Search Results - "Hilton, Mary Beth"
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GPR124 Functions as a WNT7-Specific Coactivator of Canonical β-Catenin Signaling
Published in Cell reports (Cambridge) (13-01-2015)“…G protein-coupled receptor 124 (GPR124) is an orphan receptor in the adhesion family of GPCRs, and previous global or endothelial-specific disruption of Gpr124…”
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TEM8/ANTXR1 Blockade Inhibits Pathological Angiogenesis and Potentiates Tumoricidal Responses against Multiple Cancer Types
Published in Cancer cell (14-02-2012)“…Current antiangiogenic agents used to treat cancer only partially inhibit neovascularization and cause normal tissue toxicities, fueling the need to identify…”
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3
Essential Regulation of Lung Surfactant Homeostasis by the Orphan G Protein-Coupled Receptor GPR116
Published in Cell reports (Cambridge) (30-05-2013)“…GPR116 is an orphan seven-pass transmembrane receptor whose function has been unclear. Global disruption of the Gpr116 gene in mice revealed an unexpected,…”
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4
Eradication of Tumors through Simultaneous Ablation of CD276/B7-H3-Positive Tumor Cells and Tumor Vasculature
Published in Cancer cell (10-04-2017)“…Targeting the tumor vasculature with antibody-drug conjugates (ADCs) is a promising anti-cancer strategy that in order to be realized must overcome several…”
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5
Tumor stroma-targeted antibody-drug conjugate triggers localized anticancer drug release
Published in The Journal of clinical investigation (01-07-2018)“…Although nonmalignant stromal cells facilitate tumor growth and can occupy up to 90% of a solid tumor mass, better strategies to exploit these cells for…”
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6
Cancer cell survival depends on collagen uptake into tumor-associated stroma
Published in Nature communications (18-11-2022)“…Collagen I, the most abundant protein in humans, is ubiquitous in solid tumors where it provides a rich source of exploitable metabolic fuel for cancer cells…”
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GPR124, an orphan G protein-coupled receptor, is required for CNS-specific vascularization and establishment of the blood-brain barrier
Published in Proceedings of the National Academy of Sciences - PNAS (05-04-2011)“…Every organ in the body requires blood vessels for efficient delivery of oxygen and nutrients, but independent vascular beds are highly specialized to meet the…”
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Engineering CD276/B7-H3-targeted antibody-drug conjugates with enhanced cancer-eradicating capability
Published in Cell reports (Cambridge) (26-12-2023)“…CD276/B7-H3 represents a promising target for cancer therapy based on widespread overexpression in both cancer cells and tumor-associated stroma. In previous…”
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Host-Derived Tumor Endothelial Marker 8 Promotes the Growth of Melanoma
Published in Cancer research (Chicago, Ill.) (01-08-2009)“…Tumor endothelial marker 8 (TEM8) was initially identified as a gene overexpressed in the vasculature of human tumors and was subsequently identified as an…”
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10
Combined Loss of Cdk2 and Cdk4 Results in Embryonic Lethality and Rb Hypophosphorylation
Published in Developmental cell (01-05-2006)“…Mouse knockouts of Cdk2 and Cdk4 have demonstrated that, individually, these genes are not essential for viability. To investigate whether there is functional…”
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Cdk2 and Cdk4 Activities Are Dispensable for Tumorigenesis Caused by the Loss of p53
Published in Molecular and Cellular Biology (01-05-2009)“…Article Usage Stats Services MCB Citing Articles Google Scholar PubMed Related Content Social Bookmarking CiteULike Delicious Digg Facebook Google+ Mendeley…”
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12
Rb/Cdk2/Cdk4 triple mutant mice elicit an alternative mechanism for regulation of the G₁/S transition
Published in Proceedings of the National Academy of Sciences - PNAS (13-01-2009)“…The G₁/S-phase transition is a well-toned switch in the mammalian cell cycle. Cdk2, Cdk4, and the rate-limiting tumor suppressor retinoblastoma protein (Rb)…”
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13
p21 Inhibits Cdk1 in the absence of Cdk2 to maintain the G1/S phase DNA damage checkpoint
Published in Molecular biology of the cell (01-01-2008)“…Cdk1 was proposed to compensate for the loss of Cdk2. Here we present evidence that this is possible due to premature translocation of Cdk1 from the cytoplasm…”
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COX-2 inhibition potentiates antiangiogenic cancer therapy and prevents metastasis in preclinical models
Published in Science translational medicine (25-06-2014)“…Antiangiogenic agents that block vascular endothelial growth factor (VEGF) signaling are important components of current cancer treatment modalities but are…”
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15
Rb/Cdk2/Cdk4 triple mutant mice elicit an alternative mechanism for regulation of the G 1 /S transition
Published in Proceedings of the National Academy of Sciences - PNAS (13-01-2009)“…The G 1 /S-phase transition is a well-toned switch in the mammalian cell cycle. Cdk2, Cdk4, and the rate-limiting tumor suppressor retinoblastoma protein (Rb)…”
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16
Rb/Cdk2/Cdk4 triple mutant mice elicit an alternative mechanism for regulation of the G^sub 1^/S transition
Published in Proceedings of the National Academy of Sciences - PNAS (13-01-2009)“…The G.../S-phase transition is a well-toned switch in the mammalian cell cycle. Cdk2, Cdk4, and the rate-limiting tumor suppressor retinoblastoma protein (Rb)…”
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Journal Article -
17
Rb/Cdk2/Cdk4 triple mutant mice elicit an alternative mechanism for regulation of the G sub(1)/S transition
Published in Proceedings of the National Academy of Sciences - PNAS (13-01-2009)“…The G sub(1)/S-phase transition is a well-toned switch in the mammalian cell cycle. Cdk2, Cdk4, and the rate-limiting tumor suppressor retinoblastoma protein…”
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Journal Article -
18
Rb/Cdk2/Cdk4 triple mutant mice elicit an alternative mechanism for regulation of the Gâ/S transition
Published in Proceedings of the National Academy of Sciences - PNAS (2009)“…The Gâ/S-phase transition is a well-toned switch in the mammalian cell cycle. Cdk2, Cdk4, and the rate-limiting tumor suppressor retinoblastoma protein (Rb)…”
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Journal Article -
19
GPR124 Functions as a WNT7-Specific Co-Activator of Canonical β-Catenin Signaling
Published in Cell reports (Cambridge) (31-12-2014)“…G-protein coupled receptor 124 (GPR124) is an orphan receptor in the adhesion family of GPCRs and previous global or endothelial-specific disruption of Gpr124…”
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