CD248 facilitates tumor growth via its cytoplasmic domain.

Background: Stromal fibroblasts participate in the development of a permissive environment for tumor growth, yet molecular pathways to therapeutically target fibroblasts are poorly defined. CD248, also known as endosialin or tumor endothelial marker 1 (TEM1), is a transmembrane glycoprotein expressed on activated fibroblasts. We recently showed that the cytoplasmic domain of CD248 is important in facilitating an inflammatory response in a mouse model of arthritis.

Impaired neurogenesis, learning and memory and low seizure threshold associated with loss of neural precursor cell survivin.

Background: Survivin is a unique member of the inhibitor of apoptosis protein (IAP) family in that it exhibits antiapoptotic properties and also promotes the cell cycle and mediates mitosis as a chromosome passenger protein. Survivin is highly expressed in neural precursor cells in the brain, yet its function there has not been elucidated.

Results: To examine the role of neural precursor cell survivin, we first showed that survivin is normally expressed in periventricular neurogenic regions in the embryo, becoming restricted postnatally to proliferating and migrating NPCs in the key neurogenic sites, the subventricular zone (SVZ) and the subgranular zone (SGZ).

Survivin-dependent angiogenesis in ischemic brain: molecular mechanisms of hypoxia-induced up-regulation.

Approaches to regulating angiogenesis in the brain, which may diminish parenchymal damage after stroke, are lacking. Survivin, the inhibitor of apoptosis protein, is up-regulated in vitro in vascular endothelial cells by angiogenic factors, including vascular endothelial cell growth factor (VEGF). To evaluate the in vivo role of survivin in the brain in response to hypoxia/ischemia, we used a mouse model of stroke and show that 2 days after permanent middle cerebral artery occlusion, survivin is uniquely expressed by microvessels that form in the peri-infarct and infarct regions.

Deficiency of survivin in transgenic mice exacerbates Fas-induced apoptosis via mitochondrial pathways.

Background & Aims: Survivin is an inhibitor of apoptosis protein (IAP), which also is crucial for mitosis and cell cycle progression. IAPs participate in regulating Fas ligand-induced hepatic apoptosis. The aim was to study the contribution of survivin to hepatic apoptosis by generating transgenic mice lacking survivin.