Sentence examples for may explain deficient from inspiring English sources

These findings may explain deficient cognitive functions observed in individuals born preterm.

This may explain why Bim-deficient K562 cells (sh Bim) undergo high basal SA- β-Gal-positive cell population, although it is not significantly different from K562 sh Bim/sh ATG7.

The lack of barrier protection by kc when Perforin-2 is deficient may explain why Perforin-2 knockout mice rapidly (within days; Figure 7 figure supplement 2) exhibit symptoms to epicutaneous infection with MRSA.

Since inflammation of visceral fat is a crucial trigger of atherogenesis, decreased visceral fat in PGC-1α-deficient mice may explain why these mice do not develop enhanced atherosclerosis.

This observation has important implications for the interpretation of data derived from BM chimeras and may explain previous observations where LTα-deficient splenocytes were used to reconstitute irradiated RAG-1−/− and WT mice 2, 36.

Therefore, absence of accumulated glycogen within brain samples of LAMP-2-deficient mice may explain the lack of gross abnormalities in neuronal autophagy and suggest a distinct function of LAMP-2 within the hippocampus for autophagic clearance of neuronal proteins.

Since IGF-I-stimulated Akt activity did not statistically differ between control and p110α + p110β-deficient cells, yet there was virtually no p110/IGF-IR/IRS-1 p110/IGF-IR/IRS-1 p110/IGF-IR/IRS-1nhibition in p110α + p110β-deficient myoblassociationplain the mechanism underlossg the similarity in Akt activatiof.

A role in the repair of DSB by performing DNA synthesis during alternative microhomology-mediated end-joining has been shown in Drosophila [ 18, 19] and this potential DNA repair function may explain why mouse Pol θ-deficient bone marrow and erythrocyte cells as well as human Pol θ-depleted tumor cells show increased sensitivity to ionizing radiation [ 20, 21].

One mechanism that may explain the increased mortality of Pten deficient mice is increased angiogenesis.

Possible redundancy in the functions of NPY-like ligands may explain why initial examination of NPY deficient mice suggested no skeletal changes [12], a finding contradictory to experiments showing significant increases in bone mass following loss of NPY-producing neurons from the arcuate nucleus of the hypothalamus using monosodium glutamate treatment by the same group [13].

These findings may explain the developmental abnormalities of RPS24-deficient zebrafish.