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Conversely, RNF5 KO mice exhibit delayed repair of muscle damage associated with attenuated ER stress response.
Moreover, S100A4-deficient micexhibitit delayed tumor uptake, impaired stroma organization and suppression of metastasis [4], [6] [9].
At the cellular level, calvarial osteoblasts isolated from KO mice exhibit delayed rates of differentiation and defects in matrix production and mineralization [11].
Skin γδ T cells are important mediators of inflammation and tissue repair as mice deficient in γδ T cells (δ−/− mice) exhibit delayed wound healing [1].
Lungs from connexin 43−/− mice exhibit delayed formation of alveoli, narrow airspaces, and thicker interalveolar septae.
ANGPTL4-deficient mice exhibit delayed wound reepithelialization with impaired keratinocyte migration, angiogenesis and altered inflammatory response [ 43, 44].
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As expected, db/db mice exhibited delayed wound closure compared to wild type animals (Fig. 7A).
Administration of allopregnanolone solubilized in 2-hydroxypropyl-β-cyclodextrin (CD) to Npc1−/− mice at postnatal day 7 (P7) was reported to be beneficial, with treated mice exhibiting delayed clinical onset, extended life span, and reduced ganglioside accumulation.
The Tlr3 −/− mice exhibited delayed virus clearance throughout the disease.
Mammary glands from C/EBPβ-/ virgin mice exhibited delayed ductal outgrowth, distended ducts and decreased branching [ 9, 14].
Survival analysis suggested that RIP3−/− mice exhibited delayed fatal injury, although differences in survival did not ultimately reach statistical significance.
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