The tubulointerstitial compartment comprises most of the kidney parenchyma. Inflammation in this compartment (tubulointerstitial nephritis-TIN) can be acute and resolves if the offending factor is withdrawn or may enter a chronic process leading to irreversible kidney damage. Etiologic factors differ, including different exposures, infections, and autoimmune and genetic tendency, and the initial damage can be acute, recurrent, or permanent, determining whether the acute inflammatory process will lead to complete healing or to a chronic course of inflammation leading to fibrosis.
View Article and Find Full Text PDFIn rodents with unilateral ablation of neurons supplying dopamine to the striatum, chronic treatment with the dopamine precursor L-DOPA induces a progressive increase of behavioral responses, a process known as behavioral sensitization. This sensitization is blunted in arrestin-3 knockout mice. Using virus-mediated gene delivery to the dopamine-depleted striatum of these mice, we find that the restoration of arrestin-3 fully rescues behavioral sensitization, whereas its mutant defective in c-Jun N-terminal kinase (JNK) activation does not.
View Article and Find Full Text PDFBiological activity of free arrestins is often overlooked. Based on available data, we compare arrestin-mediated signaling that requires and does not require binding to G-protein-coupled receptors (GPCRs). Receptor-bound arrestins activate ERK1/2, Src, and focal adhesion kinase (FAK).
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