We have cloned and sequenced a cDNA encoding gp34, a novel glycoprotein expressed in cells bearing human T-cell leukemia virus type I (HTLV-I). HTLV-I has a trans-acting transcriptional activator, p40tax, that is thought to be implicated in leukemogenesis through the activation of cellular enhancers. With a subline (JPX-9) of the human T-celi line Jurkat, in which p40 is inducible, gp34 was shown to be of cellular origin and to be transcriptionally activated by p40. It was also demonstrated that two species of mRNA are generated from one copy of the gp34 gene and that these mRNAs encode the identical gp34 product and differ in the 3' untranslated region. Analysis of the deduced amino acid sequence of gp34 showed that it lacks typical signal peptides; however, it has a hydrophobic stretch for membrane anchoring and four possible N-linked glycosylation sites at the carboxy-terminal portion, indicating that it belongs to the family of membrane proteins whose carboxy-terminal portion protrudes out of the cell. The gp34 gene displayed relatively delayed induction compared with other genes activated by p40. Taken together with the observation of the dependence of gp34 expression on HTLV-I p40, unlike other p4Otax-dependent genes such as those for the interleukin-2 receptor a chain and c-fos, which are expressed or induced under physiological conditions, we predict that the mechanism involved in the induction of gp34 expression by p40 is distinct from and more intricate than those for the previously characterized genes.
The possible transmission routes of hepatitis C virus (HCV) in patients without overt parenteral exposure (sporadic or community acquired form) were examined. Saliva and urine specimens obtained from type C hepatitis patients, whose sera were positive for the HCV genome, were examined by reverse transcription and polymerase chain reaction (RT-PCR). By analyzing the factors that influenced the detection of the HCV genome by PCR, we developed a single round method which enabled semiquantitative detection with higher sensitivity than that obtained with nested PCR. Single round PCR revealed that 34.8% (8 of 23) of saliva and 56.5% (13 of 23) of urine specimens from patients with type C hepatitis contained the HCV genome. The amounts of HCV genome in saliva and urine specimens correlated with those in serum. The relative amounts of HCV genome in serum, saliva, and urine from a chronic type C hepatitis patient were determined by comparing the reciprocal of the smallest volume of the specimens in which the PCR products were visualized in agarose gels (PCR units/ml), and the values were 1 x 10(5), 5 x 10(1), and 3 x 10(1) PCR units/ml for serum, saliva, and urine specimens, respectively.
We have cloned and sequenced a cDNA encoding gp34, a novel glycoprotein expressed in cells bearing human T-cell leukemia virus type I (HTLV-I). HTLV-I has a trans-acting transcriptional activator, p40tax, that is thought to be implicated in leukemogenesis through the activation of cellular enhancers. With a subline (JPX-9) of the human T-cell line Jurkat, in which p40tax is inducible, gp34 was shown to be of cellular origin and to be transcriptionally activated by p40tax. It was also demonstrated that two species of mRNA are generated from one copy of the gp34 gene and that these mRNAs encode the identical gp34 product and differ in the 3' untranslated region. Analysis of the deduced amino acid sequence of gp34 showed that it lacks typical signal peptides; however, it has a hydrophobic stretch for membrane anchoring and four possible N-linked glycosylation sites at the carboxy-terminal portion, indicating that it belongs to the family of membrane proteins whose carboxy-terminal portion protrudes out of the cell. The gp34 gene displayed relatively delayed induction compared with other genes activated by p40tax. Taken together with the observation of the dependence of gp34 expression on HTLV-I p40tax, unlike other p40tax-dependent genes such as those for the interleukin-2 receptor alpha chain and c-fos, which are expressed or induced under physiological conditions, we predict that the mechanism involved in the induction of gp34 expression by p40tax is distinct from and more intricate than those for the previously characterized genes.
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