clozapine-n-oxide and Neoplasms

clozapine-n-oxide has been researched along with Neoplasms* in 2 studies

Other Studies

2 other study(ies) available for clozapine-n-oxide and Neoplasms

Article	Year
Cancer-induced anorexia and malaise are mediated by CGRP neurons in the parabrachial nucleus. Nature neuroscience, 2017, Volume: 20, Issue:7 Anorexia is a common manifestation of chronic diseases, including cancer. Here we investigate the contribution to cancer anorexia made by calcitonin gene-related peptide (CGRP) neurons in the parabrachial nucleus (PBN) that transmit anorexic signals. We show that CGRP Topics: Adenomatous Polyposis Coli Protein; Animals; Anorexia; Behavior, Animal; Body Weight; Cachexia; Calcitonin Gene-Related Peptide; Carcinoma, Lewis Lung; Clozapine; Energy Metabolism; Female; Illness Behavior; Male; Metalloendopeptidases; Mice; Mice, Transgenic; Neoplasms; Parabrachial Nucleus; Tetanus Toxin; Tumor Cells, Cultured	2017
A genome-wide RNAi screen reveals a Trio-regulated Rho GTPase circuitry transducing mitogenic signals initiated by G protein-coupled receptors. Molecular cell, 2013, Jan-10, Volume: 49, Issue:1 Activating mutations in GNAQ and GNA11, encoding members of the Gα(q) family of G protein α subunits, are the driver oncogenes in uveal melanoma, and mutations in Gq-linked G protein-coupled receptors have been identified recently in numerous human malignancies. How Gα(q) and its coupled receptors transduce mitogenic signals is still unclear because of the complexity of signaling events perturbed upon Gq activation. Using a synthetic-biology approach and a genome-wide RNAi screen, we found that a highly conserved guanine nucleotide exchange factor, Trio, is essential for activating Rho- and Rac-regulated signaling pathways acting on JNK and p38, and thereby transducing proliferative signals from Gα(q) to the nucleus independently of phospholipase C-β. Indeed, whereas many biological responses elicited by Gq depend on the transient activation of second-messenger systems, Gq utilizes a hard-wired protein-protein-interaction-based signaling circuitry to achieve the sustained stimulation of proliferative pathways, thereby controlling normal and aberrant cell growth. Topics: Animals; Cell Line, Tumor; Cell Proliferation; Clozapine; Drosophila; Drosophila Proteins; Enzyme Activation; Female; Gene Knockdown Techniques; GTP-Binding Protein alpha Subunits; GTP-Binding Protein alpha Subunits, Gq-G11; Guanine Nucleotide Exchange Factors; Humans; Mice; Mice, Nude; Mitogen-Activated Protein Kinases; Mitogens; Mitosis; Neoplasm Transplantation; Neoplasms; NIH 3T3 Cells; Protein Serine-Threonine Kinases; Receptors, G-Protein-Coupled; rho GTP-Binding Proteins; RNA Interference; Signal Transduction; Transcription Factor AP-1	2013

Article

Year

Cancer-induced anorexia and malaise are mediated by CGRP neurons in the parabrachial nucleus.

Nature neuroscience, 2017, Volume: 20, Issue:7

Anorexia is a common manifestation of chronic diseases, including cancer. Here we investigate the contribution to cancer anorexia made by calcitonin gene-related peptide (CGRP) neurons in the parabrachial nucleus (PBN) that transmit anorexic signals. We show that CGRP

Topics: Adenomatous Polyposis Coli Protein; Animals; Anorexia; Behavior, Animal; Body Weight; Cachexia; Calcitonin Gene-Related Peptide; Carcinoma, Lewis Lung; Clozapine; Energy Metabolism; Female; Illness Behavior; Male; Metalloendopeptidases; Mice; Mice, Transgenic; Neoplasms; Parabrachial Nucleus; Tetanus Toxin; Tumor Cells, Cultured

2017

A genome-wide RNAi screen reveals a Trio-regulated Rho GTPase circuitry transducing mitogenic signals initiated by G protein-coupled receptors.

Molecular cell, 2013, Jan-10, Volume: 49, Issue:1

Activating mutations in GNAQ and GNA11, encoding members of the Gα(q) family of G protein α subunits, are the driver oncogenes in uveal melanoma, and mutations in Gq-linked G protein-coupled receptors have been identified recently in numerous human malignancies. How Gα(q) and its coupled receptors transduce mitogenic signals is still unclear because of the complexity of signaling events perturbed upon Gq activation. Using a synthetic-biology approach and a genome-wide RNAi screen, we found that a highly conserved guanine nucleotide exchange factor, Trio, is essential for activating Rho- and Rac-regulated signaling pathways acting on JNK and p38, and thereby transducing proliferative signals from Gα(q) to the nucleus independently of phospholipase C-β. Indeed, whereas many biological responses elicited by Gq depend on the transient activation of second-messenger systems, Gq utilizes a hard-wired protein-protein-interaction-based signaling circuitry to achieve the sustained stimulation of proliferative pathways, thereby controlling normal and aberrant cell growth.

Topics: Animals; Cell Line, Tumor; Cell Proliferation; Clozapine; Drosophila; Drosophila Proteins; Enzyme Activation; Female; Gene Knockdown Techniques; GTP-Binding Protein alpha Subunits; GTP-Binding Protein alpha Subunits, Gq-G11; Guanine Nucleotide Exchange Factors; Humans; Mice; Mice, Nude; Mitogen-Activated Protein Kinases; Mitogens; Mitosis; Neoplasm Transplantation; Neoplasms; NIH 3T3 Cells; Protein Serine-Threonine Kinases; Receptors, G-Protein-Coupled; rho GTP-Binding Proteins; RNA Interference; Signal Transduction; Transcription Factor AP-1

2013