Wright, M.A. and Ribera, A.B. (2010) J. Neurosci. 30, 14513.
During development, neurons migrate and position themselves in areas enabling them to fulfill their roles. A study aimed to investigate the factors involved in anchoring the neurons to their final destinations, thus preventing further migration revealed that BDNF is such a factor. When independently treating cells with Native mouse NGF 7S protein (#N-130), Recombinant human Neurotrophin-3 (NT-3) protein (#N-260) or Recombinant human BDNF protein (#B-250), only BDNF was able to anchor neurons, an event important for maintaining the identity of differentiated neurons.
Chou, W.H. et al. (2010) J. Neurosci. 30, 13955.
A lack of proper GABA(A) receptor signaling participates in various psychiatric disorders. Therefore, membrane trafficking is one crucial step controlling the integrity of GABA(A) receptor signaling. Protein kinase C (PKC) regulates membrane localization of GABA(A) γ2 receptor subunit, as shown in part in cell surface ELISA assays using Anti-GABA(A) γ2 Receptor (extracellular) Antibody (#AGA-005). Activation of PKC decreases cell surface localization of GABA(A) γ2 receptors, thereby decreasing GABA(A) receptor signaling.
Lebrun Julien, F. et al. (2010) Proc. Natl. Acad. Sci. U.S.A. 107, 3817.
The biological effects of neurotrophins are mediated in part by p75NTR. The binding of proneurotrophins to p75NTR induces cell death pathways. In adult retina, injection of Alomone Labs Recombinant mouse proNGF (cleavage resistant) protein (#N-255) activated apoptosis in retinal ganglion cells via the production of tumor necrosis factor-alpha (TNF-α) by nearby Müller cells, in a p75NTR-dependent manner. This study demonstrates that cell death induced by p75NTR can be a non-cell-autonomous event.
Reichold, M. et al. (2010) Proc. Natl. Acad. Sci. U.S.A. 107, 14490.
Mutations in the gene encoding the Kir4.1 channel are implicated in various diseases, namely renal tubulopathy (EAST) syndrome, a salt wasting disease. Kir4.1 is expressed on the basolateral membrane of the distal convoluted tubules in kidneys. In EAST syndrome, the morphology of the tubules in severely compromised. The disease causing mutations significantly affect the activity of Kir4.1 as well as modify the sensitivity of the channel towards a more alkaline pH. Throughout the study, the expression of Kir4.1 was checked in immunohistochemical staining using Alomone Labs Anti-Kir4.1 (KCNJ10) Antibody (#APC-035). Furthermore, the specificity of the antibody was verified by comparing the expression of the channel between transfected and non transfected cells in western blot analysis, and wild type and Kir4.1 knockout cells in immunocytochemical staining.