KAT6B

(redirected from MYST4)

KAT6B

A gene on chromosome 10q22.2 that encodes a histone acetyltransferase which, depending on the context, up- or downregulates transcription. KAT6B is required for RUNX2-dependent transcriptional activation and may be involved in development of the cerebral cortex. It is part of the MOZ/MORF complex, which has histone H3 acetyltransferase activity.

Molecular pathology
Defects in KAT6B are a cause of genitopatellar syndrome and Ohdo syndrome (SBBYS variant). Chromosomal defects  of KAT6B have been linked to acute myeloid leukaemias via translocation t(10;16)(q22;p13) with CREBBP.
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References in periodicals archive ?
So far, heterozygous pathogenic variants have been documented in seventeen genes (PTPN11, SOS1, SOS2, KRAS, NRAS, RAF1, SHOC2, CBL, RRAS, RIT1, RASA2, MAP3K8, SPRY1, MYST4, LZTR1, A2ML1, and PP1CB) that underlie this disorder or clinically related phenotypes [1, 2].
Bioinformatic analysis indicated a limited group of genes with conserved 3'UTR binding sites for miR-487b, including the histone acetyl transferase (HAT) Kat6b (MYST4), which is the focus of this manuscript.
We also examined the role of miR-487b in regulating the expression of Kat6b (MYST4).
Since Kat6B (MYST4, MORF) was identified as a potential target of miR-487b (Figure 1), we studied the expression of Kat6b, as well as the other members of the MYST family of HATs, in the response of macrophages to LPS (M1) and LPS/NECA (M2d) activation.
MYST4 CD109, Inhibit the IL21, PLD2 expression of BCR-ABL miR-451 Associated with TSC1, ACADSB, [75] Bcr-Abl GRSF1, MAML1, GDI1, NAMPT miR-29b Inhibits ABL1 and HAS3, SNX24, BCR/ABL1 there by CD93, SCML2, [76] inhibiting cell COL7A1, ZNF396, growth and colony HMGCR, ICOS formation miR-138 Represses BCR/ABL1 KLF12, H3F3B, [77] and CCND3, MYO5C, NXN, NEBL, increases by GATA1 PDPN, STK38 miR-212 Increases the APAF1, EP300, [78] ABCG2 expression EDNRA, CFL2, NOS1, SOX4, SOX11