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It has been reported that deletion of the hepatocyte intermediate filament proteins, keratin 8/keratin 18 heterodimers, increases apoptosis [22].
Moreover, it has been reported that deletion of the meiosis-specific Cohesin component SMC1β causes meiotic chromosome mis-segregation [12], [13].
It has also been reported that deletion of the papG gene had no effect on pilus formation; however, the pili isolated from a papG deletion strain were not adhesive [29].
It has been reported that deletion or substitution of this C-terminal residue negatively affects the biogenesis of OMPs [ 10, 11].
It has been reported that deletion of Wfs1 results in ER stress and the initiation of the UPR (Fonseca et al, 2010; Yamada, 2006).
It has previously been reported that deletion of certain genes that affect translation may confer sensitivity to multiple drugs that target translation.
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It was reported that deletion of FOB1 gene maintains rDNA repeat copy number at a constant level.
Recently it was reported that deletion in mice of the region orthologous to the 9p21 CAD interval in human affects the expression of the nearby cdkn2a and cdkn2b genes as well as the properties of proliferation of vascular cells [30].
It was reported that deletion of 6q22 in PCNSL revealed an aggressive clinical course or poor prognosis.
In previous studies, it was reported that deletion of LKB1 in skeletal muscle [ 26] or heart [ 27] resulted in loss of AMPKα2 activity, but AMPKα1 activity was only partially reduced or was up-regulated.
In the current study from F. Brad Johnson's lab, it was reported that deletion of the Sgs1 helicase, which belongs to the same RecQ family of DNA helicases as that of the WS helicase (WRN) or BS helicase (BLM), rescues the temperature sensitive phenotypes of cdc13-1 [ 1].
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