Protein AF-10 (MLLT10) ELISA Kits

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 (105) and MLLT10 Proteins (3) and many more products for this protein.

list all ELISA KIts Gene Name GeneID UniProt
MLLT10 8028 P55197
MLLT10 17354 O54826
How to order from antibodies-online
  • +1 877 302 8632
  • +1 888 205 9894 (toll-free)
  • Order online
  • orders@antibodies-online.com

Top MLLT10 ELISA Kits at antibodies-online.com

Showing 1 out of 1 products:

Catalog No. Reactivity Sensitivity Range Images Quantity Delivery Price Details
Human
  96 Tests 2 to 3 Days
$380.00
Details

More ELISA Kits for MLLT10 Interaction Partners

Human Protein AF-10 (MLLT10) interaction partners

  1. In vitro, the overexpression of MLLT10 promoted colorectal cancer (CRC) cell migration and invasion, while after MLLT10 was knocked down, the opposite results were observed. In lung metastasis sites, the knockdown of MLLT10 in SW620 cells significantly inhibited Vimentin expression, whereas the E-Cadherin was increased. These results indicate that MLLT10 regulates the metastasis of CRC cells via EMT.

  2. In a retroviral transduction/transplantation mouse model, mice transplanted with MLL/AF10(OM-LZ) cells harboring PTPN11(wt) developed myelomonocytic leukemia. Those transplanted with cells harboring PTPN11(G503A) -induced monocytic leukemia in a shorter latency. Adding PTPN11(G503A) to MLL/AF10 affected cell proliferation, chemo-resistance, differentiation, in vivo BM recruitment/clonal expansion and faster progression.

  3. 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

  4. The PZP domain of AF10 senses unmodified H3K27 to regulate DOT1L-mediated methylation of H3K79.

  5. 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).

  6. Results provide evidence that transformation driven by MLL fusions as well as the recurrent AML-associated NUP98-NSD1 fusion oncogene is critically dependent on the ability of AF10 to stimulate DOT1L activity.

  7. detection of PICALM-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

  8. In pediatric T-acute lymphoblastic leukemia, we have identified 2 RNA processing genes, that is, HNRNPH1/5q35 and DDX3X/Xp11.3 as new MLLT10 fusion partners.

  9. 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

  10. 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

  11. a new susceptibility locus for meningioma at 10p12.31 (MLLT10, rs11012732, odds ratio = 1.46, P(combined) = 1.88 x 10(-14)) was identified.

  12. FISH analysis in infant AML-M5 showed a complex rearrangement between chromosomes 10 and 11, disrupting the MLL gene, a paracentric inversion of the 11q13-q23 fragment translocated to 10p12. AF10 was the fusion partner gene of MLL in this rearrangement.

  13. ALL1 is involved in remodeling, acetylating, deacetylating, and methylating nucleosomes and/or free histones

  14. data reveal new properties for the leucine zipper domain and thus might provide new clues to understanding the mechanisms by which AF10 fusion proteins in which the PHD domain is lost might trigger leukemias in humans

  15. The patients with immunophenotype of Pre-B-acute lymphoblastic leukemia were found to carry: MLL/AF10.

  16. Data show that the nuclear isoform of FLRG lacks an intrinsic transactivation domain, but enhances AF10-mediated transcription, probably through promoting the homo-oligomerization of AF10, thus facilitating the recruitment of co-activators.

  17. CALM(PICALM)/AF10 fusion protein might interfere with normal Ikaros (IKZF1)function, and thereby block lymphoid differentiation in CALM/AF10 positive leukemias.

  18. the CALM-AF10 fusion protein can also greatly reduce global H3K79 methylation in both human and murine leukemic cells by disrupting the AF10-mediated association of hDOT1L with chromatin

Mouse (Murine) Protein AF-10 (MLLT10) interaction partners

  1. Together these data are the first to demonstrate that Af10-dependent H3K79me is essential for development of nasal processes and adjacent tissues, and consequent midfacial formation.

  2. In lung metastasis sites, the knockdown of MLLT10 in SW620 cells significantly inhibited Vimentin expression, whereas the E-Cadherin was increased. These results indicate that MLLT10 regulates the metastasis of CRC cells via EMT.

  3. Results provide evidence that transformation driven by MLL fusions as well as the recurrent AML-associated NUP98-NSD1 fusion oncogene is critically dependent on the ability of AF10 to stimulate DOT1L activity.

  4. During leukemogenesis, CALM-AF10 plays critical roles in the cytoplasm.

  5. 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

  6. further suggest that future approaches to antagonize CALM-AF10-induced transformation should incorporate strategies, which aim at blocking these key domains

  7. conclude that Mllt10/Af10-Dot1l are essential, largely dedicated activators of Wnt-dependent transcription, critical for maintenance of intestinal proliferation and homeostasis

MLLT10 Antigen Profile

Antigen Summary

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.

Gene names and symbols associated with Protein AF-10 (MLLT10) ELISA Kits

  • MLLT10, histone lysine methyltransferase DOT1L cofactor (MLLT10) antibody
  • myeloid/lymphoid or mixed-lineage leukemia; translocated to, 10 (Mllt10) antibody
  • Af10 antibody
  • B130021D15Rik antibody
  • D630001B22Rik antibody
  • mKIAA4140 antibody

Protein level used designations for Protein AF-10 (MLLT10) ELISA Kits

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

GENE ID SPECIES
8028 Homo sapiens
17354 Mus musculus
Selected quality suppliers for MLLT10 (MLLT10) ELISA Kits
Did you look for something else?