Analysis of a bovine herpesvirus 1 protein encoded by an alternatively spliced latency related (LR) RNA that is abundantly expressed in latently infected neurons.

The bovine herpes virus 1 (BoHV-1) encoded latency-related RNA (LR-RNA) is abundantly expressed in latently infected sensory neurons. A LR mutant virus with three stop codons at the amino-terminus of ORF2 does not reactivate from latency or replicate efficiently in certain tissues. ORF2 inhibits apoptosis, interacts with Notch1 or Notch3, and interferes with Notch mediated signaling.

Stress-induced cellular transcription factors expressed in trigeminal ganglionic neurons stimulate the herpes simplex virus 1 ICP0 promoter.

Alphaherpesvirinae family members can reactivate from latency following stress. The synthetic corticosteroid dexamethasone induces certain cellular transcription factors in murine and bovine trigeminal ganglionic neurons. Three dexamethasone-induced transcription factors, Krüppel-like factor 15, Slug, and SPDEF, stimulated the herpes simplex virus type 1-infected cell protein 0 (ICP0) promoter more than 150-fold.

A protein (ORF2) encoded by the latency-related gene of bovine herpesvirus 1 interacts with DNA.

Bovine herpesvirus 1 (BHV-1), like other members of the Alphaherpesvirinae subfamily, establishes latency in sensory neurons. The virally encoded latency-related RNA (LR-RNA) is expressed abundantly in latently infected sensory neurons and encodes several proteins, including ORF2. An LR mutant virus with stop codons at the amino terminus of ORF2 does not reactivate from latency after treatment with the synthetic corticosteroid dexamethasone, in part because it induces higher levels of apoptosis during the establishment of latency.

A bovine herpesvirus 1 protein expressed in latently infected neurons (ORF2) promotes neurite sprouting in the presence of activated Notch1 or Notch3.

Bovine herpesvirus 1 (BHV-1) infection induces clinical symptoms in the upper respiratory tract, inhibits immune responses, and can lead to life-threatening secondary bacterial infections. Following acute infection, BHV-1 establishes latency in sensory neurons within trigeminal ganglia, but stress can induce reactivation from latency. The latency-related (LR) RNA is the only viral transcript abundantly expressed in latently infected sensory neurons.

ICP27 protein encoded by bovine herpesvirus type 1 (bICP27) interferes with promoter activity of the bovine genes encoding beta interferon 1 (IFN-β1) and IFN-β3.

Bovine herpes virus 1 (BHV-1) infection leads to upper respiratory tract infections, conjunctivitis, and the infection predisposes cattle to secondary bacterial infections. The infected cell protein 0 (bICP0) encoded by BHV-1 suppresses antiviral innate immune signaling by interfering with expression of interferon beta (IFN-β). In contrast to humans or mice, cattle contain three IFN-β genes that have distinct transcriptional promoters.

Cellular transcription factors induced in trigeminal ganglia during dexamethasone-induced reactivation from latency stimulate bovine herpesvirus 1 productive infection and certain viral promoters.

Bovine herpesvirus 1 (BHV-1), an alphaherpesvirinae subfamily member, establishes latency in sensory neurons. Elevated corticosteroid levels, due to stress, reproducibly triggers reactivation from latency in the field. A single intravenous injection of the synthetic corticosteroid dexamethasone (DEX) to latently infected calves consistently induces reactivation from latency.

Regulation of the latency-reactivation cycle by products encoded by the bovine herpesvirus 1 (BHV-1) latency-related gene.

Like other α-herpesvirinae subfamily members, the primary site for bovine herpesvirus 1 (BHV-1) latency is ganglionic sensory neurons. Periodically BHV-1 reactivates from latency, virus is shed, and consequently virus transmission occurs. Transcription from the latency-related (LR) gene is readily detected in neurons of trigeminal ganglia (TG) of calves or rabbits latently infected with BHV-1.

Localization of sequences in a protein (ORF2) encoded by the latency-related gene of bovine herpesvirus 1 that inhibits apoptosis and interferes with Notch1-mediated trans-activation of the bICP0 promoter.

Bovine herpesvirus 1 (BHV-1) infection induces clinical symptoms in the upper respiratory tract, inhibits immune responses, and can result in life-threatening secondary bacterial infections. Following acute infection, BHV-1 establishes latency in sensory neurons within trigeminal ganglia. Periodically, reactivation from latency occurs, resulting in virus transmission.

A protein (ORF2) encoded by the latency-related gene of bovine herpesvirus 1 interacts with Notch1 and Notch3.

Like other Alphaherpesvirinae subfamily members, bovine herpesvirus 1 (BHV-1) establishes latency in sensory neurons. The latency-related RNA (LR-RNA) is abundantly expressed in latently infected sensory neurons. An LR mutant virus with stop codons at the amino terminus of the first open reading frame (ORF) in the LR gene (ORF2) does not reactivate from latency, in part because it induces higher levels of apoptosis in infected neurons.

Copper transport activity of yeast Ctr1 is down-regulated via its C terminus in response to excess copper.

Copper is an essential yet toxic trace element. The Ctr1 family of proteins plays a critical role for copper uptake in eukaryotes. However, the mechanisms of action of Ctr1 are largely unknown.

Distinct mechanisms for Ctr1-mediated copper and cisplatin transport.

The Ctr1 family of integral membrane proteins is necessary for high affinity copper uptake in eukaryotes. Ctr1 is also involved in cellular accumulation of cisplatin, a platinum-based anticancer drug. Although the physiological role of Ctr1 has been revealed, the mechanism of action of Ctr1 remains to be elucidated.

A cadmium-transporting P1B-type ATPase in yeast Saccharomyces cerevisiae.

Detoxification and homeostatic acquisition of metal ions are vital for all living organisms. We have identified PCA1 in yeast Saccharomyces cerevisiae as an overexpression suppressor of copper toxicity. PCA1 possesses signatures of a P1B-type heavy metal-transporting ATPase that is widely distributed from bacteria to humans.