A novel Bax-associating protein, named MAP-1 (Modulator of Apoptosis), has been identified in a yeast twohybrid screen. MAP-1 contains a BH3-like (BH: Bcl-2 homology) motif and mediates caspase-dependent apoptosis in mammalian cells when overexpressed. MAP-1 homodimerizes and associates with the proapoptotic Bax and the prosurvival Bcl-2 and Bcl-X L of the Bcl-2 family in vitro and in vivo in mammalian cells. Mutagenesis analyses revealed that the BH3-like domain in MAP-1 is not required for its association with Bcl-X L but is required for association with Bax and for mediating apoptosis. Interestingly, in contrast to other Bax-associating proteins such as Bcl-X L and Bid, which require the BH3 and BH1 domains of Bax, respectively, for binding, the binding of MAP-1 to Bax appears to require all three BH domains (BH1, BH2, and BH3) of Bax, because point mutation of the critical amino acid in any one of these domains is sufficient to abolish its binding to MAP-1. These data suggest that MAP-1 mediates apoptosis through a mechanism that involves binding to Bax.

SummaryThe pattern of bilirubin response to phototherapy was studied using lamps with an emission spectrum closely similar to the bilirubin absorption spectrum. A dose-response relationship was demonstrated, with increased intensity of phototherapy resulting in greater response; however, the rate of bilirubin decline progressively decreased with increasing radiance till a 'saturation' point was reached, beyond which no further response occurred with further increase in radiance, suggesting a curvilinear relationship of the nature of an asymptotic regression. At the 'saturation' point, a 24-h decline of about 50% was achieved.With extended periods of phototherapy, a gradually decreasing response to phototherapy with declining bilirubin levels was 06served. both with maximal or moderate intensitv vhototheravv; an exponential regression was suggested. At abbit 5 mg/di iktfe further decline was observed with continued phototherapy. The rate of the 24-h decline evaluated at 6-h intervals was observed to be proportional to the bilirubin level at the start of the 24-h period.

No abstract

No abstract