anti-Myeloid/lymphoid Or Mixed-Lineage Leukemia (Trithorax Homolog, Drosophila) (MLL) Antikörper

Human Myeloid/lymphoid Or Mixed-Lineage Leukemia (Trithorax Homolog, Drosophila) (MLL) Interaktionspartner

1. Data indicate zinc finger protein 64 (ZFP64) as an essential transcription factor in mixed-lineage leukemia protein (MLL)-rearranged leukemia.

2. identified a distinctive signature for patients with KMT2A (MLL) rearrangement, with high HDAC9 and MEF2D expression, regardless of age, KMT2A partner and lineage.

3. PHF20L1 associates with SOX2, antagonizes SOX2 ubiquitination and the sequential degradation induced by the MLL1/WDR5 complexes

4. Results show that MLL1 gene is down regulated by miR-193a in prostate cancer and its 3'-UTR mRNA region interacts with miR-193a.

5. We report a comparison of the specificities of the human MLL1 and TET3 CXXC domains bound to dsDNA containing either cytosine, 5mC, or an enzymatically oxidized 5mC derivatives, in CpG or non-CpG context. With respect to CXXC domain specificity towards non-modified DNA, our work extends a recent analysis, but accounts more carefully for possible confounding influences of cytosine bases away from the site of interest.

6. GNB2 transcripts were significantly upregulated in human MLL-AML compared to MLL-negative AML.

7. This study analyzed the molecular and transcriptional consequences of human KMT2A variants to further understand the contribution of KMT2A-dependent methylation to the etiology of intellectual disability and hypertrichosis in Wiedemann-Steiner syndrome.

8. Reciprocal MLL fusion may be functionally rescued by a partially truncated MLL protein in childhood acute leukemias

9. These results support the notion that the CXXC zinc finger domain of KMT2A gene is a hotspot for missense variants associated with more severe neurophenotypes.

10. MLL-partial tandem duplication was detected in 6-7% of patients with MDS that were screened by the array during the same time period

11. This system provides for rapid systematic screening of relative risk, dose dependence, and combinatorial impact of multitudes of dietary and environmental exposures on MLL-AF9 translocations

12. Acute myeloid leukemia patients with high initial MLL-partial tandem duplication levels have lower induction complete remission and survival rates.

13. The molecular characterization of MLL breakpoints suggests different etiologies in the different age groups.

14. A pivotal pathway for MLL-rearranged leukaemic maintenance.

15. our work shows that ALOX5 plays a moderate anti-tumor role and functions as a drug sensitizer, with a therapeutic potential, in MLL-rearranged AML.

16. Studied lysine methyltransferase 2A (KMT2A) genetic rearrangements in child and young adult T-lymphoblastic leukemia/lymphoma.

17. Our experience suggests that AML with KMT2A rearrangement should be considered for the differential diagnosis of infantile cases with atypical monocytosis suggestive of JMML. Cytogenetic studies, including fluorescence in situ hybridization analysis of KMT2A, may be helpful in distinguishing between AML with KMT2A rearrangement and JMML.

18. Replication stress-induced recruitment of EndoG to the MLLbcr.

19. Wiedemann-Steiner syndrome causative splice and missense variants lead to reduction of KMT2A function.

20. SETD2 is required to maintain high H3K79 di-methylation and MLL-AF9-binding to critical target genes, such as Hoxa9.

Mouse (Murine) Myeloid/lymphoid Or Mixed-Lineage Leukemia (Trithorax Homolog, Drosophila) (MLL) Interaktionspartner

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.