Generation of CRISPR/Cas9 ING5 knockout (KO) mice.
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posted on 2025-01-09, 18:35 authored by Buthaina Al Shueili, Arthur Dantas, Etienne Mahe, Tak Ho Chu, Yang Yang, Elodie Labit, Eren Kutluberk, Nicolas Lasaleta, Anand Masson, Hiba Omairi, Kenichi Ito, Roman J. Krawetz, Rajiv Midha, Gregory Cairncross, Karl RiabowolRelative ING5 mRNA levels in the brain, heart, kidney, liver, spleen, lung, and testis of ING5 KO mice compared to WT. The mRNA levels were normalized to 18S RNA. Analysis was performed for the two different mutations (1pb and 8bp deletion), using primers to amplify mRNA upstream of the mutation site (ING5_1) or downstream of the mutation site (ING5_2) as indicated by the red arrows. The graph shows mean ±SEM (n = 3).
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ing family membersh4 core histonesdiv >< paffecting gene expressiontarget histone acetyltransferasestem cell populationsstem cell maintenanceing5 targets mozcancer stem cellstumor suppressive rolefold higher ratecas9 ing5 knockouthbo1 hat complexesfold higherrate 6ing5 servinging5 functionshistone deacetylasehematopoietic cellscell lymphomascell cycletumor suppressortumor suppressionγh2ax indicatorvivo vitro type littermatesseveral tissuesprevious experimentsmultiple organshigh levelsh3k4me3 markepigenetic readersdna damagedata suggestalter acetylationactive transcriptionabnormal nuclei18 months
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