Constitutive activation of signal transducers and activators of transcription (STATs) has been associated with oncogenesis. Previously, a protein required for T-cell transformation by the DNA tumor virus herpesvirus saimiri (HVS) strain 484, designated tyrosine kinase-interacting protein (Tip-484), was shown to interact with and dramatically upregulate the activity of the STATs in an Lck-dependent manner. The minimal region of Tip-484 responsible for binding Lck was defined as a 10-residue C-terminal Src-related kinase homology domain, an 18-amino-acid spacer, and a 10-residue potential SH3 binding domain. This region is termed the LBD (for Lck binding domain). The present data show that only the LBD of Tip-484 is needed to activate Lck in vitro and in vivo. Finally, the LBD was shown to form a complex with STAT3 in vitro, and expression of the LBD in T cells led to STAT3 activation equal to that of full-length Tip-484. These studies demonstrate that the 48-amino-acid LBD of Tip-484 can perform as effectively as the full-length protein in vitro and in vivo.

Although seat belts significantly reduce the extent and severity of injuries sustained by motor vehicle occupants, seat belts are known to be associated with chest and abdominal trauma. Less commonly understood are severe neck injuries caused by the use of two-point automatic shoulder harnesses without concurrent use of a manual lap belt. Such injuries may include cervical spine fractures, craniocervical dislocations and rarely decapitation. Recognizing patterned injuries caused by seat belts and the ability to correlate autopsy findings with the circumstances surrounding the death will allow for correct interpretation of seat-belt related trauma. The four cases described detail fatal neck injuries as a result of improper seat belt use in which an automatic two-point shoulder harness was used without a manual lap restraint. In two of the cases, the victims were decapitated.