In accordance on the HMG-CoA Reductase "osteoblastic niche" model, hematopoietic stem cells (HSCs) are maintained by N-cadherin-mediated homophilic adhesion to osteoblasts at the bone marrow endosteum. In contrast to this model, we are unable to detect N-cadherin expression by HSCs, and most HSCs will not localize to the endosteal surface. It has nevertheless been advised that HSCs express lower ranges of N-cadherin that selleck chem TNF-alpha inhibitor regulate HSC maintenance. To test this, we conditionally deleted N-cadherin from HSCs and also other hernatopoietic cells in adult Mx-1-Cre(+)N-cadherin(fl/-) mice. N-cadherin deficiency had no detectable impact on HSC maintenance or hematopoiesis. N-cadherin deficiency didn't have an impact on bone marrow cellularity or lineage composition, the numbers of colony-forming progenitors, the frequency of HSCs, the ability of HSCs to sustain hematopoiesis in excess of time, or their capability to reconstitute irradiated mice in principal or secondary transplants. Loss of N-cadherin does not result in HSC depletion. N-cadherin expression by HSCs isn't required for niche function.