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Genetic deletion of p66Shc adaptor protein prevents hyperglycemia-induced endothelial dysfunction an...

Genetic deletion of p66Shc adaptor protein prevents hyperglycemia-induced endothelial dysfunction an...

https://devfeature-collection.sl.nsw.gov.au/record/TN_cdi_pubmedcentral_primary_oai_pubmedcentral_nih_gov_1829289

Genetic deletion of p66Shc adaptor protein prevents hyperglycemia-induced endothelial dysfunction and oxidative stress

About this item

Full title

Genetic deletion of p66Shc adaptor protein prevents hyperglycemia-induced endothelial dysfunction and oxidative stress

Publisher

National Academy of Sciences

Journal title

Proceedings of the National Academy of Sciences - PNAS, 2007-03, Vol.104 (12), p.5217-5222

Language

English

Formats

Publication information

Publisher

National Academy of Sciences

Subjects

Subjects and topics

More information

Scope and Contents

Contents

Increased production of reactive oxygen species (ROS) and loss of endothelial NO bioavailability are key features of vascular disease in diabetes mellitus. The p66Shc adaptor protein controls cellular responses to oxidative stress. Mice lacking p66Shc (p66Shc⁻/⁻) have increased resistance to ROS and prolonged life span. The present work was designe...

Alternative Titles

Full title

Genetic deletion of p66Shc adaptor protein prevents hyperglycemia-induced endothelial dysfunction and oxidative stress

Identifiers

Primary Identifiers

Record Identifier

TN_cdi_pubmedcentral_primary_oai_pubmedcentral_nih_gov_1829289

Permalink

https://devfeature-collection.sl.nsw.gov.au/record/TN_cdi_pubmedcentral_primary_oai_pubmedcentral_nih_gov_1829289

Other Identifiers

ISSN

0027-8424

E-ISSN

1091-6490

DOI

10.1073/pnas.0609656104

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