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The CDC42-specific inhibitor derived from ACK-1 blocks v-Ha-Ras-induced transformation

Oncogene, 1999-12, Vol.18 (54), p.7787-7793

1999

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The role of Rho GTPases in the regulation of the rearrangement of actin cytoskeleton and cell movement

Experimental & molecular medicine, 2004-08, Vol.36 (4), p.358-366

2004

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Differential Requirement for Rho Family GTPases in an Oncogenic Insulin-like Growth Factor-I Receptor-induced Cell Transformation

The Journal of biological chemistry, 2001-07, Vol.276 (28), p.26461-26471

2001

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Molecular cloning of a novel mitogen-inducible nuclear protein with a Ran GTPase-activating domain that affects cell cycle progression

Molecular and Cellular Biology, 1995-01, Vol.15 (1), p.552-560

1995

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The GTPase-activating NF1 fragment of 91 amino acids reverses v-Ha-Ras-induced malignant phenotype

The Journal of biological chemistry, 1993-10, Vol.268 (30), p.22331-22337

1993

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Proto-oncogene ras GTPase-linked induction of glutathione-S-transferase by growth factors in PC12 cells

International journal of oncology, 2000-05, Vol.16 (5), p.1043

2000

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Serum-dependent perinuclear accumulation of Cdc42 in mammalian cells

Oncology reports, 2001-01, Vol.8 (1), p.71

2001

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Comparative studies on the sensitivity of polymerase chain reaction and microscopic examination for the detection of Trypanosoma evansi in experimentally infected mice

Comparative immunology, microbiology and infectious diseases, 1998-07, Vol.21 (3), p.215-223

1998

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Rsr1 and Rap1 GTPases are activated by the same GTPase-activating protein and require threonine 65 for their activation

The Journal of biological chemistry, 1991-09, Vol.266 (26), p.16992-16995

1991

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Midkine (MK), a Retinoic Acid (RA)-Inducible Gene Product, Produced in E. coli Acts on Neuronal and HL60 Leukemia Cells

Growth factors (Chur, Switzerland), 1993, Vol.8 (2), p.119-134

1993

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Differential expression and characterization of proto-oncogene product Ha-Ras GTPase in camel tissues

International journal of oncology, 1997-07

1997

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rho GAP of 28 kDa (GAP2), but not of 190 kDa (p190), requires Asp65 and Asp67 of rho GTPase for its activation

The Journal of biological chemistry, 1993-12, Vol.268 (36), p.27160-27163

1993

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The GTPase and Rho GAP domains of p190, a tumor suppressor protein that binds the Mr 120,000 Ras GAP, independently function as anti-ras tumor suppressors

Cancer research (Chicago, Ill.), 1997, Vol.57 (12), p.2478-2484

1997

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A synthetic nanofibrillar matrix promotes in vivo-like organization and morphogenesis for cells in culture

Biomaterials, 2005-10, Vol.26 (28), p.5624-5631

2005

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Asparagine 26, glutamic acid 31, valine 45, and tyrosine 64 of ras proteins are requirred for their oncogenicity

The Journal of biological chemistry, 1992, Vol.267 (3), p.1415-1418

1992

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Three dimensional nanofibrillar surfaces induce activation of Rac

Biochemical and biophysical research communications, 2005-06, Vol.331 (2), p.428-434

2005

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Identification of a Neurite Outgrowth-Promoting Motif within the Alternatively Spliced Region of Human Tenascin-C

The Journal of neuroscience, 2001-09, Vol.21 (18), p.7215-7225

2001

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Tenascin-C Contains Domains That Independently Regulate Neurite Outgrowth and Neurite Guidance

The Journal of neuroscience, 1999-10, Vol.19 (19), p.8443-8453

1999

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Neurite guidance by the FnC repeat of human tenascin-C: neurite attraction vs. neurite retention

The European journal of neuroscience, 2005-10, Vol.22 (8), p.1863-1872

2005

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Requirement of Activated Cdc42-Associated Kinase for Survival of v-Ras-Transformed Mammalian Cells

