KAT6B

Official Full Name

lysine acetyltransferase 6B

Organism

Homo sapiens

Gene ID

23522

Background

The protein encoded by this gene is a histone acetyltransferase and component of the MOZ/MORF protein complex. In addition to its acetyltransferase activity, the encoded protein has transcriptional activation activity in its N-terminal end and transcriptional repression activity in its C-terminal end. This protein is necessary for RUNX2-dependent transcriptional activation and could be involved in brain development. Mutations have been found in patients with genitopatellar syndrome. A translocation of this gene and the CREBBP gene results in acute myeloid leukemias. Three transcript variants encoding different isoforms have been found for this gene. [provided by RefSeq, Mar 2012]

Synonyms

qkf; MORF; MOZ2; GTPTS; MYST4; ZC2HC6B; querkopf

Cat.No.	Product Name	Price
CSC-DC007897	Panoply™ Human KAT6B Knockdown Stable Cell Line	Inquiry
CSC-SC007897	Panoply™ Human KAT6B Over-expressing Stable Cell Line	Inquiry

Cat.No.	Product Name	Price
AD10463Z	Human MYST4 adenoviral particles	Inquiry
LV19037L	human MYST4 (NM_012330) lentivirus particles	Inquiry

Cat.No.	Product Name	Price
SHH322455	shRNA set against Human KAT6B (NM_012330.3)	Inquiry
SHH348574	shRNA set against Mouse MYST4 (NM_017479.3)	Inquiry

Cat.No.	Product Name	Price
MiUTR3H-08013	KAT6B miRNA 3'UTR clone	Inquiry
CDCB184035	Rabbit KAT6B ORF clone (XM_002718403.2)	Inquiry
CDCL122615	Human KAT6B ORF clone (NM_001256468.1)	Inquiry
CDCL122617	Human KAT6B ORF clone (NM_001256469.1)	Inquiry
CDCR253492	Mouse Myst4 ORF Clone(NM_017479.3)	Inquiry

Detailed Information

Recent Research

KAT6B (also named as MORF, MYST4), a histone acetyltransferase, has been implicated in leukemogenic and other tumorigenic processes. KAT6B and its homologous paralog MOZ (monocytic leukemic zinc-finger protein) have been shown to be involved in many biological processes, such as transcriptional regulation, DNA repair, the cell cycle and signal transduction.

Small cell lung cancer (SCLC) is an aggressive tumor with the feature of accelerated growth, frequent metastases and premature death. Some reports identified the presence of homozygous deletions of the candidate KAT6B, and the loss of the corresponding transcript, in SCLC cell lines and primary tumors. It has been shown, in vitro and in vivo, that the depletion of KAT6B expression enhances cancer growth, whilst its restoration induces tumor suppressor-like features. Importantly, KAT6B exerts its tumor inhibitory role through a newly defined type of histone H3 Lys23 acetyltransferase activity.

Tongue squamous cell carcinoma (TSCC) is the most common oral cancer. It has been found a strong correlation between miR-22 expression and chemosensitivity to cisplatin (CDDP) in TSCC patients. Mechanistically, miR-22 over-expression or KAT6B knockdown inhibited PI3K/Akt/NF-κB signaling in TSCC cells, possibly via down-regulating the activators of PI3K/Akt/NF-κB signaling, such as S100A8, PDGF and VEGF.

KAT6B is widely expressed in various mouse and human tissues. It has demonstrated that KAT6B acts as coactivators for different transcription factors such as Runxs, Hox, ETV6, PU.1, and P53; KAT6B translocation is also associated with childhood AML or therapeutic myelodysplastic syndromes, in which the KAT6B gene is fused to that of CBP. KAT6B is also disrupted in multiple cases of uterine leiomyomata. KAT6B has been shown to be coactivators of Runx genes. Runx2 functions as a novel oncogenic effector for T-cell lymphoma. Runx1 is an important regulator of fetal liver hematopoiesis, and its gene is frequently rearranged in leukemia patients. The expression levels of KAT6B may affect roles of Runx proteins in the development of T-cell lymphoma and leukemogenesis.

In addition, some reports showed that KAT6B is strongly suppressed in macrophages by lipopolysaccharide (LPS) (M1 activation), while KAT6A, its partner in the MOZ/MORF complex, is reciprocally up-regulated. This pattern of expression is not altered by LPS together with the adenosine receptor agonist NECA (M2d activation). In addition, MYST3 was reciprocally up-regulated by LPS, while MYST1, MYST2, and MYST5 were only marginally aﬀected. Furthermore, the expression of KAT6B positively correlates with mandibular prognathism, and with Class II myosin heavy chain (MHCs type IIA and IIX) expression in masseter muscle.

References:

Shukla S, et al. The Kat in the HAT: The Histone Acetyl Transferase Kat6b (MYST4) Is Downregulated in Murine Macrophages in Response to LPS. Mediators of Inflammation, 2018, 2018(4):1-11.
Simó-Riudalbas L, et al. KAT6B Is a Tumor Suppressor Histone H3 Lysine 23 Acetyltransferase Undergoing Genomic Loss in Small Cell Lung Cancer. Cancer Research, 2015, 75(18):3936.
Desh H, et al. Molecular motor MYO1C, acetyltransferase KAT6B and osteogenetic transcription factor RUNX2 expression in human masseter muscle contributes to development of malocclusion. Archives of Oral Biology, 2014, 59(6):601-607.
Gu Y, Liu H, et al. miR-22/KAT6B axis is a chemotherapeutic determiner via regulation of PI3k-Akt-NF-kB pathway in tongue squamous cell carcinoma. Journal of Experimental & Clinical Cancer Research Cr, 2018, 37.

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