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

MLL encodes a transcriptional coactivator that plays an essential role in regulating gene expression during early development and hematopoiesis. De plus, nous expédions Myeloid/lymphoid Or Mixed-Lineage Leukemia (Trithorax Homolog, Drosophila) Anticorps (63) et beaucoup plus de produits pour cette protéine.

afficher tous les protéines Gène GeneID UniProt
MLL 4297 Q03164
MLL 214162 P55200
Rat MLL MLL 315606  
Comment commander chez anticorps-enligne
  • +1 877 302 8632
  • +1 888 205 9894 (toll-free)
  • Commandez enligne

Top Myeloid/lymphoid Or Mixed-Lineage Leukemia (Trithorax Homolog, Drosophila) Protéines sur

Showing 3 out of 3 products:

Catalogue No. Origin Source Conjugué Images Quantité Fournisseur Livraison Prix Détails
Cellules d'insectes Souris His tag „Crystallography Grade“ protein due to multi-step, protein-specific purification process 1 mg Connectez-vous pour afficher 70 Days
Cellules d'insectes Humain His tag „Crystallography Grade“ protein due to multi-step, protein-specific purification process 1 mg Connectez-vous pour afficher 70 Days
Escherichia coli (E. coli) Humain GST tag Recombinant MLL / HRX - SET protein gel. MLL / HRX - SET protein was run on a 10% SDS-PAGE gel and stained with Coomassie blue. 50 μg Connectez-vous pour afficher 1 to 2 Days

MLL Protéines protéines par origine et source

Origin Exprimée danse Conjugué
Human ,
Mouse (Murine)

Plus protéines pour Myeloid/lymphoid Or Mixed-Lineage Leukemia (Trithorax Homolog, Drosophila) (MLL) partenaires d'interaction

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

  1. 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.

  2. Whole exome sequencing reveals a MLL de novo mutation associated with mild developmental delay and without 'hairy elbows': expanding the phenotype of Wiedemann-Steiner syndrome.

  3. Diagnosis and relapse: cytogenetically normal acute myelogenous leukemia without FLT3-ITD or MLL-PTD.

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

  5. 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

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

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

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

  9. 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.

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

  11. 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.

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

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

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

  15. One of the USP10 targets is TP53. Wildtype TP53 is usually rescued from proteasomal degradation by USP10. As most KMT2A leukemias display wildtype p53 alleles, one might argue that the disruption of an USP10 allele can be classified as a pro-oncogenic event.

  16. this work highlights that MLLr AML comprises of an AML subgroup affecting younger patients with poor prognosis. The allo-HSCT in MRD-negative patients could be the best therapeutic option.

  17. Myeloid Zinc Finger 1 and GA Binding Protein Co-Operate with Sox2 in Regulating the Expression of Yes-Associated Protein 1 in Cancer Cells

  18. This study demonstrates a tractable approach for respecifying iPSC-derived blood cells into highly engraftable hematopoietic stem and progenitor cells (HSPCs) through transient expression of a single transcription factor, MLL-AF4

  19. the influence of TGFbeta/SMADs on MLL- and MLL-AF4-mediated 5-LO promoter activation

  20. Chromosomal translocations involving MLL1 appear to directly perturb the regulation of multiple chromatin-associated complexes to allow inappropriate expression of developmentally regulated genes and thus drive leukemia development. [review]

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

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

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

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

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

  5. Kmt2a is also important in memory formation

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

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

  8. 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.

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

  10. 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.

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

  12. 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.

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

  14. 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.

  15. 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.

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

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

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

  19. 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.

  20. We have demonstrated that the Mll1 gene is critical to Th1 differentiation in humans and mice

Profil protéine Myeloid/lymphoid Or Mixed-Lineage Leukemia (Trithorax Homolog, Drosophila) (MLL)

Profil protéine

This gene encodes a transcriptional coactivator that plays an essential role in regulating gene expression during early development and hematopoiesis. The encoded protein contains multiple conserved functional domains. One of these domains, the SET domain, is responsible for its histone H3 lysine 4 (H3K4) methyltransferase activity which mediates chromatin modifications associated with epigenetic transcriptional activation. This protein is processed by the enzyme Taspase 1 into two fragments, MLL-C and MLL-N. These fragments reassociate and further assemble into different multiprotein complexes that regulate the transcription of specific target genes, including many of the HOX genes. Multiple chromosomal translocations involving this gene are the cause of certain acute lymphoid leukemias and acute myeloid leukemias. Alternate splicing results in multiple transcript variants.

Gene names and symbols associated with MLL

  • lysine methyltransferase 2A (KMT2A)
  • lysine (K)-specific methyltransferase 2A (Kmt2a)
  • lysine methyltransferase 2A (Kmt2a)
  • 6430520K01 Protéine
  • ALL-1 Protéine
  • All1 Protéine
  • Cxxc7 Protéine
  • HRX Protéine
  • HTRX1 Protéine
  • mKIAA4050 Protéine
  • Mll Protéine
  • MLL/GAS7 Protéine
  • Mll1 Protéine
  • MLL1A Protéine
  • TET1-MLL Protéine
  • TRX1 Protéine
  • WDSTS Protéine

Protein level used designations for MLL

CDK6/MLL fusion protein , CXXC-type zinc finger protein 7 , MLL-AF4 der(11) fusion protein , MLL/GAS7 fusion protein , MLL/GMPS fusion protein , histone-lysine N-methyltransferase 2A , lysine N-methyltransferase 2A , myeloid/lymphoid or mixed-lineage leukemia (trithorax homolog, Drosophila) , myeloid/lymphoid or mixed-lineage leukemia protein 1 , trithorax-like protein , zinc finger protein HRX , histone-lysine N-methyltransferase MLL , myeloid/lymphoid or mixed-lineage leukemia 1 , trithorax Drosophila , Mixed-lineage leukemia (also acute lymphocytic leukemia 1 or tritorax Drosophila gene)

4297 Homo sapiens
214162 Mus musculus
315606 Rattus norvegicus
Fournisseurs de qualité sélectionnés pour Myeloid/lymphoid Or Mixed-Lineage Leukemia (Trithorax Homolog, Drosophila) Protéines (MLL)
Avez-vous cherché autre chose?