is a transcription factor, which acts like a software program that has the ability to control the function of other genes.
"As such, Meis1
could possibly be used as an on/off switch for making adult heart cells divide.
Its function in prostate cancer has not been well explored, but its regulation on the same set of genes together with MEIS1
in modules 7 and 9 suggests it may present as a coregulator with MEIS1
to be functional.
To test this idea, the researchers introduced an active form of beta-catenin into the progenitor cells after activating Hoxa9 and Meis1. Once injected into mice, these progenitor cells later induced leukemia.
Most young children with AML develop the disease as a result of what researchers call mixed lineage leukemia fusion proteins, which can activate the Hoxa9 and Meis1 genes.
The researchers have said that a large proportion of the millions of people who suffer from the syndrome have this mutated MEIS1 gene.
While common variants (different versions) of MEIS1 and BTBD9, another associated gene, have been found in families with a high incidence of restless legs syndrome, Vilarino-Guell said that it is not clear that those variants are capable of causing disease.
For example, pluripotency and sell-renewal marker MEIS1 was upregulated, while NANOG expression was downregulated at P15 in both normal hPDLSCs and MS-hPDLSCs.
Peak scoring networks from NANOG, MEIS1, and SIX3, which regulate stemness properties, in P15 hPDLSCs (a) and P15 MS-hPDLSCs (b) are shown.
Gene Fold changes MSC versus ALI versus ALI + MSC ALI + MSC control control versus control versus ALI Hhex 2.34 ** -1.14 3.17 ** 3.60 (##) Hoxa1 -1.27 2.55 ** 3.13 ** 1.23 Hoxa3 1.77 -1.01 -2.86 ** -2.86 (##) Hoxa5 2.09 ** -2.44 ** 1.97 4.81 (##) Hoxa9 1.97 1.88 11.16 ** 5.94 (##) Hoxb5 3.16 ** 2.07 ** 4.85 ** 2.34 (##) Hoxb7 3.17 ** 1.96 3.55 ** 1.81 Hox c9 2.11 ** 1.63 2.38 ** 1.46 Hoxd8 1.42 1.32 -3.01 ** -4.00 (##) Lhx2 2.03 ** 1.38 3.97 ** 2.88 (##) Meis1
-1.04 2.97 ** 1.47 -2.02 (##) ** p < 0.01 versus control; (##) P < 0.01 versus ALI.
The pathway gene expression modulation is similar for hGMSCs and hPDLSCs displaying the overexpression of transcripts such as FOXC1, MEIS1, STAT3, and ZFHX3 while hDPSCs reveal a unique gene signature with the overexpression of only three transcripts (GBX2, JARID2, and SKIL).
In fact, the intracellular pathways were differentially regulated, showing the specific activation of HESX1, MEIS1, and TCF7L1 in hPDLSCs; the activation of CDYL, GATA6, SALL1, and SMARCAD1 in hGMSCs; and the activation of GBX2, JARID2, and SKIL in hDPSCs.