Sentence examples for mutation or knockdown from inspiring English sources

Nearly all of these models have been constructed via mutation or knockdown of a single gene, or by heterologous expression of a transgene.

This proinflammatory transcriptional response provides a useful readout for characterizing the consequences of mutation or knockdown of host genes involved in the immune response.

Also, bro-1, a cofactor of rnt-1, interacts with rnt-1 and its mutation or knockdown affects hypoplasia of hypodermal seam cells (Kagoshima et al. 2007; Shim and Lee 2008).

Surprisingly, SMC3 knockdown resulted in detectable chromatin decompaction at only one of the tested loci and not at the loci that were most susceptible to NIPBL mutation or knockdown.

In murine embryoid bodies and human CD34+ cord blood cells ectopic Klf1 expression suppressed both Fli-1 expression and Mk progenitor formation, whereas mutation or knockdown of Klf1 (or its human homologue) was found to increase Mk differentiation (Frontelo et al, 2007; Bouilloux et al, 2008).

In other studies, we found that toxic inhibition of complex III (cIII) by antimycin or cIV by cyanide, or phenotypes resulting from mutations or knockdown of cIV subunits or the cIV assembly factor Surf1 in Drosophila, could be mitigated by concomitant expression of the mitochondrial alternative oxidase (AOX) from Ciona intestinalis (Fernández-Ayala et al. 2009; Kemppainen et al. 2014).

Genetic mutations or knockdowns can be identified, given that their phenotypic consequence regarding leukocyte behavior during inflammation lies within the sensitivity threshold of the ChIn assay.

These defects are similar to those reported for other zebrafish USH gene mutations or knockdowns (Ernest et al., 2000; Söllner et al., 2004; Seiler et al., 2005) and indicate reduced function of both the auditory and vestibular systems.

Having assessed their predicted properties, the next step was to assess whether disruption of their expression by mutation or RNAi knockdown causes readily observable phenotypes.

A specific 3′UTR-targeting site, localized within the retained intron between exons 6 and 7, was identified, and its mutation, or miR-574-5p miR-574-5p miR-574-5phe degradation of CerS1-2 mRNA.

When MMCs are intact but RPMs are impaired for other reasons (e.g., disruption of the SUN/KASH bridge, tubulin depolymerization, ATP depletion, spd-3 mutation, or dynein knockdown), chromosome pairing is severely reduced or absent and SCs start to be formed between non-homologs.