Description: Thymic stromal lymphopoietin (TSLP) has recently been identified as an important factor capable of driving dendritic cell maturation and activation. TSLP is a four-helix-bundle cytokine that is expressed mainly by barrier epithelial cells and is a potent activator of several cell types such as myeloid dendritic cells. TSLP is involved in the positive selection of regulatory T cells, maintenance of peripheral CD4+ T cell homeostasis and the induction of CD4+ T cell-mediated allergic reaction. TSLP is also capable of supporting the growth of fetal liver and adult B cell progenitors and their differentiation to the IgM-positive stage of B cell development. Amino acid sequence analysis has shown poor homology between human and mouse TSLP although they exhibit similar biological functions and are expressed in similar tissues. The TSLP receptor (TSLP-R) will bind TSLP in a low-affinity fashion in transfected cells; co-transfection with IL-7R cDNA results in high-affinity binding and a functional heteromeric complex. This heteromeric receptor requires stat5 for TSLP-mediated signal transduction and is inhibited by SOCS1. Despite their predicted molecular weight, TSLP and TSLP-R often migrate at a higher molecular weight in SDS-PAGE. Antibody #4209 recognizes only mouse protein; #4025 recognizes both mouse and rat proteins. Antibodies #4021 and #4207 are specific for human proteins.;;For images please see PDF data sheet

Description: SLIT and NTRK-like proteins comprise a six member protein family consisting of homologous transmembrane proteins (Slitrk1-6) that share two conserved leucine-rich repeat domains in the extracellular domain and have significant homology to Slit, a secreted axonal growth-controlling protein. These proteins are also homologous to trk neurotrophin receptors in their intracellular domains. Expression of Slitrk proteins is highly restricted to neural and brain tumor tissues, but varies within the family. For example, Slitrk1 is expressed primarily in mature neurons and Slitrk2 is expressed primarily in neurons in the ventricular layer of the brain. Overexpression of Slitrk1 in transfected neuronal cells induced unipolar neurites, while expression of the other Slitrk proteins inhibited neurite outgrowth, suggesting that these proteins are involved in the control of neurite outgrowth. Deletion analysis of Slitrk2 indicated that the functional difference between Slitrk2 and Slitrk1 is within their intracellular domains. While Slitrk1 variants have been suggested associated with Tourette’s Syndrome, it is thought to play only a minor role if at all.;;For images please see PDF data sheet