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Thus, male infertility in Ing2−/− mice is attributed to quantitative and qualitative defects in mature spermatozoa.
We demonstrate that the increased number of γδ T cells in Id3−/− mice is attributed to the increase in SAP-dependent cells.
Rather, the low human T cell reconstitution rate in our control mice is attributed to inefficient engraftment of pro-T cells derived from bone marrow and poor thymic selection of human thymocytes.
Longevity of Ames dwarf mice is attributed to their resistance to oxidative stress.
Because FGF21 is an important metabolic regulator, we next investigated whether the atherosclerosis-prone phenotype of DKO mice is attributed to impaired glucose or lipid metabolism.
Previously we established that increased O2- production in STZ-induced diabetic mice is attributed to eNOS uncoupling, which was significantly attenuated by Ang II signaling blockers [ 16].
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The increased lipid accumulation in Ces1g deficient mice was attributed to activation of hepatic SREBP1c processing leading to increased lipogenesis.
The preservation of the renal function in USAG-1-/ mice was attributed to the enhancement of endogenous BMP signaling and action [39].
This increased clearance of E. coli by CD14-deficient mice was attributed to a rapid infiltration of neutrophils (PMNs) in the peritoneal cavity that was significantly delayed in normal mice [50].
The normal ERG responses in the rdgB2 and transthyretin knockout mice were attributed to likely functional compensation mechanisms and this explanation could well apply to the results obtained here.
LPS-induced mortality in Idh1 KO mice was attributed to massive hepatocyte apoptosis or cytotoxicity.
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