Sentence examples for deficiency in the expression of from inspiring English sources

A deficiency in the expression of TLR2 and 4 may also explain the lack response of these cells to NTHi as well.

In a previous study, we evaluated the role of the mitochondrial NAD-dependent IDH by generating transgenic plants displaying mild deficiency in the expression of this gene (Sienkiewicz-Porzucek et al. 2010).

IFN-resistant melanoma cells contain reduced levels of ISGF3a components, particularly of STAT-1, indicating that the non-responsiveness of melanoma cell lines to type I IFN may be due to a deficiency in the expression of ISGF3 components [ 7].

The expression of sucrase-isomaltase (SI), lactase-phlorizin hydrolase (LCT), trehalase (TREH), and maltase-glucoamylase (MGAM) are necessary for digesting sucrose, lactase, trehalose, and maltose, respectively, and deficiency in the expression of any of these enzymes results in severe digestive problems [ 54, 55].

These data suggest that the deficiency in the expression of ALK-1 receptors could be altering the ability of the cholinergic neurons studied to respond appropriately to factors such as TGF-β and BMP, which have a known neurotrophic activity and promote cholinergic differentiation, maintaining the cholinergic phenotype of differentiated cells (Lopez-Coviella et al., 2000; Schnitzler et al., 2010).

Genotyping to detect deficiencies in the expression of enzymes, e.g. those involved in metabolic activation or inactivation, may explain interindividual differences in susceptibility.

While the effects of the CAS on blood coagulation measured as activated partial thromboplastin time shortening are well documented, genetic mutations that result in deficiencies in the expression of either plasma prekallikrein (PPK) or factor XII (FXII) are not associated with spontaneous bleeding or increased bleeding risk during surgery.

Two or three deficiencies in the expression of ERCC1, XPF or PMS2 occur simultaneously in the majority of the 49 colon cancers evaluated by Facista et al. The chart in this section shows some frequent DNA damaging agents, examples of DNA lesions they cause, and the pathways that deal with these DNA damages.

Jurkat E6.1 T cells have deficiencies in the expression of lipid phosphatases PTEN and SHIP, leading to the constitutive activation of AKT, a serine-threonine kinase important for cell survival, and other downstream signaling molecules [16], [17], [18].

The reason for the distorted phosphorylation of PLCγ1 and Vav1 does not appear to be due to deficiencies in the expression of PTEN and SHIP, since we have recently shown that inhibition of PI3K does not alter the site specific phosphorylation of these proteins (NCO and JCDH, manuscript submitted).

It is well known that deficiencies in the expression of APM components can hinder or entirely abolish anticancer immune-responses by preventing proper CTL-induced cell lysis as a consequence of a reduced level of MHC-Class I antigen presentation [32], [33], [34].