Argyros et al. [ 13] reported the co-culture fermentation of an organic acid-deficient engineered T. saccharolyticum with a highly cellulolytic organism, C. thermocellumi, to produce ethanol from crystalline cellulose.
In the present study, influences of 3-HPA and lactate on 1,3-PD fermentation was investigated using two strains (KG1 and KG1Δldh (lactate dehydrogenase-deficient strain engineered from KG1)), and then 1,3-PD fermentation process was optimized by strategic glycerol feeding to keep the 3-HPA below the inhibitory level [[9]].
These studies have collectively shown that Hunk plays a vital role in promoting mammary tumorigenesis, as Hunk knockdown via shRNA in xenograft tumor models or crossing MMTV-neu or Pten-deficient genetically engineered mouse models into a Hunk knockout (Hunk-/) background impairs mammary tumor growth in vivo.
PI16-deficient mice were engineered and found to generate higher levels of processed chemerin than wildtype mice.
Electrophysiological recordings were carried out in the connexin-deficient N2A cells engineered to express wild-type or mutant connexins.
Properdin-deficient mice were genetically engineered through gene-specific targeting to be deficient of properdin and were shown to lack properdin in their serum [ 29].
Bacteria deficient for RNaseIII were engineered to produce high quantities of specific dsRNA segments.
To investigate the functional significance of this editing in vivo, we engineered mice deficient in GluR6 Q/R site editing.
The role of specific α2AR subtypes (α2a, α2b, and α2c) was characterized with hemodynamic measurements obtained from strains of genetically engineered mice deficient in either α2b or α2c receptors.
A recombinant P. aeruginosa PAO1ΔpscD::exlBA strain, deficient for T3SS but engineered to express ExlA, gained lytic capacity on endothelial cells and full virulence in mice, demonstrating that ExlA is necessary and sufficient for pathogenicity.
Recent studies using novel analytical tools, including basophil-depleting antibodies and genetically engineered mice deficient only in basophils, have illuminated the crucial and nonredundant roles for basophils in protective immunity against both ecto- and endoparasites.
