Full list of author information is available at the end of the articleBackground IgA nephropathy, a mesangial proliferative glomeruloneph-ritis, is the most common primary glomerulonephritis worldwide, and as many as 20-30 % of patients with IgA ne-phropathy progress to end-stage renal failure after 20– 25 years [1-4]. It is characterized by in the beginning phase with expansion of glomerular mesangial matrix and me-sangial cell proliferation, and a subsequent progression phase with glomerulosclerosis, tubulointerstitial fibrosis and ongoing loss in renal function, which is a hallmark of many chronic glomerulonephritis [5]. The progress from glomerulonephritis to end-stage renal disease and the need for renal replacement therapy can even be seen when the initial glomerulonephritic phase has been resolved, sug-gesting a self-perpetuated and intrarenal mechanism is ope-rating during the disease progression.

Abstract The goal of this study was to determine the role of tyrosine phosphorylation in transducing deformation-stimu-lated vascular smooth muscle growth. Rat aorta-derived vas-cular smooth muscle cells were cultured on flexible silicone elastomer membranes and subjected to cyclic deformation (15

Copyright: © 2015 Mathur R. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use,

from HER2 tyrosine kinase inhibition

INTRODUCTION. There are more than 90 protein tyrosine kinases in the human genome of which 30 have been implicated in cancer. The oncogenic tyrosine kinases promote growth factor independent cell proliferation, protect cells from apoptosis and render cells resistant to genotoxic therapies. We have

of new class of agents such as monoclonal antibodies, proteasome inhibitors and immunomodulatory derivatives has sparked further search for treatment agents with novel targets to inhibit. The B cell receptor activating pathway involving the Bruton’s tyrosine kinase (BTK) is crucial in B cell production

involve novel agents targeting molecular aberrations present in subsets of NSCLC. We evaluated 88 human NSCLC tumors of diverse histology and identified Mer and Axl as receptor tyrosine kinases (RTKs) overexpressed in 69 % and 93%, respectively, of tumors relative to surrounding normal lung tissue. Mer

Updated Version Access the most recent version of this article at: doi: 10.1158/0008-5472.CAN-04-3379

Abstract not found

Spleen tyrosine kinase inhibition prevents tissue damage after ischemia-reperfusion