These receptors are mediators of growth signals and thus determine cell fate. They are cell surface allosteric enzymes consisting of a single transmembrane domain that separates the intracellular kinase domain from the extracellular ligand-binding domain. Ligand binding to the ectodomain results in allosteric alterations leading to receptor homo- or heterodimerization, kinase activation, and trans-autophosphorylation. Subsequent tyrosine phosphorylation on residues within the carboxyl terminal tail of the receptors enables the recruitment and activation of signaling effectors containing Src homology 2 domain and phosphotyrosine binding domain that will lead to the initiation of various signaling cascades. The ErbB receptors are expressed in various tissues of epithelial, mesenchymal and neuronal origin. Under normal physiological conditions, activation of the ErbB receptors is controlled by the spatial and temporal expression of their ligands, which are members of the EGF family of growth factors. Abnormal function of the ErbB receptors and their ligands is involved in human cancer and already serve as target for several cancer drugs. As a major risk LDN-193189 ALK inhibitor factor for type 2 diabetes and cardiovascular complications, obesity is currently reaching epidemic proportions worldwide, largely stemming from complex interactions between genetic factors and environmental influences such as overnutrition. In mammals, multiple mechanisms act in an integrated manner to balance energy storage and expenditure, and chronic disruption of energy balance leads to excessive accumulation of fat in the adipose tissue. In addition to energy storage, the adipose tissue is also known to serve as a critical endocrine organ that releases a variety of adipokines, eliciting an array of metabolic effects on lipid and glucose metabolism. Even though these vectors have proven extremely useful, there are limited drug selection markers available, and different vector backbones can be required to express cDNAs or shRNAs/miRNAs. We sought to extend the versatility of viral vectors by developing third generation, self-inactivating lentiviral vectors with an expanded range of drug selection markers, promoters, and epitope tags. Furthermore, we wanted to improve their flexibility, allowing the investigator to rapidly change promoters and/or drug selection markers without extensive recloning. We report here a series of 59 vectors to express cDNAs, shRNAs and miRNAs, either constitutively or inducibly, in mammalian cells. These vectors are based on the Gateway System whereby a cDNA, shRNA or miRNA is cloned into an Entry vector which is recombined in vitro with the viral Destination vector of choice. This system offers two main advantages: First, the recombination is very efficient and rapid.