Anoikis is an apoptotic phenomenon of epithelial cells which are detached from cell-cell and cell-matrix contacts. Anoikis may contribute to renal tubulo-degeneration, and, therefore, be implicated in disorders such as acute renal failure. MDCK are an epithelial model to study the function and pathology of renal tubuli. We characterize the function of tyrosine receptor kinase TrkB in cell survival. TrkB, full length and kinase truncated forms, were originally cloned by Dr. D. Middlemas (Memphis, USA), and GFP-tagged kindly gifted by Dr. V. Leßmann (Magdeburg, Germany). GFP-TrkB constructs were overexpressed in MDCKII cells. Anoikis was committed by suspension culture of MDCK. Apoptosis, necrosis and cell viability were monitored by zeiosis, DNA-histone ELISA, cell counting, LDH- as well as MTT-assay. In GFP-TrkB transfected cells, viability was increased 1.7- to 2.1-fold (-/+BDNF). Apoptosis was 2.1- to 2.6-fold (-/+BDNF) or necrosis 1.4 to 2- fold (-/+BDNF) decreased. Protection against anoikis was less effective in kinase truncated forms of GFP-TrkB but viability was saved 2- to 3.8-fold (-/+BDNF). Viability in non-transfected cells was 1.7-fold increased by BDNF with minor attenuating effects on anoikis. In conclusion, TrkB controls cell survival presumably by kinase- as well as non-kinase-domain effects.