mRAS) metastatic colorectal cancer (mCRC) in vivo and in patients (pts)

Annals of oncology, 2022-09, Vol.33, p.S704

2022

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Oncoprotein-mediated signalling cascade stimulates c-Jun activity by phosphorylation of serines 63 and 73

Molecular and Cellular Biology, 1992-08, Vol.12 (8), p.3507-3513

1992

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Different requirements for formation of Jun: Jun and Jun: fos complexes

Genes & development, 1989-12, Vol.3 (12B), p.2091-2100

1989

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PAK4 mediates morphological changes through the regulation of GEF-H1

Journal of cell science, 2005-05, Vol.118 (9), p.1861-1872

2005

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Requirement for PAK4 in the Anchorage-independent Growth of Human Cancer Cell Lines

The Journal of biological chemistry, 2002-01, Vol.277 (1), p.550-558

2002

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P3.07-006 Pemetrexed Exerts Intratumor Immunomodulatory Effects and Enhances Efficacy of Immune Checkpoint Blockade in MC38 Syngeneic Mouse Tumor Model

Journal of thoracic oncology, 2017-11, Vol.12 (11), p.S2300-S2300

2017

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Malignant wound management: what dressings do nurses use?

Journal of wound care, 2001-03, Vol.10 (3), p.65-69

2001

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Villin Sequence and Peptide Map Identify Six Homologous Domains

Proceedings of the National Academy of Sciences - PNAS, 1988-07, Vol.85 (14), p.4986-4990

1988

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Abstract B12: The ALK inhibitor PF-06463922 shows significant response as a single agent in ALK/MYCN driven models of neuroblastoma

Cancer research (Chicago, Ill.), 2016-03, Vol.76 (5_Supplement), p.B12-B12

2016

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The Serine/Threonine Kinase Nek6 Is Required for Cell Cycle Progression through Mitosis

The Journal of biological chemistry, 2003-12, Vol.278 (52), p.52454-52460

2003

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Control of transcription factors by signal transduction pathways: the beginning of the end

Trends in biochemical sciences (Amsterdam. Regular ed.), 1992-10, Vol.17 (10), p.418-422

1992

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Loss of Transcriptional Silencing Causes Sterility in Old Mother Cells of S. cerevisiae

Cell, 1996-02, Vol.84 (4), p.633-642

1996

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The mammalian ultraviolet response is triggered by activation of src tyrosine kinases

Cell, 1992-12, Vol.71 (7), p.1081-1091

1992

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

Nature (London), 1991-05, Vol.351 (6322), p.122-127

1991

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

Cell, 1988-12, Vol.55 (5), p.875-885

1988

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Contribution of the epithelial-mesenchymal (EMT) phenotype to the sensitivity of colorectal cancer cell lines to the p21-activated kinase inhibitor, PF-3758309

Journal of clinical oncology, 2011-02, Vol.29 (4_suppl), p.438-438

2011

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

Nature (London), 1991-12, Vol.354 (6353), p.494-496

1991

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Transcriptional interference between c-Jun and the glucocorticoid receptor: Mutual inhibition of DNA binding due to direct protein-protein interaction

Cell, 1990-09, Vol.62 (6), p.1205-1215

1990

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Activation of protein kinase C decreases phosphorylation of c-Jun at sites that negatively regulate its DNA-binding activity

Cell, 1991-02, Vol.64 (3), p.573-584

1991

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Casein kinase II is a negative regulator of c-Jun DNA binding and AP-1 activity

Cell, 1992-09, Vol.70 (5), p.777-789

1992

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The ALK inhibitor PF-06463922 is effective as a single agent in neuroblastoma driven by expression of ALK and MYCN

Activation of cAMP and mitogen responsive genes relies on a common nuclear factor

c-Jun N-terminal phosphorylation correlates with activation of the JNK subgroup but not the ERK subgroup of mitogen-activated protein kinases

397P Early decreases in KRAS mutant allele frequency (MAF) predicts clinical benefit to the PLK1 inhibitor onvansertib in combination with FOLFIRI/bev in 2L treatment of metastatic colorectal carcinoma (mCRC)

Altering the specificity of signal transduction cascades: positive regulation of c‐Jun transcriptional activity by protein kinase A

366P The PLK1 inhibitor onvansertib overcomes irinotecan resistance in RAS-mutated (mRAS) metastatic colorectal cancer (mCRC) in vivo and in patients (pts)

Oncoprotein-mediated signalling cascade stimulates c-Jun activity by phosphorylation of serines 63 and 73

Different requirements for formation of Jun: Jun and Jun: fos complexes

PAK4 mediates morphological changes through the regulation of GEF-H1

Requirement for PAK4 in the Anchorage-independent Growth of Human Cancer Cell Lines

P3.07-006 Pemetrexed Exerts Intratumor Immunomodulatory Effects and Enhances Efficacy of Immune Checkpoint Blockade in MC38 Syngeneic Mouse Tumor Model

Malignant wound management: what dressings do nurses use?

Villin Sequence and Peptide Map Identify Six Homologous Domains

Abstract B12: The ALK inhibitor PF-06463922 shows significant response as a single agent in ALK/MYCN driven models of neuroblastoma

The Serine/Threonine Kinase Nek6 Is Required for Cell Cycle Progression through Mitosis

Control of transcription factors by signal transduction pathways: the beginning of the end

Loss of Transcriptional Silencing Causes Sterility in Old Mother Cells of S. cerevisiae

The mammalian ultraviolet response is triggered by activation of src tyrosine kinases

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

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

Contribution of the epithelial-mesenchymal (EMT) phenotype to the sensitivity of colorectal cancer cell lines to the p21-activated kinase inhibitor, PF-3758309

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

Transcriptional interference between c-Jun and the glucocorticoid receptor: Mutual inhibition of DNA binding due to direct protein-protein interaction

Activation of protein kinase C decreases phosphorylation of c-Jun at sites that negatively regulate its DNA-binding activity

Casein kinase II is a negative regulator of c-Jun DNA binding and AP-1 activity

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