Commonwealth of Dominica: socio-economic assessment of the damage and losses caused by hurricane Dean

Includes bibliography

Belize: macro socio-economic assessment of the damage and losses caused by hurricane Dean

Includes bibliography

História ambiental no Brasil: o percurso historiográfico de Warren Dean

Pós-graduação em História - FCLAS

Allegacion en derecho por el Dean, Cabildo y Canonigos de la Santa Iglesia Colegial de la ciudad de Gandia con el colegio ... San Francisco de Borja y San Sebastian de la Compañia de Iesus de dicha ciudad.

Precede al tit.: "Iesus, Maria, Iosef..."

Por el Cabildo y Dean de la Santa Iglesia de Valencia con el Duque de Segorve y Cardona...

El texto alude al año 1635

Sermon panegirico ... que para celebrar la beatificacion de el B. Juan de Ribera hizo en el dia 22 de Enero de 1797 el Illmo Sr. dean y cabildo de la Santa Metropolitana ... Iglesia de Sevilla

Fecha y lugar de imp. constan en tít

3.6 William Masterson, Law School Dean, University of Missouri

https://bluetigercommons.lincolnu.edu/lgaines_sec1/1019/thumbnail.jpg

Suppression of tumor necrosis factor-induced cell death by inhibitor of apoptosis c-IAP2 is under NF-κB control

Members of the NF-κB/Rel and inhibitor of apoptosis (IAP) protein families have been implicated in signal transduction programs that prevent cell death elicited by the cytokine tumor necrosis factor α (TNF). Although NF-κB appears to stimulate the expression of specific protective genes, neither the identities of these genes nor the precise role of IAP proteins in this anti-apoptotic process are known. We demonstrate here that NF-κB is required for TNF-mediated induction of the gene encoding human c-IAP2. When overexpressed in mammalian cells, c-IAP2 activates NF-κB and suppresses TNF cytotoxicity. Both of these c-IAP2 activities are blocked in vivo by coexpressing a dominant form of IκB that is resistant to TNF-induced degradation. In contrast to wild-type c-IAP2, a mutant lacking the C-terminal RING domain inhibits NF-κB induction by TNF and enhances TNF killing. These findings suggest that c-IAP2 is critically involved in TNF signaling and exerts positive feedback control on NF-κB via an IκB targeting mechanism. Functional coupling of NF-κB and c-IAP2 during the TNF response may provide a signal amplification loop that promotes cell survival rather than death.

In vitro reconstitution of human replication factor C from its five subunits.

Replication factor C (RFC, also called Activator I) is part of the processive eukaryotic DNA polymerase holoenzymes. The processive elongation of DNA chains requires that DNA polymerases are tethered to template DNA at primer ends. In eukaryotes the ring-shaped homotrimeric protein, proliferating cell nuclear antigen (PCNA), ensures tight template-polymerase interaction by encircling the DNA strand. Proliferating cell nuclear antigen is loaded onto DNA through the action of RFC in an ATP-dependent reaction. Human RFC is a protein complex consisting of five distinct subunits that migrate through SDS/polyacrylamide gels as protein bands of 140, 40, 38, 37, and 36 kDa. All five genes encoding the RFC subunits have been cloned and sequenced. A functionally identical RFC complex has been isolated from Saccharomyces cerevisiae and the deduced amino acid sequences among the corresponding human and yeast subunits are homologous. Here we report the expression of the five cloned human genes using an in vitro coupled transcription/translation system and show that the gene products form a complex resembling native RFC that is active in supporting an RFC-dependent replication reaction. Studies on the interactions between the five subunits suggest a cooperative mechanism in the assembly of the RFC complex. A three-subunit core complex, consisting of p36, p37, and p40, was identified and evidence is presented that p38 is essential for the interaction between this core complex and the large p140 subunit.