IndraLab

Statements


| 8

sparser
"The observation that CRM1 binds Hoxa chromatin in CALM-AF10 expressing MEFs led us to question whether CRM1 is also present at HOXA loci in leukemia cells."

sparser
"We have demonstrated that in addition to mediating nuclear export of CALM-AF10, the interaction of CRM1 with CALM-AF10 directly regulates HOXA cluster gene expression."

sparser
"We have demonstrated that a CRM1-AF10 fusion protein phenocopies CALM-AF10 in its ability to bind and activate Hoxa and Meis1 genes and to induce leukemia, supporting a model in which CRM1 enables the tethering of CALM-AF10 to Hoxa and Meis1 effector genes, thereby recruiting the AF10/DOT1L transcriptional complex and causing leukemia."

sparser
"CALM-AF10 interacts with Crm1 via a Nuclear Export Signal (NES) contained in the CALM moiety, and mutation of the NES or pharmacological inhibition of the Crm1/NES interaction abolishes the ability of CALM-AF10 to bind to and activate the transcription of Hoxa genes."

sparser
"Interaction of CALM-AF10 with CRM1 is necessary to upregulate Hoxa gene expression."

sparser
"Together, these results suggest that the interaction of CALM-AF10 with CRM1 is necessary for upregulation of Hoxa cluster gene expression."

sparser
"Our results thus far support a model in which CALM-AF10 must interact with CRM1 (via the NES) to upregulate Hoxa gene transcription."

sparser
"Our observation that CALM-AF10 interacts with Hoxa chromatin in a CRM1-dependent manner led us to hypothesize that CRM1 itself may bind Hoxa loci thus allowing for recruitment of CALM-AF10."