Recent Obeticholic Acid nmr commentaries in the area underscore the potential impact of this paradigm shift. These articles concur with the notion that signaling pathways drive cancer progression, and are a rich source of targets for therapeutic development [5] and [20]. Both biological network models and gene-interference studies are cutting edge techniques that have greatly added to our understanding of cancer systems. As such, future endeavors merging these growing fields will enhance understanding of cancer systems and improve ability to manipulate a complicated disease. The authors declare that there are no conflicts of interest. The authors would like to thank our

funding sources: NSF Graduate Research Fellowship Program (JLW), NCI Integrative Cancer Biology Program grant U54-CA112967 (DAL/EF/MH), and NCI grant U01-CA155758 (DAL/MH). “
“Somatostatin

(SOM) is a 14 amino acid neuropeptide originally identified as somatotropin release-inhibiting factor in the Ribociclib research buy hypothalamus (Brazeau et al., 1973). It is distributed widely in the brain and is coreleased with amino acid neurotransmitters. Under normal conditions, SOM is exclusively expressed in cortical GABAergic interneurons (Somogyi et al., 1984). In the hippocampal CA1 area, at least five distinct neuron types express SOM (Baude et al., 1993, Chittajallu et al., 2013, Katona et al., 1999 and Klausberger et al., 2004) and some SOM-expressing GABAergic cell types also project to extrahippocampal areas (Gulyás et al., 2003 and Jinno et al., 2007), including the entorhinal cortex in the mouse (Melzer et al., 2012). All of these neurons probably release SOM and GABA within the dendritic domain of pyramidal cells and also innervate other interneurons (Gulyás and et al., 2003, Jinno et al., 2007 and Katona et al.,

1999). Some interneurons, including the bistratified cells, also express neuropeptide tyrosine (NPY), a powerful inhibitor of glutamate release (Colmers et al., 1985). Taken together, it appears that the primary role of SOM-expressing interneurons is the regulation of dendritic inputs and signal integration. Indeed, the bistratified cell was recently shown to be a key controller of pyramidal cell output in vitro (Lovett-Barron et al., 2012 and Lovett-Barron et al., 2014). The SOM-expressing bistratified and O-LM cell types in the CA1 area have nonoverlapping axonal arbors and are each selectively associated with one of the major glutamatergic inputs to pyramidal cells. Bistratified cells innervate the dendritic zones of pyramidal cells receiving input from the CA3 area (Buhl et al., 1994), whereas O-LM cells innervate the entorhinal input zone (McBain et al., 1994). Both cell types coexpress parvalbumin (PV), a calcium-binding protein that is also expressed by axoaxonic cells and one type of basket cell (Klausberger et al., 2003 and Klausberger et al., 2004).