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Histone acetyltransferase that acetylates lysine residues in histone H3 and histone H4 (in vitro). Additionally we are shipping and many more products for this protein.
Showing 10 out of 55 products:
Human Polyclonal MYST3 Primary Antibody for EIA, WB - ABIN953593
Paggetti, Largeot, Aucagne, Jacquel, Lagrange, Yang, Solary, Bastie, Delva: Crosstalk between leukemia-associated proteins MOZ and MLL regulates HOX gene expression in human cord blood CD34+ cells. in Oncogene 2010
Show all 5 references for ABIN953593
Human Polyclonal MYST3 Primary Antibody for ELISA - ABIN4234137
Rokudai, Aikawa, Tagata, Tsuchida, Taya, Kitabayashi: Monocytic leukemia zinc finger (MOZ) interacts with p53 to induce p21 expression and cell-cycle arrest. in The Journal of biological chemistry 2008
Histone acetyltransferase (show HAT Antibodies) sactivity of Moz regulates homeobox (show PRRX1 Antibodies) expression and segsmental identity.
Results show that Moz and Hox (show MSH2 Antibodies) genes function in cranial neural crest cells, but not in the ectoderm or endoderm, to specify the support skeleton.
In this study we report the frequency of FGFR1 (show FGFR1 Antibodies) and KAT6A involvement in patients with hematological malignancies and 8p11 abnormalities.
These data suggest that KAT6A may be a novel oncogene (show RAB1A Antibodies) in breast cancers bearing the 8p11-p12 (show POLE4 Antibodies) amplicon.
findings establish that MOZ and BMI1 (show BMI1 Antibodies) play opposing roles during the onset of Hox (show MSH2 Antibodies) gene expression in the ES cell model and during body segment identity specification in vivo.
We have identified KAT6A mutations as a frequent cause of syndromic developmental delay with microcephaly and dysmorphic features.
Heterozygous truncating mutations in KAT6A, as well as deletions of the same locus, cause a syndrome characterized by intellectual disability, craniosynostosis, cardiac defects, feeding difficulties, and distinct facial features.
MOZ-TIF2 (show NCOA2 Antibodies)/BRPF1 (show BRPF1 Antibodies) complex upregulates HOX (show MSH2 Antibodies) genes mediated by MOZ-dependent histone acetylation, leading to the development of leukemia.
The double PHD (show PDC Antibodies) finger domain of MOZ/MYST3 induces alpha-helical structure of the histone H3 (show HIST3H3 Antibodies) tail to facilitate acetylation and methylation sampling and modification.
Symplekin (show SYMPK Antibodies) interacts and co-localizes with both MOZ and MLL (show MLL Antibodies) in immature hematopoietic cells. Its inhibition leads to a decrease of the HOXA9 (show HOXA9 Antibodies) protein level but not of Hoxa9 (show HOXA9 Antibodies) mRNA.
Studies indicate the critical function of MOZ (MYST3 or KAT6A(1)) in haematopoiesis.
MYST3-CREBBP (show CREBBP Antibodies) rearrangement harbors a distinctive microRNA signature targeting RET proto-oncogene (show RET Antibodies) in acute myeloid leukemia (show BCL11A Antibodies) with translocation (8;16)(p11 (show S100A10 Antibodies);p13).
the expression of MOZ-TIF2 (show NCOA2 Antibodies) fusion protein represses the transcription of p16INK4a (show CDKN2A Antibodies) and p19ARF (show CDKN2A Antibodies) and blocks senescence.
Study establishes that MOZ is an upstream inhibitor of the INK4A-ARF (show CDKN2A Antibodies) pathway, and suggests that inhibiting MOZ may be one way to induce senescence in proliferative tumor cells.
these data suggest that the molecular pathogenesis of ventricular septal defectss in Moz germline mutant mice is due to loss of MOZ-dependant activation of mesodermal Tbx1 (show TBX1 Antibodies) and Tbx5 (show TBX5 Antibodies) expression.
MOZ regulates B-cell progenitors and, consequently, Moz haploinsufficiency dramatically retards MYC (show MYC Antibodies)-induced lymphoma development
These results suggest a critical requirement for MOZ HAT (show HAT Antibodies) activity to silence p16(INK4a (show CDKN2A Antibodies)) expression and to protect stem cells from early entrance into replicative senescence.
MOZ regulates B-cell memory formation, controlling memory compartment composition, an activity that is B cell-intrinsic and required for establishing the germinal center gene expression program.
MOZ interacts with the gene Tbx1 which influences heart and aortic arch development and is involved in DiGeorge syndrome.
The show that lack of the histone acetyltransferase (show HAT Antibodies) MOZ (MYST3/KAT6A) phenocopies DiGeorge syndrome, and the MOZ complex occupies the Tbx1 (show TBX1 Antibodies) locus, promoting its expression and histone 3 lysine 9 acetylation.
Moz is essential for a fundamental property of hematopoietic stem cells, the ability to reconstitute the hematopoietic system of a recipient after transplantation and that Moz is specifically required in the stem cell compartment.
MOZ is required for maintenance of hematopoietic stem cells, and that it plays a role in differentiation of erythroid and myeloid cells.
Histone acetyltransferase that acetylates lysine residues in histone H3 and histone H4 (in vitro). Component of the MOZ/MORF complex which has a histone H3 acetyltransferase activity. May act as a transcriptional coactivator for RUNX1 and RUNX2 (By similarity).
MYST histone acetyltransferase (monocytic leukemia) 3
, histone acetyltransferase MYST3
, monocytic leukemia zinc finger protein
, histone acetyltransferase MYST3-like
, K(lysine) acetyltransferase 6A
, MOZ, YBF2/SAS3, SAS2 and TIP60 protein 3
, Monocytic leukemia zinc finger protein
, histone acetyltransferase KAT6A
, runt-related transcription factor binding protein 2
, runt-related transcription factor-binding protein 2
, zinc finger protein 220
, monocytic leukemia zinc finger homolog
, MYST protein 3