LDL receptor and its family members serve as the cellular receptors for vesicular stomatitis virus.

Vesicular stomatitis virus (VSV) exhibits a remarkably robust and pantropic infectivity, mediated by its coat protein, VSV-G. Using this property, recombinant forms of VSV and VSV-G-pseudotyped viral vectors are being developed for gene therapy, vaccination, and viral oncolysis and are extensively used for gene transduction in vivo and in vitro. The broad tropism of VSV suggests that it enters cells through a highly ubiquitous receptor, whose identity has so far remained elusive.

C/EBP-beta regulates endoplasmic reticulum stress-triggered cell death in mouse and human models.

Endoplasmic reticulum (ER) stress elicits the unfolded protein response (UPR), initially aimed at coping with the stress, but triggering cell death upon further stress. ER stress induces the C/EBP-beta variant Liver-enriched Activating Protein (LAP), followed by the dominant-negative variant, Liver Inhibitory Protein (LIP). However, the distinct role of LAP and LIP in ER stress is unknown.

Antiviral and immunoregulatory activities of IFN-gamma depend on constitutively expressed IL-1alpha.

IFN-gamma induces its immunoregulatory activities by activating genes mainly through the Jak-STAT signaling pathway. Here we show that what was considered to be intrinsic IFN-gamma activities depend largely on the basal level of NF-kappaB, which is maintained by constitutively expressed IL-1alpha. The IL-1 receptor antagonist and antibodies to IL-1alpha, but not to IL-1beta, inhibited the antiviral activity of IFN-gamma by 90%, whereas no inhibition of type I IFN activity was observed.

Differential role and tissue specificity of interleukin-1alpha gene expression in atherogenesis and lipid metabolism.

Objective: We examined the role of IL-1alpha and IL-1beta expressed by bone marrow-derived cells in atherogenesis and lipid metabolism.

Methods And Results: We first studied the effect of atherogenic diet on wild-type C57BL/6 IL-1alpha or IL-1beta deficient mice. IL-1alpha KO resulted in a comparatively higher total cholesterol levels, compared to WT and IL-1beta KO mice (398+/-10; 266+/-19; 223+/-13 mg/dl, respectively, p<0.

The precursor form of IL-1alpha is an intracrine proinflammatory activator of transcription.

Although most cytokines are studied for biological effects after engagement of their specific cell surface membrane receptors, increasing evidence suggests that some function in the nucleus. In the present study, the precursor form of IL-1alpha was overexpressed in various cells and assessed for activity in the presence of saturating concentrations of IL-1 receptor antagonist to prevent receptor signaling. Initially diffusely present in the cytoplasm of resting cells, IL-1alpha translocated to the to nucleus after activation by endotoxin, a Toll-like receptor ligand.