Molecular cancer research, 2005-05, Vol.3 (5), p.297-305

2005

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G proteins, phosphoinositides, and actin‐cytoskeleton in the control of cancer growth

Microscopy research and technique, 1999-10, Vol.47 (1), p.61-66

1999

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Localisation of a gene for an autosomal recessive syndrome of macrocephaly, multiple epiphyseal dysplasia, and distinctive facies to chromosome 15q26

Journal of medical genetics, 2001-06, Vol.38 (6), p.369-373

2001

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Construction of a Cell-Permeable CDC42 Binding Fragment of ACK That Inhibits v-Ha-Ras Transformation

Annals of the New York Academy of Sciences, 1999-01, Vol.886 (1), p.285-288

1999

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The minimal fragments of c-Raf-1 and NF1 that can suppress v-Ha-Ras-induced malignant phenotype

The Journal of biological chemistry, 1994-12, Vol.269 (48), p.30105-30108

1994

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Asparagine 26, glutamic acid 31, valine 45, and tyrosine 64 of Ras proteins are required for their oncogenicity

The Journal of biological chemistry, 1992-01, Vol.267 (3), p.1415-1418

1992

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The CDC42-specific inhibitor derived from ACK-1 blocks v-Ha-Ras-induced transformation

The role of Rho GTPases in the regulation of the rearrangement of actin cytoskeleton and cell movement

Differential Requirement for Rho Family GTPases in an Oncogenic Insulin-like Growth Factor-I Receptor-induced Cell Transformation

Molecular cloning of a novel mitogen-inducible nuclear protein with a Ran GTPase-activating domain that affects cell cycle progression

The GTPase-activating NF1 fragment of 91 amino acids reverses v-Ha-Ras-induced malignant phenotype

Proto-oncogene ras GTPase-linked induction of glutathione-S-transferase by growth factors in PC12 cells

Serum-dependent perinuclear accumulation of Cdc42 in mammalian cells

Comparative studies on the sensitivity of polymerase chain reaction and microscopic examination for the detection of Trypanosoma evansi in experimentally infected mice

Rsr1 and Rap1 GTPases are activated by the same GTPase-activating protein and require threonine 65 for their activation

Midkine (MK), a Retinoic Acid (RA)-Inducible Gene Product, Produced in E. coli Acts on Neuronal and HL60 Leukemia Cells

Differential expression and characterization of proto-oncogene product Ha-Ras GTPase in camel tissues

rho GAP of 28 kDa (GAP2), but not of 190 kDa (p190), requires Asp65 and Asp67 of rho GTPase for its activation

The GTPase and Rho GAP domains of p190, a tumor suppressor protein that binds the Mr 120,000 Ras GAP, independently function as anti-ras tumor suppressors

A synthetic nanofibrillar matrix promotes in vivo-like organization and morphogenesis for cells in culture

Asparagine 26, glutamic acid 31, valine 45, and tyrosine 64 of ras proteins are requirred for their oncogenicity

Three dimensional nanofibrillar surfaces induce activation of Rac

Identification of a Neurite Outgrowth-Promoting Motif within the Alternatively Spliced Region of Human Tenascin-C

Tenascin-C Contains Domains That Independently Regulate Neurite Outgrowth and Neurite Guidance

Neurite guidance by the FnC repeat of human tenascin-C: neurite attraction vs. neurite retention

Requirement of Activated Cdc42-Associated Kinase for Survival of v-Ras-Transformed Mammalian Cells

G proteins, phosphoinositides, and actin‐cytoskeleton in the control of cancer growth

Localisation of a gene for an autosomal recessive syndrome of macrocephaly, multiple epiphyseal dysplasia, and distinctive facies to chromosome 15q26

Construction of a Cell-Permeable CDC42 Binding Fragment of ACK That Inhibits v-Ha-Ras Transformation

The minimal fragments of c-Raf-1 and NF1 that can suppress v-Ha-Ras-induced malignant phenotype

Asparagine 26, glutamic acid 31, valine 45, and tyrosine 64 of Ras proteins are required for their oncogenicity

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