Yet, Iqgap2-/- colonic cell proliferation and apoptosis rates were Ropivacaine hydrochloride similar to those of WT controls. Moreover, our results also indicate that Iqgap2-/- mice had significantly less myeloid infiltrating cells in colons and lower number of circulating white blood cells, including neutrophils and monocytes. The only morphological aberration observed in Iqgap2-/- colons was hyperplasia of goblet cells irrespective of DSS treatment. The Iqgap2-deficient mouse studied here is a whole body knockout model, which allowed us to uncover IQGAP2 complex function in both colon-specific and systemic inflammatory response. Still, dissecting the precise molecular mechanisms of IQGAP2 involvement in inflammation will require generation of tissue-specific Iqgap2-deficient models. Based on the results of this study, and also the ability of the IQGAP2 scaffold to play the role of a signal transducer in multiple signaling pathways and the recent report of IQGAP2��sability to Indacaterol Maleate directly bind NF��B, we propose that IQGAP2 modulates inflammatory response by functioning as an adaptor protein in the TLR4/NF-��B signaling pathway in both colonic epithelial and stromal cells. We hypothesize that IQGAP2 may positively regulate NF-��B stability and activation through spatial and/or temporal control of My D88, Rac1 or Akt. NF-��B activation has been shown to occur in aRac1/PI3K-dependent manner. IQGAP2 may regulate NF-��B signaling by stabilizing Rho GTPase Rac1. A recent study in a large cohort of IBD patients identified a single nucleotide polymorphism rs10951982 in the Rac1 gene leading to increased Rac1 expression and higher susceptibility to IBD. The same study also showed that a conditional deletion of Rac1 in mouse neutrophils and macrophages resulted in these mice being protected from DSS-induced colitis. Therefore IQGAP2 interaction withRac1 may be crucial for its role in colonic inflammation. It is also feasible to propose that IQGAP2 realizes its pro-inflammatory action through interaction with p38 or ERK1/2, both involved in control of NF-��B and cytokine production.