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MLLT10 encodes a transcription factor and has been identified as a partner gene involved in several chromosomal rearrangements resulting in various leukemias. Additionally we are shipping MLLT10 Antibodies (130) and MLLT10 Proteins (3) and many more products for this protein.
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In a retroviral transduction/transplantation mouse model, mice transplanted with MLL/AF10(OM-LZ) cells harboring PTPN11 (show PTPN11 ELISA Kits)(wt) developed myelomonocytic leukemia. Those transplanted with cells harboring PTPN11 (show PTPN11 ELISA Kits)(G503A) -induced monocytic leukemia in a shorter latency. Adding PTPN11 (show PTPN11 ELISA Kits)(G503A) to MLL/AF10 affected cell proliferation, chemo-resistance, differentiation, in vivo BM recruitment/clonal expansion and faster progression.
Our results provide evidence for new loci influencing abdominal visceral (BBS9, ADCY8, KCNK9) and subcutaneous (MLLT10/DNAJC1/EBLN1) fat, and confirmed a locus (THNSL2) previously reported to be associated with abdominal fat in women
The PZP (show PZP ELISA Kits) domain of AF10 senses unmodified H3K27 to regulate DOT1L (show DOT1L ELISA Kits)-mediated methylation of H3K79.
we report that variants at the MLLT10 locus are unlikely to alter risk of glioma, and they have no prognostic value among patients with high-grade tumors (glioblastoma).
Results provide evidence that transformation driven by MLL fusions as well as the recurrent AML (show RUNX1 ELISA Kits)-associated NUP98 (show NUP98 ELISA Kits)-NSD1 fusion oncogene (show RAB1A ELISA Kits) is critically dependent on the ability of AF10 to stimulate DOT1L (show DOT1L ELISA Kits) activity.
detection of PICALM (show PICALM ELISA Kits)-MLLT10 fusion transcript occurs in 7% of children with T-lineage ALL and is not associated with a poorer outcome for patients treated with contemporary, intensive chemotherapy
In pediatric T-acute lymphoblastic leukemia, we have identified 2 RNA processing genes, that is, HNRNPH1 (show HNRNPH1 ELISA Kits)/5q35 and DDX3X (show DDX3X ELISA Kits)/Xp11.3 as new MLLT10 fusion partners.
results strongly indicate that the differential regulation of these three genes is not due to the break point effect but as a consequence of the CALM/AF10 fusion gene expression, though the mechanism of regulation is not well understood
In leukemia cells, full-length CALM-AF10 localized to the nucleus with no consistent effect on growth factor endocyctosis, and suppressed histone H3 lysine 79 methylation regardless of the presence of clathrin
a new susceptibility locus for meningioma at 10p12.31 (MLLT10, rs11012732, odds ratio = 1.46, P(combined) = 1.88 x 10(-14)) was identified.
During leukemogenesis, CALM-AF10 plays critical roles in the cytoplasm.
further suggest that future approaches to antagonize CALM-AF10-induced transformation should incorporate strategies, which aim at blocking these key domains
conclude that Mllt10/Af10-Dot1l (show DOT1L ELISA Kits) are essential, largely dedicated activators of Wnt (show WNT2 ELISA Kits)-dependent transcription, critical for maintenance of intestinal proliferation and homeostasis
This gene encodes a transcription factor and has been identified as a partner gene involved in several chromosomal rearrangements resulting in various leukemias. Multiple transcript variants encoding different isoforms have been found for this gene.
ALL1-fused gene from chromosome 10 protein
, protein AF-10
, type I AF10 protein
, type III AF10 protein
, type IV AF10 protein
, myeloid/lymphoid or mixed lineage-leukemia translocation to 10 homolog