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Cholera- and Anthrax-Like Toxins

issuu.com/rfieldhouse/docs/journal.pcbi.1001029...
Computer tools helped us uncover and understand potent protein toxins that empower bacterial pathogens against plants, animals and man. These toxins are potential drug targets and researchers can use them to make vaccines. New toxin knowledge aids the long-term goal of finding alternatives to antibiotics, to which pathogens are becoming more resistant. The toxins share similar structure despite low sequence identity, so our search links sequence and structure features. We present a ranked list and computational characterization of six new toxins combined with cell-based tests.
Uploaded by rfieldhouse on 01/05/2011
Digital publication details: 19 pages.

Human tumor-derived p53 exhibit binding site selectivity and TS for transactivation

issuu.com/charlesjdicomo/docs/oncogene-1998-di_como-2...
We examined the e fficacy by which p53 mutants bind to and activate reporters in an Saccharomyces cerevisiae-based assay. Analysis of 19 human tumor-derived p53 mutants, spanning the DNA binding domain of p53 and including the `hot-spot' class, revealed a broad array of transcriptional transactivation abilities at 248C, 308C and 378C, despite the fact that each mutant had originally been identified as being inactive for transactivation in yeast against a single p53-responsive RGC site-containing reporter. Strikingly, however, in contrast to the other tumor derived mutants, all of the previously identified `hot-spot' mutants were completely inactive with all sites tested. Finally, we found that transcriptional activity in vivo does not necessarily correlate with DNA binding in vitro.
Uploaded by charlesjdicomo on 12/19/2012
Digital publication details: 13 pages.

Molecular Biology Essentials

issuu.com/psygeo/docs/molecular_biology_essentials_20...
Life Technologies Molecular Biology Catalogue 2011/12
Uploaded by psygeo on 10/01/2011
Digital publication details: 300 pages.

Gene Therapy & Molecular Biology Volume 4 Issue A

issuu.com/gtmb/docs/vol4a...
Gene Therapy & Molecular Biology Volume 4 Issue A
Uploaded by gtmb on 02/15/2009
Digital publication details: 424 pages.

pharmaceutical microbio

issuu.com/sohailsaqi/docs/pharmaceutical_microbiology...
good book fro pharmcy students
Uploaded by sohailsaqi on 02/04/2011
Digital publication details: 383 pages.

Gene Therapy & Molecular Biology Volume 1 Issue A - Part 2

issuu.com/gtmb/docs/vol1a2...
Gene Therapy & Molecular Biology Volume 1 Issue A - Part 2
Uploaded by gtmb on 02/15/2009
Digital publication details: 236 pages.

Gene Therapy & Molecular Biology Volume 11 Issue B

issuu.com/gtmb/docs/vol11b2...
Gene Therapy & Molecular Biology Volume 11 Issue B
Uploaded by gtmb on 02/15/2009
Digital publication details: 459 pages.

Product List

issuu.com/steff.cocks/docs/prodlist2012-13...
Product List EU
Uploaded by steff.cocks on 05/27/2013
Digital publication details: 84 pages.

CNS Cell Model Systems

issuu.com/filarete/docs/cns_cell_model_systems...
Production and delivery of products and services for advanced reserach in neurosciences. Reference point for industrial applications in the field of neuropharmaceuticals, neurodevices and neurodiagnostics
Uploaded by filarete on 06/15/2010
Digital publication details: 7 pages.

p73 Function Is Inhibited by Tumor-Derived p53Mutants in Mammalian Cells

issuu.com/charlesjdicomo/docs/mol._cell._biol.-1999-d...
We show that both p73a and p73b activate the transcription of reporters containing a number of p53-responsive promoters in the p53-null cell line H1299. However, a number of significant differences were observed between p53 and p73 and even between p73a and p73b. Additionally, a Saccharomyces cerevisiae-based reporter assay revealed a broad array of transcriptional transactivation abilities by both p73 isoforms at 37°C. Our data suggest the possibility that in some tumor cells, an outcome of the expression of mutant p53 protein may be to interfere with the endogenous p73 protein.
Uploaded by charlesjdicomo on 12/19/2012
Digital publication details: 13 pages.
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