mouse monoclonal primary antibodies against ir (beta-subunit)  (Santa Cruz Biotechnology)

Journal:

Article Title: Role for neuronal insulin resistance in neurodegenerative diseases

doi: 10.1073/pnas.0308724101

Figure Lengend Snippet: Abolished IR expression and insulin-stimulated signaling in NIRKO neurons. (A) Immunoblot analysis of IR expression on protein extracts from microdissected individual brain regions of control and NIRKO mice. (B) IR and IGF-1-IR expression in cultured neurons from control and NIRKO mice analyzed by Western blot. The blots were probed with a polyclonal antiserum specific for the β-subunit of the IGF-IR and the β-subunit IR. (C) Immunoblot analysis of insulin-stimulated tyrosine phosphorylation of the IR β-subunit (top blot) and of cellular proteins (second blot) on protein extracts from control and NIRKO mice. Insulin-stimulated activation of Akt and Erk by Western blot analysis using phospho-specific antibodies against Akt (Ser-473) and Erk (Tyr-204) from control and NIRKO hypothalami (third and fourth blots) also are shown. Insulin-stimulated IRS-1- and IRS-2-associated phosphatidylinositol 3-kinase activity from control and NIRKO hypothalami (fifth and sixth blots) was determined 15 min after i.v. injection of 5 milliunits of insulin. (D) Immunohistochemistry with anti-PIP3 (Upper) and anti-pSTAT3 (Lower) antibodies. Sections through the hypothalamus were prepared from control (Wild) or NIRKO mice that had been injected with vehicle alone, 5 milliunits of insulin, or 10 μg of leptin per g of body weight through the tail vein at 30 min before harvesting.

Article Snippet: Primary antibodies against the IR β-subunit, insulin-like growth factor (IGF)-IR β-subunit, and Tau (Santa Cruz Biotechnology); Akt, pAkt, glycogen synthase kinase (GSK)3β, and pGSK3β (Upstate Biotechnology, Lake Placid, NY); and AT8 and AT180 (Innogenetic, Ghent, Belgium) were used.

Techniques: Expressing, Western Blot, Cell Culture, Activation Assay, Activity Assay, Injection, Immunohistochemistry