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Human Monoclonal MYST3 Primary Antibody for ChIP, IP - ABIN2668559
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 2 Pubmed References
Human Polyclonal MYST3 Primary Antibody for WB - ABIN2668560
Yu, Liang, Cao, Wang, Gao, Lin, Schiff, Wang, Li: Identification of MYST3 as a novel epigenetic activator of ERα frequently amplified in breast cancer. in Oncogene 2016
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.
Given the similar findings in animal models and our patient's phenotypes, we hypothesize that KAT6A could play a role in development of the brain, face, and heart in humans
MYST3 binds to the proximal promoter region of ERalpha (show ESR1 Antibodies) gene, and inactivating mutations in its HAT (show MGEA5 Antibodies) domain abolished its ability to regulate ERalpha (show ESR1 Antibodies), suggesting MYST3 functioning as a histone acetyltransferase (show HAT Antibodies) that activates ERalpha (show ESR1 Antibodies) promoter.
Studies show that misregulation of MOZ/MORF (show KAT6B Antibodies) results in tumorigenesis and developmental disorders. Results also provide evidence that these 2 proteins play important role in regulating cell proliferation and stem cell maintenance. [review]
The demonstrate that the histone acetylation-binding double PHD finger (DPF) domains of human MOZ (also known as KAT6A) and DPF2 (also known as BAF45d) accommodate a wide range of histone lysine acylation with the strongest preference for propionylation (Kcr).
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.
Loss of MOZ in adult mice leads to the rapid loss of hematopoietic stem cells as defined by transplantation.
Our work revealed that MOZ and BMI1 (show BMI1 Antibodies) regulate HSCs in a synergistic manner by acting on distinct processes required to maintain HSCs.
BRPF2 (show BRPF1 Antibodies)-MOZ complexes play an important role in the differentiation of embryonic stem cells via H3K14 acetylation.
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.
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