Development and evaluation of a VP1-ELISA for detection of antibodies to duck hepatitis type 1 virus.

The VP1-encoding gene of the duck hepatitis type 1 virus (DHV-1) HP-1 strain was cloned and expressed in Escherichiacoli. The open reading frame (ORF) of VP1 comprised 714 bp and encoded 238 amino acids, with a predicated molecular mass of 26.5 kDa.

Specific reduction of fas-associated protein with death domain (FADD) in clear cell renal cell carcinoma.

Fas-associated protein with death domain (FADD) plays a major role in the execution of apoptosis. Attenuation of apoptosis is a hallmark of cancer. Through systemic examination of FADD in renal cell carcinoma (RCC) and adjacent nontumor kidney tissues from 85 patients, we demonstrated a significant reduction of FADD in clear cell RCC (ccRCC) compared to the respective nontumor kidney tissues.

Interaction of p14ARF with Brca1 in cancer cell lines and primary breast cancer.

We report an association between p14ARF and Brca1 in which both proteins co-immunoprecipitate (co-IP) in DU145 cells. The N-terminal 64 residues of p14ARF encoded by exon 1beta are sufficient for this association. Inside the cell, ectopic p14ARF co-localizes with ectopic and endogenous Brca1 in A375 cells.

Co-existence of high levels of the PTEN protein with enhanced Akt activation in renal cell carcinoma.

Recruiting Akt to the membrane-bound phosphatidylinositol (3,4,5) trisphosphate (PIP3) is required for Akt activation. While PI3 kinase (PI3K) produces PIP3, PTEN dephosphorylates the 3-position phosphate from PIP3, thereby directly inhibiting Akt activation. PTEN is the dominant PIP3 phosphatase, as knockdown of PTEN results in increases in Akt activation in mice.

ATM activation is accompanied with earlier stages of prostate tumorigenesis.

The ATM (ataxia telangiectasia mutated) kinase plays an essential role in maintaining genome integrity by coordinating cell cycle arrest, apoptosis, and DNA damage repair. Phosphorylation of ATM at serine 1981 (ATMpSer1981) by DNA damage activates ATM, which subsequently phosphorylates H2AX Ser139 (gammaH2AX), Chk2 Thr68 (Chk2pThr68), and p53 Ser15 (p53pSer15). To determine the role of the ATM pathway in prostate cancer tumorigenesis, we have analyzed 35 primary prostate cancer specimens for ATMpSer1981 (ATM activation), Chk2pThr68, gammaH2AX, and p53pSer15 by immunohistochemistry (IHC) in normal glands, prostatic intraepithelial neoplasias (PINs), and carcinomas.