Type 1 X Type 8 Adenylyl Cyclase double Knockout Mice (DKO strain)

Introduction Production of cAMP by adenylyl cyclase (AC) provides an important mechanism for the regulation of neuronal physiology. The calcium-stimulated AC isoforms have been strongly implicated in the alteration of neuronal function. Targeted inactivation of the calciumstimulated AC type I (AC1) results in defective spatial learning, motor coordination, and hippocampal and cerebellar long-term potentiation. AC8 is a critical molecule for the translation of increased intracellular calcium to altered protein kinase A and/or CREBmediated changes in gene expression that impact upon induction of long term depression and the response to stress. AC8 is expressed in the non-excitable mouse parotid cell and is predominantly involved in the regulation of muscarinic augmentation of cAMP synthesis. Technology description Dr Daniel Storm’s laboratory has generated mice deficient in AC1 and AC8 by homologous recombination in R1 (129/Sv × 129/Sv-CP)F1 embryonic stem cells. Injection of the ES clone 3D6 into C57BL/6 blastocysts resulted in the production of several male chimeras that transmitted the mutant allele through their germline. AC1/AC8 DKO mice demonstrate a compromise in calcium-stimulated AC activity in the hippocampus, hypothalamus, thalamus, and brainstem. This transgenic mouse offers a powerful tool for dissecting the multiple pathways that exist in a cell to regulate cAMP synthesis Related Publication(s)
Methods in Enzymolog, 345: 206-231, 2002 Neuron, 23: 787-798, 1999 For more information on this technology contact:
Ariadna Santander Agreements Manager Technology Licensing [email protected] 206-543-1138

Type of Offer: Licensing



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