Abstracts from Society for Neuroscience (SFN) Chicago, IL • October 17-21, 2009
Abstracts from Society for Neuroscience (SFN) Chicago, IL • October 17-21, 2009 Read More »
Targeting Tools: Bombesin-SAP
Bombesin-SAP (Cat. #IT-40) specifically targets and eliminates gastrin- releasing peptide receptor (GRPR)-positive cells. This targeted toxin (molecular weight 31.8 kDa) is a chemical conjugate of bombesin and the ribosome-inactivating protein, saporin. Please see cover article (pp. 1, 6) for an example of its experimental use.
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Targeting Tools: Anti-Basigin
This mouse monoclonal antibody (Cat. #AB-42; Clone P2C2) recognizes human Basigin. The antibody is purified by ammonium sulfate precipitation on conditioned medium and then further purified through Protein-A. The antibody is routinely tested by flow cytometry. The immunoglobulin superfamily protein basigin (EMMPRIN/CD147) is a cell surface glycoprotein expressed by tumor cells that stimulates matrix metalloproteinase
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Targeting Tools: Oxytocin-SAP
Oxytocin-SAP (Cat. #IT-46) is a conjugate (molecular weight 31 kDa) between the native oxytocin peptide and saporin. Oxytocin is a nine amino acid peptide with a structure similar to vasopressin, and is a hormone released by the posterior pituitary. Peripheral activity of oxytocin is linked primarily to lactation and labor-related uterine contractions. Within the brain,
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Cover Article: Ablation of GRPR+ Neurons in the Spinal Cord by Bombesin-Saporin Knocks Out Itch Sensation in Mice Without Affecting Pain Circuit
Contributed by Zhou-Feng Chen, Yang-Gang Sun, Zhong-Qiu Zhao, Xiu-Li Meng, Jun Yin, Xian-Yu Liu; Washington University Pain Center School of Medicine, Dept of Anesthesiology, St. Louis, MO 63141 Unlike pain, itch sensation evokes scratching response instead of withdrawal behavior. However, itch and pain sensations share many similarities. Like chronic pain, chronic itch is a major clinical
Targeting Article: SBIR Grant Funded: Selective Activation in Neuronal Populations
ATS has been awarded a Phase I SBIR grant to develop a new line of products. Dr. Douglas Lappi is the Principal Investigator and Brian Russell is the Lead Scientist on the project. Molecules targeted towards cell surface markers have been used for years to identify specific cell types. It has been demonstrated over the
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Cover Article: Depletion of Microglia by Mac-1-SAP in Mouse Hippocampal Slice Cultures Enhances Ischemia-Like Neurodegeneration
Contributed by Maria Montero (a), Berta Gonzalez (b), Jens Zimmer (a)(a) Anatomy and Neurobiology, University of Southern Denmark, Denmark(b) Histology Unit, Autonomous University of Barcelona, Spain Microglial cells contribute about 12% of the cells in the brain, acting as “biosensors” for homeostatic regulation in normal and pathological conditions.[3,13] Resting microglial cells in the adult brain
Targeting Tools: Hug-M-ZAP
This secondary conjugate (molecular weight 210 kDa) recognizes YOUR human monoclonal IgM antibody. Hug-M-ZAP (IT-43) is a chemical conjugate of affinity-purified goat anti-human IgM and the ribosome-inactivating protein, saporin. Hug-M- ZAP uses your primary human monoclonal IgM antibody to target and eliminate cells and can be used to evaluate the potential of a primary antibody
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Targeting Tools: CTB-SAP
CTB-SAP (Cat. #IT-14) is a conjugate between the cell-binding component of cholera toxin (the B chain) and saporin. CTB binds to GM1 (monosialotetrahexosylganglioside), which is present on the surface of different neurons. It has been suggested to be involved in many problems (besides the most famous in the gut: cholera) of neuronal systems: Parkinson’s, motor
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Cover Article: Deletion of Catecholaminergic Neurons by Anti-DBH-Saporin Disrupts Hypothalamic MAP Kinase and CREB Activation
Contributed by Arshad M. Khan, Kimberly L. Rapp, Todd A. Ponzio, Graciela Sanchez-Watts and Alan G. Watts; Dept. of Biological Sciences and Neuroscience Research Institute, University of Southern California, Los Angeles, CA; and Laboratory for Neurochemistry, National Institute of Neurological Disorders and Stroke, National Institutes of Health, Bethesda, MD The brain has evolved adaptive mechanisms for