Diabetes Reduces Autophosphorylation of Retinal Insulin Receptor and Increases Protein-Tyrosine Phosphatase-1B Activity | Zendy

Raju V. S. Rajala | Zendy; Brandt Wiskur | Zendy; Masaki Tanito | Zendy; Michelle C. Callegan | Zendy; Ammaji Rajala | Zendy

AI Assistant Blog Pricing

Home ZAIA Blog

Open Access

Diabetes Reduces Autophosphorylation of Retinal Insulin Receptor and Increases Protein-Tyrosine Phosphatase-1B Activity

Author(s) -

Raju V. S. Rajala,

Brandt Wiskur,

Masaki Tanito,

Michelle C. Callegan,

Ammaji Rajala

Publication year - 2009

Publication title -

investigative ophthalmology and visual science

Language(s) - English

Resource type - Journals

SCImago Journal Rank - 1.935

H-Index - 218

eISSN - 1552-5783

pISSN - 0146-0404

DOI - 10.1167/iovs.08-2851

Subject(s) - autophosphorylation , retina , insulin receptor , irs1 , biology , phosphorylation , retinal , phosphatase , protein tyrosine phosphatase , western blot , microbiology and biotechnology , chemistry , biochemistry , medicine , endocrinology , insulin , protein kinase a , insulin resistance , neuroscience , gene

Protein-tyrosine phosphatase-1B (PTP1B) has been implicated in the negative regulation of insulin signaling. The expression, activity, and functional role of PTP1B in the retina are unknown. In this study, the authors examined the relationship between the retinal insulin receptor (IR) and PTP1B in normal and diabetic mouse retinas.

The content you want is available to Zendy users.

Already have an account? Click here to sign in.

Having issues? You can contact us here

Accelerating Research