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Human Monoclonal MYST3 Primary Antibody pour 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. dans Oncogene 2010
Show all 2 Pubmed References
Human Polyclonal MYST3 Primary Antibody pour 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. dans Oncogene 2016
Human Polyclonal MYST3 Primary Antibody pour ELISA - ABIN4234137
Rokudai, Aikawa, Tagata, Tsuchida, Taya, Kitabayashi: Monocytic leukemia zinc finger (MOZ) interacts with p53 to induce p21 expression and cell-cycle arrest. dans The Journal of biological chemistry 2008
Histone acetyltransferase (Montrer HAT Anticorps) sactivity of Moz regulates homeobox (Montrer PRRX1 Anticorps) expression and segsmental identity.
Results show that Moz and Hox (Montrer MSH2 Anticorps) genes function in cranial neural crest cells, but not in the ectoderm or endoderm, to specify the support skeleton.
Overexpression of KAT6A or TRIM24 (Montrer TRIM24 Anticorps) promoted PIK3CA (Montrer PIK3CA Anticorps) expression, AKT (Montrer AKT1 Anticorps) phosphorylation, and cell proliferation.
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 (Montrer ESR1 Anticorps) gene, and inactivating mutations in its HAT (Montrer MGEA5 Anticorps) domain abolished its ability to regulate ERalpha (Montrer ESR1 Anticorps), suggesting MYST3 functioning as a histone acetyltransferase (Montrer HAT Anticorps) that activates ERalpha (Montrer ESR1 Anticorps) promoter.
Studies show that misregulation of MOZ/MORF (Montrer KAT6B Anticorps) 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 (Montrer FGFR1 Anticorps) and KAT6A involvement in patients with hematological malignancies and 8p11 abnormalities.
These data suggest that KAT6A may be a novel oncogene (Montrer RAB1A Anticorps) in breast cancers bearing the 8p11-p12 (Montrer POLE4 Anticorps) amplicon.
findings establish that MOZ and BMI1 (Montrer BMI1 Anticorps) play opposing roles during the onset of Hox (Montrer MSH2 Anticorps) 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.
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 (Montrer BMI1 Anticorps) regulate HSCs in a synergistic manner by acting on distinct processes required to maintain HSCs.
BRPF2 (Montrer BRPF1 Anticorps)-MOZ complexes play an important role in the differentiation of embryonic stem cells via H3K14 acetylation.
the expression of MOZ-TIF2 fusion protein represses the transcription of p16INK4a and p19ARF and blocks senescence.
Study establishes that MOZ is an upstream inhibitor of the INK4A-ARF 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 (Montrer TBX1 Anticorps) and Tbx5 (Montrer TBX5 Anticorps) expression.
MOZ regulates B-cell progenitors and, consequently, Moz haploinsufficiency dramatically retards MYC (Montrer MYC Anticorps)-induced lymphoma development
These results suggest a critical requirement for MOZ HAT activity to silence p16(INK4a) 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