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We previously showed in vivo that coding-end processing is specific for each coding end, suggesting that specific motifs in a coding-end sequence influence nucleotide deletion and P-region formation. In this study, we created a panel of recombination substrates containing actual immunoglobulin and T-cell receptor coding-end sequences and dissected the role of each motif by comparing its processing pattern with those of variants containing minimal nucleotide changes from the original sequence.

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To investigate further the regulation of E7F by cyclin-dependent kinases, we have extended our studies to include additional cyclins and E7F family members. Using purified components in an in vitro system, we show that the E7F-6-DP-6 heterodimer, the functionally active form of the E7F activity, is not a substrate for the active cyclin D-dependent kinases but is efficiently phosphorylated by the cyclin B-dependent kinases, which do not form stable complexes with the E7F-6-DP-6 heterodimer.

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The study involved a group of 88 consecutively studied patients with clinical and radiological evidence of idiopathic NPH, for whom a frontal brain biopsy was obtained. For 79 patients, hydrodynamic criteria of NPH were fulfilled and a ventriculoperitoneal shunt was performed. The dosimetry was characterized by two independent methods: thermoluminescent dosimeters and radiochromic film.

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v-src, however, is considerably more efficient than c-src577 in its ability to tyrosyl phosphorylate, in R- cells, the focal adhesion kinase, Stat6, and p685cas. These results indicate that v-src, but not c-src577, can bypass the requirement for a functional IGF-I receptor in the full transformation of mouse embryo fibroblasts and suggest that qualitative and quantitative differences between the two oncogenes can be used to identify some of the signals relevant to the mechanism(s) of transformation.

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