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Shih-Yi Wu

Publications and source records attributed to Shih-Yi Wu.

2 recordsLinked to original sources

Induction of the early growth response 1 gene by Epstein-Barr virus lytic transactivator Zta.

Early growth response 1 (Egr-1) is a cellular transcription factor involved in diverse biologic functions. Egr-1 has been associated with Epstein-Barr virus (EBV) infection, but it is still unknown whether any EBV protein regulates Egr-1 expression. In this study, we first showed that EBV reactivation is involved in upregulation of Egr-1 and that Egr-1 can be induced by Zta, an EBV lytic transactivator. Zta not only binds to the Egr-1 promoter but also activates the ERK signaling pathway to trigger binding of Elk-1 to the Egr-1 promoter. In addition, knockdown of Egr-1 significantly reduces the spontaneous expression of Zta and Rta in EBV-infected 293 cells, suggesting that a positive-feedback network involving Egr-1 is required for EBV reactivation. This study also implies that Zta has the potential to affect expression of certain genes through Egr-1.

Base Sequence↗

Ring (Y) in two azoospermic men.

We have identified two azoospermic men with r(Y) in 312 infertile men presenting with non-obstructive azoospermia or oligozoospermia. Their karyotypes were 45,X [9]/46,X, r(Y)(p11q11) [11] (case 1), and 46,X,r(Y)(p11q11) (case 2), respectively. In both cases, the Yp breakpoints were located within the pseudoautosomal region. Both cases had extensive deletions of azoospermia factors (AZFs). Case 1 also had deletion of the putative growth controlling gene (GCY) and the Yq breakpoint was located between sY741 and USP9Y. The Yq breakpoint was located between sY105 and sY109 in case 2. Both cases did not have Turner stigmata except short stature in case 1. By a combination of cytogenetic and molecular genetic tools, we showed r(Y) arose from breakage in both arms of the chromosome with subsequent fusion of two broken ends of the centric fragment to form a continuous ring. Spermatogenic defects in men with r(Y) may result from deletion of Y-linked AZFs combined with synaptic failure.

Adult↗