Researchers have created a mutant mouse that lives 30 per cent longer despite eating more and weighing less — all thanks to the loss of a single protein called type 5 adenylyl cyclase (AC5). News@Nature.com

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Anonymous's picture
Anonymous says:

excellent news.. can you divulge exactly what researchers and where/ when etc?

posted on Mon, 02/25/2008 - 1:45am
ARTiFactor's picture
ARTiFactor says:

Good questions (stupid paywall). I scored the abstract for free at Science. The researchers were Julia A. Chester and Val J. Watts, Department of Psychological Sciences, Purdue University, West Lafayette, IN 47907, USA and Department of Medicinal Chemistry and Molecular Pharmacology, Purdue University, West Lafayette, IN 47907, USA respectively. The paper title was "Adenylyl Cyclase 5: A New Clue in the Search for the "Fountain of Youth"?"

Abstract: The adenylyl cyclase (AC)­–cyclic adenosine monophosphate (cAMP) signaling pathway is involved in a number of important physiological functions in both the peripheral and central nervous systems. A report now indicates that genetic disruption of AC5 increases mouse life span and confers resistance to aging-related conditions, including bone loss and cardiomyopathies. It is proposed that these beneficial effects may be the result of the increased activity of second messenger signaling proteins such as mitogen-activated or extracellular signal–regulated protein kinase kinase (MAPKK, also known as MEK) and extracellular signal–regulated kinase (ERK), or of enzymes such as manganese superoxide dismutase (MnSOD) that promote cell survival through protection against oxidative stress and apoptosis. These intriguing findings should stimulate additional research aimed at dissecting the complex cellular mechanisms regulated by AC isoforms and may lead to novel genetic and pharmacological approaches to delay aging-related conditions and to extend life span.

posted on Mon, 02/25/2008 - 11:34am

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