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Switching of the Relative Dominance Between Feedback Mechanisms in Lipopolysaccharide-Induced NF-κB Signaling
Dueling feedback loops set the threshold for mounting an effective innate immune response to infection. Rewiring NF-κB Signaling The bacterial product lipopolysaccharide (LPS) stimulates nuclearExpand
OmpC and OmpF are required for growth under hyperosmotic stress above pH 8 in Escherichia coli
Aims:  To investigate the requirement of outer membrane porins for osmotic adaptation at alkaline pH in Escherichia coli.
Cannabinoids Inhibit Insulin Receptor Signaling in Pancreatic β-Cells
OBJECTIVE Optimal glucose homeostasis requires exquisitely precise adaptation of the number of insulin-secreting β-cells in the islets of Langerhans. Insulin itself positively regulates β-cellExpand
Cannabinoids Induce Pancreatic β-Cell Death by Directly Inhibiting Insulin Receptor Activation
Activation of cannabinoid 1 receptors prevents insulin receptors from promoting β-cell survival in the pancreas. Death by Cannabinoids Cannabinoid receptors are located in the brain and in theExpand
Insulin and Glucagon Regulate Pancreatic α-Cell Proliferation
Type 2 diabetes mellitus (T2DM) results from insulin resistance and β-cell dysfunction, in the setting of hyperglucagonemia. Glucagon is a 29 amino acid peptide hormone, which is secreted fromExpand
New Determinant for the CaVβ2 Subunit Modulation of the CaV1.2 Calcium Channel*
Cavβ subunits support voltage gating of Cav1.2 calcium channels and play important role in excitation-contraction coupling. The common central membrane-associated guanylate kinase (MAGUK) region ofExpand
High-Throughput Screening for CYP21A1P-TNXA/TNXB Chimeric Genes Responsible for Ehlers Danlos Syndrome in Patients with Congenital Adrenal Hyperplasia.
Many patients with congenital adrenal hyperplasia (CAH) due to 21 hydroxylase deficiency have CAH-X syndrome, a connective tissue dysplasia consistent with hypermobility type Ehlers Danlos syndromeExpand
Calmodulin-dependent gating of Cav1.2 calcium channels in the absence of Cavβ subunits
It is generally accepted that to generate calcium currents in response to depolarization, Cav1.2 calcium channels require association of the pore-forming α1C subunit with accessory Cavβ and α2δExpand