Downregulation of Fer induces PP1 activation and cell-cycle arrest in malignant cells.

Fer is a nuclear and cytoplasmic intracellular tyrosine kinase. Herein we show that Fer is required for cell-cycle progression in malignant cells. Decreasing the level of Fer using the RNA interference (RNAi) approach impeded the proliferation of prostate and breast carcinoma cells and led to their arrest at the G0/G1 phase.

Fer kinase sustains the activation level of ERK1/2 and increases the production of VEGF in hypoxic cells.

Fer is a nuclear and cytoplasmic tyrosine kinase that is ubiquitously expressed in mammalian cells. Herein we show that Fer sustains a key signaling step in hypoxic cells. Knock-down of the Fer protein using a specific siRNA decreased the production of VEGF by the hypoxic cells.

Fer is a downstream effector of insulin and mediates the activation of signal transducer and activator of transcription 3 in myogenic cells.

Fer is an intracellular tyrosine kinase that associates with signal transducer and activator of transcription 3 (Stat3) in mammalian cells. However, the signaling pathways in which this interaction plays a functional role have not been revealed. Herein, we show that insulin up-regulates the levels of the fer mRNA and Fer protein in myoblasts that undergo insulin-induced myogenic differentiation.