Zobrazeno 1 - 10
of 14
pro vyhledávání: '"Jamie W. Meyer"'
Autor:
Karena Sisco, Marian L. Miller, Ilona Bodi, Vikram Prasad, John N. Lorenz, Michelle L. Nieman, Yigang Wang, Sandra J. Engle, Jamie W. Meyer, Thomas Doetschman, Muhammad Ashraf, Gary E. Shull
Publikováno v:
Journal of Biological Chemistry. 283:31303-31314
To analyze the cardiac functions of AE3, we disrupted its gene (Slc4a3) in mice. exchange coupled with Na+-dependent acid extrusion can mediate pH-neutral Na+ uptake, potentially affecting Ca2+ handling via effects on Na+/Ca2+ exchange. AE3 null mice
Autor:
Jamie W. Meyer, Mark E. Schmitt
Publikováno v:
FEBS Letters. 472:1-4
An increasing body of evidence has demonstrated that NADPH oxidase plays a critical role in several early steps leading toward the development of atherosclerosis. These effects appear to be carried out by both the ability of O2− to act as a small s
Autor:
Robert O'Donnell, David K. Johnson, Ming-Mei Chang, Linda M. Ziegler, James A. Holland, Jamie W. Meyer
Publikováno v:
Endothelium. 6:113-121
In order to study the major cellular source of reactive oxygen species (ROS) in perturbed human endothelial cells (EC), the effect of thrombin, a phospholipase A2 activator, on cultured EC ROS generation has been investigated. EC were incubated with
Autor:
Small Rf, Jamie W. Meyer, James A. Holland, Sauro, Linda M. Ziegler, Schillinger Kj, Mark E. Schmitt, Patel, Larry F. Lemanski, Raja W. Abdul-Karim, David K. Johnson
Publikováno v:
Endothelium. 5:191-207
The effects of arachidonic acid metabolism and NADPH oxidase inhibitor on the hydrogen peroxide (H2O2) generation and endocytotic activity of cultured human endothelial cells (EC) exposed to atherogenic low-density lipoprotein (LDL) levels have been
Autor:
Jamie W. Meyer, Kurt J. Schillinger, Vinu Patel, Lydia Kauffman, Linda M. Ziegler, Raja W. Abdul-Karim, Larry F. Lemanski, David K. Johnson, James A. Holland
Publikováno v:
Endothelium. 4:207-218
In order to study the signal transduction mechanism of endothelial perturbation, the effects of phorbol 12-myristate 13-acetate (PMA) and phorbol 12,13-dibutyrate (PDBu), both protein kinase C (PKC) activators, on cultured human endothelial cell (EC)
Publikováno v:
Journal of Cellular Physiology. 166:144-151
Cultured human umbilical vein endothelial cells(EC) exposed to atherogenic low-density lipoprotein (LDL) levels have augmented reactive oxygen species generation. Confluent EC were incubated with 30-330 mg/dl LDL cholesterol and cellular hydrogen per
Autor:
Vikram, Prasad, Ilona, Bodi, Jamie W, Meyer, Yigang, Wang, Muhammad, Ashraf, Sandra J, Engle, Thomas, Doetschman, Karena, Sisco, Michelle L, Nieman, Marian L, Miller, John N, Lorenz, Gary E, Shull
Publikováno v:
The Journal of biological chemistry. 283(46)
To analyze the cardiac functions of AE3, we disrupted its gene (Slc4a3) in mice. \documentclass[10pt]{article} \usepackage{amsmath} \usepackage{wasysym} \usepackage{amsfonts} \usepackage{amssymb} \usepackage{amsbsy} \usepackage{mathrsfs} \usepackage{
Publikováno v:
American journal of physiology. Gastrointestinal and liver physiology. 291(4)
The mechanism of apical Na+-dependent H+ extrusion in colonic crypts is controversial. With the use of confocal microscopy of the living mouse distal colon loaded with BCECF or SNARF-5F (fluorescent pH sensors), measurements of intracellular pH (pHi)
Autor:
William H. Beierwaltes, Adetola Shodeinde, Jamie W. Meyer, Young-Hee Kim, Mark A. Knepper, John N. Lorenz, Truyen D. Pham, Kathryn A. Hassell, Michael P. Fischer, John R. Dietz, Gary E. Shull, Susan M. Wall, Wonkyong Shin
Publikováno v:
American journal of physiology. Renal physiology. 290(2)
NKCC1 null mice are hypotensive, in part, from the absence of NKCC1-mediated vasoconstriction. Whether these mice have renal defects in NaCl and water handling which contribute to the hypotension is unexplored. Therefore, we asked 1) whether NKCC1 (
Publikováno v:
American journal of physiology. Renal physiology. 287(6)
In the medullary thick ascending limb (MTAL) of rat kidney, inhibiting basolateral Na+/H+ exchange with either amiloride or nerve growth factor (NGF) results secondarily in inhibition of apical Na+/H+ exchange, thereby decreasing transepithelial HCO3