The parts of the molecule that pass through membrane are called transmembrane domains. ❋ Unknown (2009)
Those "transmembrane" protein gateways match the architecture of the membrane, with a hydrophobic center section bounded by two water soluble, or hydrophilic, layers. ❋ Unknown (2010)
Given this overlap in infection and human cell engraftment patterns, it may also be possible to deliver molecules in addition to cytokines, such as transmembrane receptors, that require direct cell-to-cell contact to mediate their effects. ❋ Ryan M. O'Connell Et Al. (2010)
The mutation, called G551D, is in a gene called the cystic fibrosis transmembrane conductance regulator. ❋ Jonathan D. Rockoff (2012)
Peter Mitchell who proposed an elaborate but basically "unphysical" mechanism for this transmembrane proton transport received a Nobel Prize. ❋ SETI Institute (2011)
Langzhou Song et al., “Structure of staphylococcal alpha-hemolysin, a heptameric transmembrane pore,” Science 274 1996, 1859–1866. ❋ Kevin Davies (2010)
For example, we know that cystic fibrosis manifests due to an irregularity in the ability to produce cystic fibrosis transmembrane conductance regulator (CFTR). ❋ Unknown (2009)
It consists of 5 cadherin repeats (EC1 ~ EC5) in the extracellular domain, one transmembrane domain, and an intracellular domain that binds p120-catenin and beta-catenin. ❋ Unknown (2007)
It turned out to be a cAMP-activated choride channel and was termed cystic fibrosis transmembrane conductance regulator (CFTR). ❋ Unknown (2007)
Returning to the case of cystic fibrosis, a PMG for an individual without the disease referred to one of a variety of transmembrane ion-channel templates along with all the epigenetic factors involved in the generation of the normal polypeptide product. ❋ Darden, Lindley (2009)
Individuals receive two copies of the cystic fibrosis transmembrane conductance regulator (CFTR) gene, one from each parent. ❋ Darden, Lindley (2009)
Mutations in the P. falciparum digestive vacuole transmembrane protein PfCRT and evidence for their role in chloroquine resistance. ❋ Michael J. Behe (2007)
But it does not just bind the toxin “passively” – upon binding, a non-selective ion channel is opened, leading to dissipation of transmembrane ion gradients, and all of the resulting events that accompany collapse of proton-motive force. ❋ Unknown (2007)
These experiments, which might have been the last performed by the hands of Jessell, led to the isolation of genes encoding the seven transmembrane domain serotonin receptor, ❋ Unknown (2005)
