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Traditionally, conflict resolution in an input-I. INTRODUCTION buffered switch is solved by finding a matching between inputs and outputs per time slot To do this, a switch not only needs to gather the information of the virtual output queues at the inputs, but also uses the gathered information to compute a matching. As such, both the communication(More)
The ORF45 gene of Kaposi's sarcoma-associated herpesvirus (KSHV) encodes a multifunctional tegument protein. Here, we characterize the transcriptional control of the ORF45 gene and show that its promoter can be activated by ORF50 protein, a latent-lytic switch transactivator. The ORF45 promoter can also be induced by sodium butyrate (SB), a histone(More)
UNLABELLED The orf47-orf46-orf45 gene cluster of Kaposi's sarcoma-associated herpesvirus (KSHV) is known to serially encode glycoprotein L (gL), uracil DNA glycosylase, and a viral tegument protein. Here, we identify two novel mRNA variants, orf47/45-A and orf47/45-B, alternatively spliced from a tricistronic orf47-orf46-orf45 mRNA that is expressed in the(More)
Femoral nerve injury is a rare complication after femoral angiography. Symptoms including quadri-ceps weakness and atrophy, absent or reduced knee jerk and sensory impairment along the anterior thigh and medial lower leg have been found. This leads to both muscular weakness and sensory deficit, which impairs walking and interferes with quality of life.(More)
The switch of Kaposi's sarcoma-associated herpesvirus (KSHV) from latency to lytic replication is a key event for viral dissemination and pathogenesis. MLN4924, a novel neddylation inhibitor, reportedly causes the onset of KSHV reactivation but impairs later phases of viral lytic program in infected cells. Thus far, the molecular mechanism involved in the(More)
The switch between latency and the lytic cycle of Kaposi's sarcoma-associated herpesvirus (KSHV) is controlled by the expression of virally encoded ORF50 protein. Thus far, the regulatory mechanism underlying the protein stability of ORF50 is unknown. Our earlier studies have demonstrated that a protein abundance regulatory signal (PARS) at the ORF50(More)
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