anti-Myeloid/lymphoid Or Mixed-Lineage Leukemia 1 (MLL1) Anticorps

Mouse (Murine) Myeloid/lymphoid Or Mixed-Lineage Leukemia 1 (MLL1) interaction partners

1. Results suggest that myeloid-lymphoid or mixed-lineage leukemia protein (MLL1) is indispensable for retinal neurogenesis and function development.

2. Distinct pathways affected by menin versus MLL1/MLL2 in MLL-rearranged acute myeloid leukemia.

3. Provide molecular insights into how SETD2 mutations accelerate MLLr leukemogenesis.

4. Wild-type MLL1 is a regulator of pre-BCR signaling.

5. Targeting PRMT5 using small-molecule inhibitors in the treatment of leukemias harboring MLL rearrangements.

6. Kmt2a is also important in memory formation

7. Collectively, these data indicated that ATR or ATM inhibition represent potential therapeutic strategies for the treatment of AML, especially MLL-driven leukemias.

8. Epigenomic profiling indicates an abnormal H3K79me2 pattern on MLL-fusion targeted genes, but the molecular mechanism underlying this epigenetic dependency is not well understood.

9. NUP98-HOXA9 interacts with MLL via the NUP98 second FG repeat domain. In the absence of MLL (in knockout mice), NUP98-HOXA9-induced cell immortalization and leukemogenesis are severely inhibited. MLL is important for the recruitment of NUP98-HOXA9 to the HOXA locus and for NUP98-HOXA9-induced HOXA gene expression. MLL is crucial for NUP98-HOXA9 leukemia initiation.

10. Atg5-dependent autophagy contributes to the development of acute myeloid leukemia in an MLL-AF9-driven mouse model.

11. These results define an important role for MLL1 in regulating macrophage-mediated inflammation in wound repair and identify a potential target for the treatment of chronic inflammation in diabetic wounds.

12. these results implicate an important role for MLL1-dependent epigenetic regulation of macrophage antimicrobial functions

13. These results reveal a cooperative transcriptional activation mechanism of AEP and DOT1L and suggest a molecular rationale for the simultaneous inhibition of the MLL fusion-AF4 complex and DOT1L for more effective treatment of MLL-rearranged leukemia.

14. This study demonstrated that Kmt2a regulates synaptic plasticity in striatal neurons and provides an epigenetic drug target for anxiety and dopamine-mediated behaviors.

15. Inactivation of Kmt2a in Men1-deficient mice accelerated pancreatic islet tumorigenesis and shortened the average life span. Increases in cell proliferation were observed in mouse pancreatic islet tumors upon inactivation of both Kmt2a and Men1.

16. Data suggest that RAS-homolog enriched in brain protein (Rheb1) promotes MLL-AF9 fusion protein initiated acute myeloid leukemia (AML) progression through target of rapamycin complex 1 (mTORC1) signaling pathway.

17. HoxBlinc RNA Recruits Set1/MLL Complexes to Activate Hox Gene Expression Patterns and Mesoderm Lineage Development.

18. MLL1 and DOT1L cooperate with meningioma-1 to induce acute myeloid leukemia.

19. Set1 role in cellular reprogramming and its interactions with Dpy30,Myc,Sox2 and Ash2l reprogramming factors

20. The present study examined the mechanism underlying the development of KMT2A (MLL)-rearranged infant leukemia in response to in utero exposure to etoposide in a mouse model.