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anti-Human MLL5 Anticorps:
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In the duloxetine-treated subsample (N=186), we observed suggestive associations with ZNF385D (rs4261893; beta=-0.46, P=1.55 x 10(-5)), NCAM1 (rs2303377; beta=0.45, P=1.76 x 10(-5)) and MLL5 (rs117986340; beta=0.91, P=3.04 x 10(-5)).
three dimensional structure of MLL5 SET domain unveils the structural basis for its lack of methyltransferase activity
MLL5 preserves spindle bipolarity through maintaining cytosolic PLK1 in a nonaggregated form.
MLL5 interacts with OGT and USP7 to form a stable ternary complex. Upregulation of MLL5 expression was correlated with increased expression of OGT and USP7 in human primary cervical adenocarcinomas.
Suggest a role for MLL5 and H3.3 in maintaining self-renewal hierarchies in adult glioblastomas.
O-GlcNAcylation of MLL5beta at T440 residue is critical for MLL5 recruitment to the HPV16/18-long control region through its interaction with AP-1.
Improved outcome is observed in decitabine-treated patients who express MLL5 at high levels.
KMT2E expression retained association with poor acute promyelocytic leukaemia remission rate and shorter survival while the association with disease-free survival was of marginal significance.
NMR solution structure of the MLL5 PHD domain
these results indicate that the suppression of MLL genes, especially MLL2 and MLL5, take part in modulating breast carcinogenesis.
MLL5 is a cellular ligand for the natural cytotoxicity receptor NKp44.
findings provide first insights into the molecular basis for the recruitment, exclusion, and regulation of MLL5 at chromatin
MLL5 can associate with HCF-1 and then be recruited to E2F1-responsive promoters to stimulate H3K4 trimethylation and transcriptional activation.
MLL5 functionally interacts with Borealin, facilitates the expression of chromosomal passenger complex, and hence contributes to mitotic fidelity and genomic integrity.
A new isoform, MLL5beta, truncated in exon 14, regulates E6 & E7 transcription in cervical carcinoma cells. Interaction of MLL5beta with the AP-1-binding site at the distal region of the HPV18 long control region activated E6/E7 transcription.
High MLL5 expression levels are associated with a favorable outcome and may improve risk and treatment stratification in acute myeloid leukemia
Phosphorylation of MLL5 may have an indispensable role in the mitotic progression in mixed lineage leukemia cells.
MLL5 forms intranuclear protein complexes that may play an important role in chromatin remodeling and cellular growth suppression.
These findings provide evidence that MLL5 might be an important cell cycle regulator, participating in cell cycle regulatory network machinery at multiple cell cycle stages.
MLL5 protein has been classified into a distinct subfamily with SETD5, because its SET domain and domain architecture show high homology with SETD5 rather than the members in MLL subfamily (i.e. MLL, MLL2, MLL3 and MLL4)
MLL5 has a role in suppressing antiviral innate immune response by facilitating STUB1-mediated RIG-I degradation
toxic reactive oxygen species levels in Mll5(-/-) mice are critically dependent on type 1 interferon (IFN-1) signaling, which triggers mitochondrial accumulation of full-length Bid.[IFN-1]
inactivation of the Mll5 gene in mice results in a 30% reduction in the average representation of hematopoietic stem cells and in functional impairment of long-term hematopoietic repopulation potential under competitive conditions
MLL5 is a key regulator of normal hematopoiesis
findings establish several nonredundant functions for Mll5, including an essential role in regulating proliferation and functional integrity of hematopoietic stem/progenitor cells
MLL5 plays an integral role in novel chromatin regulatory mechanisms that suppress inappropriate expression of S-phase-promoting genes and maintain expression of determination genes in quiescent cells.
This gene is a member of the myeloid/lymphoid or mixed-lineage leukemia (MLL) family and encodes a protein with an N-terminal PHD zinc finger and a central SET domain. Overexpression of the protein inhibits cell cycle progression. Alternate transcriptional splice variants have been characterized.
histone-lysine N-methyltransferase 2E
, histone-lysine N-methyltransferase MLL5
, lysine N-methyltransferase 2E
, myeloid/lymphoid or mixed-lineage leukemia 5 (trithorax homolog, Drosophila)
, myeloid/lymphoid or mixed-lineage leukemia protein 5
, myeloid/lymphoid or mixed-lineage leukemia 5
, myeloid/lymphoid or mixed-lineage leukemia protein 5 homolog