Characterization of a New Allele of the Human ERBB2 Gene by Allele-Specific Competition Hybridization

Genomics ◽  
1993 ◽  
Vol 15 (2) ◽  
pp. 426-429 ◽  
Author(s):  
Ali Ehsani ◽  
Jennifer Low ◽  
R.Bruce Wallace ◽  
Anna M. Wu
2003 ◽  
Vol 33 (4) ◽  
pp. 469-475 ◽  
Author(s):  
Julian C. Knight ◽  
Brendan J. Keating ◽  
Kirk A. Rockett ◽  
Dominic P. Kwiatkowski

2003 ◽  
Vol 358 (1434) ◽  
pp. 1133-1140 ◽  
Author(s):  
C. Nathan Hancock ◽  
Katsuhiko Kondo ◽  
Brian Beecher ◽  
Bruce McClure

Plants have many ways to regulate the type of pollen that arrives on the stigma surface. Once there, further control mechanisms regulate compatibility. The latter controls are largely based on biochemical interactions that support compatible pollination and prevent incompatible matings. S–RNase–based self–incompatibility (SI) systems are the most phylogenetically widespread mechanisms for controlling pollination. Studies of Nicotiana establish a firm link between SI and unilateral interspecific incompatibility. Although implicated in both inter– and intraspecific compatibility, S–RNase operates through at least three distinct genetic mechanisms that differ in their dependence on non–S–RNase factors. Identification and characterization of these non–S–RNase factors is currently an area of active research. Searching for genetic and biochemical interactions with S–RNase can identify candidate non–S–RNase factors. HT–protein is one factor that is required for S –allele–specific pollen rejection in the Solanaceae. Major style arabinogalactan proteins such as TTS interact biochemically with S–RNase. These glycoproteins are known to interact with compatible pollen tubes and have long been suggested as possible recognition molecules. Their binding to S–RNase implies a link between stylar systems for compatibility and incompatibility. Thus, genetic and biochemical studies suggest a highly networked picture of pollen–pistil interactions.


Vox Sanguinis ◽  
1995 ◽  
Vol 68 (2) ◽  
pp. 121-128 ◽  
Author(s):  
B.R. DuPont ◽  
S.G. Grant ◽  
S.H. Oto ◽  
W.L. Bigbee ◽  
R.H. Jensen ◽  
...  

2006 ◽  
Vol 50 (3) ◽  
pp. 1075-1078 ◽  
Author(s):  
E. T. Y. Leung ◽  
P. L. Ho ◽  
K. Y. Yuen ◽  
W. L. Woo ◽  
T. H. Lam ◽  
...  

ABSTRACT Multiplex allele-specific PCRs detecting katG codon 315 and mabA (bp −15) mutations could specifically identify 77.5% of isoniazid-resistant Mycobacterium tuberculosis strains in the South China region. One clinical isolate harboring InhA Ile194Thr was characterized to show strong association with isoniazid resistance in Mycobacterium tuberculosis.


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