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FLASH GENE

Symbol

ACTL6B

contributors: mct - updated : 06-06-2019

HGNC name	actin-like 6B
HGNC id	160

FLASH GENE DNA RNA EXPRESSION PROTEIN DISORDER ANIMAL & CELL MODELS

EXPRESSION

Type	restricted

expressed in	(based on citations)
organ(s)	System Organ level 1 Organ level 2 Organ level 3 Organ level 4 Level Pubmed Species Stage Rna symbol Nervous brain       specific

cell lineage

cell lines

fluid/secretion

at STAGE

PROTEIN

PHYSICAL PROPERTIES

STRUCTURE

motifs/domains

small member of actin-typical domain

HOMOLOGY

interspecies	homolog to yeast S. cerevisiae SWI/SNF complex
	homolog to Drosophila SWI/SNF complex
	ortholog to murine Actl6
	homolog to C.elegans ZK616.4

intraspecies

homolog to BAF53A

Homologene

FAMILY

member of a family of actin-related proteins (ARPs)

CATEGORY

DNA associated , protooncogene

SUBCELLULAR LOCALIZATION	intracellular
	intracellular,nucleus,nucleolus

basic FUNCTION	involved in the regulation of genes by structural modulation of their chromatin specifically in the brain
	required for maximal ATPase activity of BRG1 and for association of the complex with chromatin/matrix
	role for ACTL6B in nucleus accumbens (NAc) neuronal function required for cocaine-associated memories, and also BDNF/TrkB activation in the NAc may overcome memory and plasticity deficits linked to ACTL6B mutations
	critical role of ACTL6B in the lateral amygdala neurons for memory consolidation during long-term memory formation
	role for ACTL6B in neurodevelopment

CELLULAR PROCESS	nucleotide, chromatin organization, remodeling
	nucleotide, transcription, regulation

PHYSIOLOGICAL PROCESS

text	structural constituent of cytoskeleton
	establishment and/or maintenance of chromatin architecture

PATHWAY

metabolism

signaling

a component	subunit of the BAF (BRG1/brm-associated factor) complex
	component of the chromatin remodeling machinery including the BAF complex

INTERACTION

DNA

binding

RNA

small molecule

protein	binding to BRG1 and BRM
	deleting HDAC3 can ameliorate the impairments in both long-term memory and synaptic plasticity caused by ACTL6B mutation
	BDNF rescues ACTL6B-dependent synaptic plasticity and cocaine-associated memory in the nucleus accumbens
	ACTL6B expression was induced upon neural cells becoming post-mitotic

cell & other

REGULATION

Other

is induced after learning, and such increase of ACTL6B level facilitates memory consolidation likely by regulating learning-related spine structural plasticity

ASSOCIATED DISORDERS

corresponding disease(s)

MREES

Susceptibility

Variant & Polymorphism

Candidate gene

Marker

Therapy target

ANIMAL & CELL MODELS

Actl6b knock-out (KO) mouse have deficits in dendritic spine and synapse function, leading to impaired long-term memory and poor survival