Ex vivo therapeutic base and prime editing using chemically derived hepatic progenitors in a mouse model of tyrosinemia type 1. Kim et al.

Published: 11-05-2021| Version 1 | DOI: 10.17632/rf6wscfvhw.1
Contributor:
Sangsu Bae

Description

Bipotent differentiation capacity of HT1-mCdHs. (A) Gene expression levels of mature hepatocyte-specific markers determined by RT-qPCR. Gapdh was used as an internal control. Data are mean ± SD (n=9). Data were analyzed by the t test, *p<0.05, **p<0.01, ***p<0.001. (B) Activated gene sets in HT1-mCdH-Heps as generated by GSEA using liver-specific (left) and hepatocyte-specific (right) genes. NES reflects the degree of over-representation for each group at the peak of the entire set. Statistical significance was calculated by nominal p value of the NES by using an empirical phenotype-based permutation test. (C) Blue-Pink O' Gram displaying differentially expressed liver-specific genes in HT1-mCdHs and HT1-mCdH-Heps. (D) Bright-field image of HT1-mCdH-Chols, which have been cultured under conditions to induce cholangiocytic differentiation. Scale bars, 100 μm. (E) Gene expression levels of cholangiocyte-specific markers in HT1-mCdH-Chols measured by RT-qPCR. Gapdh was used as an internal control. Data are mean ± SD (n=9). Data were analyzed by the t test, *p<0.05, **p<0.01, ***p<0.001.

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