Figure 2
Figure 2. MST1 expression. (A) MST1 transcript levels were quantified as the -fold difference of mRNA levels for MST1 normalized against the housekeeping gene ACTA1 (β-actin). Data are representative of 2 independent experiments performed in duplicate. (B) MST1 transcript levels were quantified as the -fold difference in mRNA levels for MST1 (normalized to ACTA1) in control sorted naive (CD4+ CD45RA+; CD8+ CD45RA+ CCR7+) and memory subpopulations of CD4 (CD4+ CD45RO+) and CD8 (CD8+ CD45RO+ CCR7−) T cells, as well as double-negative, double-positive, and single-positive thymocytes. Data are representative of 3 independent experiments performed in duplicate. (C) MST1 transcript levels in control and patient T cells. Data are representative of 5 independent experiments performed in duplicate. (D) A Western blot analysis of MST1 protein expression in lymphocytes from a healthy control, 2 heterozygous individuals (F2M, F1M), and 2 MST1-deficient patients with different homozygous nonsense mutations. Actin was used as the loading control. Data are representative of 5 independent experiments.

MST1 expression. (A) MST1 transcript levels were quantified as the -fold difference of mRNA levels for MST1 normalized against the housekeeping gene ACTA1 (β-actin). Data are representative of 2 independent experiments performed in duplicate. (B) MST1 transcript levels were quantified as the -fold difference in mRNA levels for MST1 (normalized to ACTA1) in control sorted naive (CD4+ CD45RA+; CD8+ CD45RA+ CCR7+) and memory subpopulations of CD4 (CD4+ CD45RO+) and CD8 (CD8+ CD45RO+ CCR7) T cells, as well as double-negative, double-positive, and single-positive thymocytes. Data are representative of 3 independent experiments performed in duplicate. (C) MST1 transcript levels in control and patient T cells. Data are representative of 5 independent experiments performed in duplicate. (D) A Western blot analysis of MST1 protein expression in lymphocytes from a healthy control, 2 heterozygous individuals (F2M, F1M), and 2 MST1-deficient patients with different homozygous nonsense mutations. Actin was used as the loading control. Data are representative of 5 independent experiments.

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