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J John Cohen

Publications and source records attributed to J John Cohen.

4 recordsLinked to original sources
PubMed2004

The biological effects of five feline IFN-alpha subtypes.

IFN-alpha has been shown to induce both antiviral and antiproliferative activities in animals. This report describes the biological activity of five recently identified feline IFN-alpha subtypes expressed in the Chinese hamster ovary (CHO) cell line (rfeIFN-alpha1[CHO], rfeIFN-alpha2[CHO], rfeIFN-alpha3[CHO], rfeIFN-alpha5[CHO] and rfeIFN-alpha6[CHO]) and the feIFN-alpha6 subtype expressed in and purified from Pichia pastoris (rfeIFN-alpha6[P. pastoris]). The rfeIFN-alpha[CHO] subtypes were tested for antiviral activity against either Vesicular stomatitis virus (VSV) or feline calicivirus (FCV) infected feline embryonic fibroblast cell line (AH927) or Crandell feline kidney cell line (CRFK). Antiviral activity was induced against both VSV and FCV infected AH927 cells and VSV infected CRFK cells by all five of the rfeIFN-alpha[CHO] subtypes and rfeIFN-alpha6[P. pastoris]. In addition, the IFN-alpha inducible Mx gene (associated with antiviral activity) was upregulated in vivo 24 h following treatment with rfeIFN-alpha6[P. pastoris], compared to baseline levels seen prior to treatment. All of the rfeIFN-alpha[CHO] subtypes and rfeIFN-alpha6[P. pastoris] exhibited antiproliferative activity in the FeT-J cell line (an IL-2 independent feline T-cell line). Both necrosis and apoptosis were observed in rfeIFN-alpha6[P. pastoris]-treated FeT-J cells. The rfeIFN-alpha3[CHO] subtype consistently exhibited lower antiviral and antiproliferative activity compared to that observed with the other four rfeIFN-alpha[CHO] subtypes. In summary, this paper demonstrates that five previously described feIFN-alpha subtypes induce both antiviral and antiproliferative activities in vitro and are capable of upregulating the feMx gene in vivo.

Animals↗
PubMed2003

Quantitative structure-activity relationships of phenolic compounds causing apoptosis.

A study of a variety of phenolic compounds (simple phenols, estradiol, bisphenol A, diethylstilbesterol) on their action on L1210 leukemia cells led to the formulation of the following QSAR for apoptosis:log 1/C=-3.16 Clog P+2.77 CMR-3.76n=11, r(2)=0.939, s=0.630, q(2)=0.892C is the molar concentration causing 25% apoptosis, Clog P is the calculated octanol/water partition coefficient and CMR is the calculated molecular refractivity. Our results imply the significance of characterization of the phenolic compounds with apoptotic activity and the development of new agents for cancer therapy.

Algorithms↗
PubMed2003

Hydroquinone and catechol interfere with T cell cycle entry and progression through the G1 phase.

Cigarette smoking causes profound suppression of pulmonary T cell responses, which is associated with increased susceptibility to respiratory tract infections and decreased tumor surveillance. Hydroquinone (HQ) and catechol, at concentrations comparable to those found in cigarette smoke, are potent inhibitors of T cell activation and proliferation. We have previously shown that HQ and catechol inhibit ribonucleotide reductase, the rate-limiting enzyme in DNA synthesis. In this report we demonstrate that HQ and catechol also inhibit blastogenesis by interfering with T cell cycle entry and progression through the G(1) phase. In an attempt to localize the point in the cell cycle where arrest occurred, a set of key markers of activation and cell cycle progression were examined, including induction of c-Myc, up regulation of RNA synthesis, surface expression of CD71, and induction of E2F-dependent gene expression. Addition of HQ or catechol prior to stimulation inhibited each of these events without decreasing cell viability. However, production of IL-2 and surface expression of CD69 and CD25 were not affected, indicating that HQ and catechol inhibit only certain cell cycle events. These studies provide further indication of the regulatory pathways by which cigarette smoke inhibits T cell responses in the lungs of smokers.

Antigens, CD↗